Obsessive-compulsive: A form of personality (or personality disorder) marked by obsessions and compulsions.
Saturday, June 18, 2011
Oath of Maimonides
Oath of Maimonides: A prayer that is said to have been written by the 12th-century physician-philosopher Moses Maimonides. Like the famous oath of Hippocrates, the prayer of Maimonides is often recited by new medical graduates. This prayer, which is also called the "Prayer of Moses Maimonides", is now thought to have been written, not by Maimonides, but by Marcus Herz, a German physician, pupil of the the German philosopher Immanual Kant, and physician to the great English philantropist Moses Mendelssohn. The prayer first appeared in print in 1793 which may be when it was written. Irrespective of who wrote it, it is an extraordinary prayer. It reads as follows: "Almighty God, Thou has created the human body with infinite wisdom. Ten thousand times ten thousand organs hast Thou combined in it that act unceasingly and harmoniously to preserve the whole in all its beauty the body which is the envelope of the immortal soul. They are ever acting in perfect order, agreement and accord. Yet, when the frailty of matter or the unbridling of passions deranges this order or interrupts this accord, then forces clash and the body crumbles into the primal dust from which it came. Thou sendest to man diseases as beneficent messengers to foretell approaching danger and to urge him to avert it. "Thou has blest Thine earth, Thy rivers and Thy mountains with healing substances; they enable Thy creatures to alleviate their sufferings and to heal their illnesses. Thou hast endowed man with the wisdom to relieve the suffering of his brother, to recognize his disorders, to extract the healing substances, to discover their powers and to prepare and to apply them to suit every ill. In Thine Eternal Providence Thou hast chosen me to watch over the life and health of Thy creatures. I am now about to apply myself to the duties of my profession. Support me, Almighty God, in these great labors that they may benefit mankind, for without Thy help not even the least thing will succeed. "Inspire me with love for my art and for Thy creatures. Do not allow thirst for profit, ambition for renown and admiration, to interfere with my profession, for these are the enemies of truth and of love for mankind and they can lead astray in the great task of attending to the welfare of Thy creatures. Preserve the strength of my body and of my soul that they ever be ready to cheerfully help and support rich and poor, good and bad, enemy as well as friend. In the sufferer let me see only the human being. Illumine my mind that it recognize what presents itself and that it may comprehend what is absent or hidden. Let it not fail to see what is visible, but do not permit it to arrogate to itself the power to see what cannot be seen, for delicate and indefinite are the bounds of the great art of caring for the lives and health of Thy creatures. Let me never be absent- minded. May no strange thoughts divert my attention at the bedside of the sick, or disturb my mind in its silent labors, for great and sacred are the thoughtful deliberations required to preserve the lives and health of Thy creatures. "Grant that my patients have confidence in me and my art and follow my directions and my counsel. Remove from their midst all charlatans and the whole host of officious relatives and know-all nurses, cruel people who arrogantly frustrate the wisest purposes of our art and often lead Thy creatures to their death. "Should those who are wiser than I wish to improve and instruct me, let my soul gratefully follow their guidance; for vast is the extent of our art. Should conceited fools, however, censure me, then let love for my profession steel me against them, so that I remain steadfast without regard for age, for reputation, or for honor, because surrender would bring to Thy creatures sickness and death. "Imbue my soul with gentleness and calmness when older colleagues, proud of their age, wish to displace me or to scorn me or disdainfully to teach me. May even this be of advantage to me, for they know many things of which I am ignorant, but let not their arrogance give me pain. For they are old and old age is not master of the passions. I also hope to attain old age upon this earth, before Thee, Almighty God! "Let me be contented in everything except in the great science of my profession. Never allow the thought to arise in me that I have attained to sufficient knowledge, but vouchsafe to me the strength, the leisure and the ambition ever to extend my knowledge. For art is great, but the mind of man is ever expanding. "Almighty God! Thou hast chosen me in Thy mercy to watch over the life and death of Thy creatures. I now apply myself to my profession. Support me in this great task so that it may benefit mankind, for without Thy help not even the least thing will succeed."
Oat cell cancer
Oat cell cancer: A type of lung cancer in which the cells look like oats. Also called small cell lung cancer.
Prevalence of Viral Illness Immediately Prior to Presentation of Anorexia Nervosa
Professor Mike Thomas,
University of Chester, UK
Abstract
Purpose: The study investigated the prevalence of illness, particularly viral, immediately prior to the onset of anorexia nervosa during puberty.
Design and Method: A retrospective evaluation of clinical care records which identified viral onset illness. Two hundred records were scrutinised of which ninety-seven explicitly recorded the DSM-IV-TR (2000) criteria for Anorexia Nervosa diagnosis.Findings: Thirteen individuals were identified as having experienced a viral illness during puberty and immediately prior to onset of Anorexia Nervosa presentation.
Implications: Further research should be undertaken to ascertain correlation between viral illness and pubescent onset of Anorexia Nervosa. Further work using a clinical inter-disciplinary approach should be undertaken to gain more knowledge regarding the potential for post-viral effects to influence digestion and psychological balance during puberty.
Background
The study objective was to obtain the prevalence of adolescent onset viral-based illnesses prior to the development of severe and enduring eating disorders to provide additional data which builds upon earlier observations and which has practice implications for mental health interventions. Park et al. (1995) commented that the pathogenesis of eating disorders remains indistinct and fragmented and despite some advances in several areas the situation remains similar today. Their work is often cited as an interesting observation yet little further work has built upon their proposal that there may be a possible post-viral disruption involving corticotrophin-releasing hormones (CRH) regulation.
The influence of the hypothalamic-pituitary-adrenal axis in the regulation of eating patterns has been known for nearly half a century. There has been observation of anorexia nervosa symptoms amongst patients diagnosed with hypothalamic and mid-brain tumours (Lewin, Mattingly & Millis, 1972); whilst others discussed anorexia nervosa as a type of depressive illness closely mimicking post-viral depression (Cantwell, Struzenberger, Burroughs, Salkin & Green, 1977) or found a clear relationship between anorexia nervosa and other diagnostic criteria for physical illness (Patton, Wood & Johnson-Sabine, 1986); whilst Park et al. (1995) indicated a possible post-viral disturbance of neuroendocrine responses.
Others such as Maes, Goosens, Scharp, Metzer, D’Hondt and Cosyns (1994) have examined lowered serum prolyl-endopetidase enzyme activity amongst clients diagnosed with major depression and concluded that peptides play a part in the pathophysiology of depression. This is of interest because low mood is a known presenting symptom by clients experiencing anorexia nervosa and is considered by the Diagnostic and Statistical Manual of Mental Disorders IV (DSM IV 1994) as a co-morbid condition amongst clients experiencing bulimia nervosa. Park et al (1995) described four individuals with a diagnosis of severe restrictive anorexia nervosa who self-reported earlier episodes of glandular-fever like illnesses immediately before the onset of eating disorders. One was a nineteen year old woman who had presented with monospot positive glandular fever which caused loss of appetite, weight, menses and mood. Within three months of post-recovery she was diagnosed with anorexia nervosa (Body Mass Index (BMI) = 11.7). Neither she nor her immediate family had any previous psychiatric history and there was no previous history of dieting or of bingeing. At the age of seven years she reported a resolved case of “arthritis” but had no other relevant or significant physical ill-health. Despite regaining weight leading to discharge the woman was readmitted due to rapid relapse. The second client was a thirty-three year old woman with a twelve year history of sub-clinical eating disorder leading to a diagnosis of anorexia nervosa at the age of thirty years. The client had a co-morbid condition of multiple sclerosis and connective tissue disorder and recalled her eating disorder precipitating immediately after suffering glandular fever at the age of eighteen years. The woman was also diagnosed with irritable bowel syndrome. The third client, a woman age twenty-nine years, had a history of restrictive anorexia nervosa since the age of seventeen years following presentation of glandular fever-like symptoms when she was sixteen. Investigations demonstrated adenoviral infection but monospot was negative. There was no family history of mental health problems. The woman had a recurrent urinary tract infection at the age of twelve years which was treated with steroids. There were no other relevant or notable physical illnesses. At the time of the study she was admitted with a BMI of 10. The final case was a thirty-five year old woman with a history of restrictive anorexia nervosa. She recalled at the age of fifteen years a severe episode of pharyngitis and a loss of twelve kilograms in weight. Six months later she was referred to the mental health services and diagnosed with anorexia nervosa. At the age of twenty-nine years the client was diagnosed with a co-morbid obsessive-compulsive disorder and anorexia nervosa. For the past six years the client had spent all but nine months as an in-patient.
Park et al. (1995) suggested that there may be a possibility that viral infections could be a factor in many more cases of eating disorders but these may not be noted unless the infection is of such severity to invoke retention in the individuals memory or a referral to a medical practitioner who would record such illnesses in case notes. They postulated that the loss of appetite and weight commonly presented during a viral illness may precipitate anorexia nervosa in vulnerable individuals or that post-viral melancholy may precipitate a co-morbid depressive anorexia nervosa. Such a proposal replicates other similar conclusions by Cantwell et al. (1977) and Goodwin (1990) and additionally they put forward a further alternative that there may be viral induced alterations in neuroendocrine functions which precipitates restrictive eating disorders. The actual mechanism may be masked by clinical interventions to deal with weight loss and abnormalities in hypothalamic-pituitary results may be due to a primary post-viral cause or be caused by restricted food input and sudden weight loss. Weight gain causes a rebalance in results and may be hiding original sources. For example corticotrophin sensitivity to the inhibitory effects of free fatty acids is preserved in individuals experiencing anorexia nervosa despite persistent adrenal hyperactivity (Lanfranco, Giannotti, Picu, Giordano, Daga, Mondelli, Malfi, Fassino, Ghigo & Arvat, 2006) whilst plasma levels of homovanillic acid (pHVA) recover to within normal levels when individuals experiencing anorexia nervosa gain weight alongside psychopathological improvements suggesting a dopaminergic dysfunction amongst individuals with co-morbid depression (Castro, Deulofeu, Baeza, Casulai, Saura, Laizaro, Puig, Toro & Bernado, 2008). Interestingly Park et al’s (1995) study points out that similar abnormality had been found in the hypothalamic-pituitary-adrenal axis in patients with myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS). This is supported by Chia, Chia, Voeller, Lee and Changs’ (2009) more recent study demonstrating three patients with acute enterovirus infections who subsequently developed ME/CFS and who provided evidence of persistent viral infections through the presentation of VP1 and RNA found in the stomach.
Cooling May Reduce Brain Lesions in Newborns
THURSDAY, Nov. 5 (HealthDay News) -- Babies who are deprived of oxygen at birth often go on to have lifetime disabilities, but research has shown that cooling infants can help prevent problems.
Now, a new study reports that the cooling actually reduces the number of brain lesions in the babies.
Oxygen starvation at birth can cause a condition called hypoxic-ischemic encephalopathy, which can be fatal. Oxygen starvation also accounts for about 20 percent of cerebral palsy cases.
An earlier study found that chilling infants who suffer from oxygen deprivation can help reduce rates of cerebral palsy and improve their motor skills later in life. In the new study, reported online Nov. 5 and in the January issue of The Lancet Neurology, researchers investigated whether MRI scans would reveal fewer cerebral lesions in infants who were cooled.
That turned out to be the case. After reviewing MRI brain scans of 131 infants, they found 30 to 40 percent fewer lesions in areas of the brain where neurological development occurs. The infants who underwent cooling were three times more likely than those who didn't to have normal scans.
The scans also allowed doctors to predict with more than an 80 percent degree of certainty whether the infants would die or be disabled by the time they were 18 months old. The accuracy rate was 84 percent for the infants who were cooled and 81 percent for those who were not.
SOURCE: The Lancet Neurology, news release, Nov. 4, 2009 HealthDay
Now, a new study reports that the cooling actually reduces the number of brain lesions in the babies.
Oxygen starvation at birth can cause a condition called hypoxic-ischemic encephalopathy, which can be fatal. Oxygen starvation also accounts for about 20 percent of cerebral palsy cases.
An earlier study found that chilling infants who suffer from oxygen deprivation can help reduce rates of cerebral palsy and improve their motor skills later in life. In the new study, reported online Nov. 5 and in the January issue of The Lancet Neurology, researchers investigated whether MRI scans would reveal fewer cerebral lesions in infants who were cooled.
That turned out to be the case. After reviewing MRI brain scans of 131 infants, they found 30 to 40 percent fewer lesions in areas of the brain where neurological development occurs. The infants who underwent cooling were three times more likely than those who didn't to have normal scans.
The scans also allowed doctors to predict with more than an 80 percent degree of certainty whether the infants would die or be disabled by the time they were 18 months old. The accuracy rate was 84 percent for the infants who were cooled and 81 percent for those who were not.
SOURCE: The Lancet Neurology, news release, Nov. 4, 2009 HealthDay
Defibrillator, implantable cardiac
Defibrillator, implantable cardiac: A device put within the body that is designed to recognize certain types of abnormal heart rhythms (arrhythmias) and correct them. Defibrillators continuously monitor the heart rhythm in order to detect rapid arrhythmias such as Ventricular tachycardia (rapid regular beating of the ventricles, the bottom chambers of the heart); and Ventricular fibrillation (rapid irregular beating of the venticles). These ventricular arrhythmias impair the pumping efficiency of the heart and greatly raise the risks of fainting (syncope) and sudden cardiac arrest. They tend to develop in people with coronary artery disease and heart muscle diseases (cardiomyopathies). They are life- threatening. A defibrillator can be implanted within the body by far less invasive techniques than in the past because the devices, aside from being more technologically advanced, are smaller. (An implantable defibrillator is about the size of a minicassette). The defibrillator corrects the heart rhythm by delivering precisely calibrated and timed electrical shocks, when needed, to restore a normal heartbeat.
Decongestants
Decongestants: Drugs that shrink the swollen membranes in the nose and make it easier to breath. Decongestants can be taken orally or by nasal spray. Decongestant nasal spray should not be used for more than five days without the doctor"s advice, and if so, usually only when accompanied by a nasal steroid. Many decongestant nasal sprays often cause a rebound effect if taken too long. A rebound effect is the worsening of symptoms when a drug is discontinued. This is a result of a tissue dependence on the medication. Decongestants should not be used by patients with high blood pressure (hypertension) unless under doctor’s supervision.
Deafness-ichthyosis-keratitis syndrome
Daily Prayer of a Physician
Daltonism
Daltonism: Daltonism refers to colorblindness of the red-green type (also known as deuteranopia or deuteranomaly). The term "Daltonism" comes from the name of the English chemist and physicist, John Dalton (1766-1844). Born in a village in Cumberland where his father, Joseph, was a weaver in poor circumstances, Dalton was educated by his father and John Fletcher, teacher in a Quaker school. When Fletcher retired in 1778, Dalton took his place. In 1793 he was appointed teacher of mathematics and natural philosophy at New College in Manchester. In 1803 he put forth the facts embodied in his law of partial pressures: the pressure of a mixture of gases is the sum of the pressures which would be exerted separately by the several constituents if each alone were present. Dalton's reputation largely rests upon his great Atomic Theory. It was said of Dalton that, "into society he rarely went, and his only amusement was a game of bowls on Thursday afternoons." In the first scientific paper he published, Dalton described his (and his brother's) affliction of colorblindness with defective perception of red and green (Dalton, J: Extraordinary facts relating to the vision of colours, with observation. Mem Literary Philos Soc Manchester 5: 28-45, 1798). It is the first recognized account of red-green colorblindness.
Abdominal aneurysm
Abdominal aneurysm: An aneurysm situated within the abdomen (belly). An aneurysm is a localized widening (dilatation) of an artery, vein, or the heart. At the area of an aneurysm, there is typically a bulge and the wall is weakened and may rupture. The word ôaneurysmö comes from the Greek ôaneurysmaö meaning ôa widening.ö An aneurysm may involve the aorta, the largest artery in the body, as it courses down through the abdomen. Because of the great volume of blood flowing under high pressure in the aorta, rupture of an abdominal aortic aneurysm is a surefire catastrophe.
ACEBUTOLOLHYDROCHLORIDECAPSULES, USP200 mg and 400 mg
Acebutolol hydrochloride is a selective, hydrophilic beta-adrenoreceptor blocking agent with mild intrinsic sympathomimetic activity for use in treating patients with hypertension and ventricular arrhythmias. It is marketed in capsule form for oral administration. Acebutolol Hydrochloride Capsules, USP are available in two strengths which contain 200 or 400 mg of acebutolol as the hydrochloride salt. The inactive ingredients are gelatin, methylparaben, povidone, pregelatinized starch, propylparaben, sodium lauryl sulfate, stearic acid, titanium dioxide, FD&C Blue #1, FD&C Red #40, D&C Yellow #10, D&C Red #28, FD&C Blue #2, and black iron oxide.
Acebutolol HCl is a white or slightly off-white powder freely soluble in water, and less soluble in alcohol. Chemically it is defined as the hydrochloride salt of (±) N-[3-Acetyl-4-[2-hydroxy-3-[(1-methylethyl)amino]propoxy]phenyl] butanamide.
Acebutolol HCl is a white or slightly off-white powder freely soluble in water, and less soluble in alcohol. Chemically it is defined as the hydrochloride salt of (±) N-[3-Acetyl-4-[2-hydroxy-3-[(1-methylethyl)amino]propoxy]phenyl] butanamide.CLINICAL PHARMACOLOGY
Acebutolol is a cardioselective, beta-adrenoreceptor blocking agent, which possesses mild intrinsic sympathomimetic activity (ISA) in its therapeutically effective dose range.
Pharmacodynamics
β1-cardioselectivity has been demonstrated in experimental animal studies. In anesthetized dogs and cats, acebutolol is more potent in antagonizing isoproterenol-induced tachycardia (β1) than in antagonizing isoproterenol-induced vasodilatation (β2). In guinea pigs and cats, it is more potent in antagonizing this tachycardia than in antagonizing isoproterenol-induced bronchodilatation (β2). ISA of acebutolol has been demonstrated in catecholamine-depleted rats by tachycardia induced by intravenous administration of this agent. A membrane-stabilizing effect has been detected in animals, but only with high concentrations of acebutolol.
Clinical studies have demonstrated β1-blocking activity at the recommended doses by: a) reduction in the resting heart rate and decrease in exercise-induced tachycardia; b) reduction in cardiac output at rest and after exercise; c) reduction of systolic and diastolic blood pressures at rest and postexercise; d) inhibition of isoproterenol-induced tachycardia.
The β1-selectivity of acebutolol has also been demonstrated on the basis of the following vascular and bronchial effects:
Clinical studies have demonstrated β1-blocking activity at the recommended doses by: a) reduction in the resting heart rate and decrease in exercise-induced tachycardia; b) reduction in cardiac output at rest and after exercise; c) reduction of systolic and diastolic blood pressures at rest and postexercise; d) inhibition of isoproterenol-induced tachycardia.
The β1-selectivity of acebutolol has also been demonstrated on the basis of the following vascular and bronchial effects:
Pharmacokinetics and Metabolism
Acebutolol is well absorbed from the GI tract. It is subject to extensive first-pass hepatic biotransformation, with an absolute bioavailability of approximately 40% for the parent compound. The major metabolite, an N-acetyl derivative (diacetolol), is pharmacologically active. This metabolite is equipotent to acebutolol and in cats is more cardioselective than acebutolol; therefore, this first-pass phenomenon does not attenuate the therapeutic effect of acebutolol. Food intake does not have a significant effect on the area under the plasma concentration-time curve (AUC) of acebutolol although the rate of absorption and peak concentration decreased slightly.
The plasma elimination half-life of acebutolol is approximately 3 to 4 hours, while that of its metabolite, diacetolol, is 8 to 13 hours. The time to reach peak concentration for acebutolol is 2.5 hours and for diacetolol, after oral administration of acebutolol hydrochloride, 3.5 hours.
Within the single oral dose range of 200 to 400 mg, the kinetics are dose proportional. However, this linearity is not seen at higher doses, probably due to saturation of hepatic biotransformation sites. In addition, after multiple dosing the lack of linearity is also seen by AUC increases of approximately 100% as compared to single oral dosing. Elimination via renal excretion is approximately 30% to 40% and by non-renal mechanisms 50% to 60%, which includes excretion into the bile and direct passage through the intestinal wall.
Acebutolol hydrochloride has a low binding affinity for plasma proteins (about 26%).
Acebutolol and its metabolite, diacetolol, are relatively hydrophilic and, therefore, only minimal quantities have been detected in the cerebrospinal fluid (CSF).
Drug interaction studies with tolbutamide and warfarin indicated no influence on the therapeutic effects of these compounds. Digoxin and hydrochlorothiazide plasma levels were not affected by concomitant acebutolol administration. The kinetics of acebutolol were not significantly altered by concomitant administration of hydrochlorothiazide, hydralazine, sulfinpyrazone, or oral contraceptives.
In patients with renal impairment, there is no effect on the elimination half-life of acebutolol, but there is decreased elimination of the metabolite, diacetolol, resulting in a two- to three-fold increase in its half-life. For this reason, the drug should be administered with caution in patients with renal insufficiency (see PRECAUTIONS). Acebutolol and its major metabolite are dialyzable.
Acebutolol crosses the placental barrier, and is secreted in breast milk.
In geriatric patients, the bioavailability of acebutolol and its metabolite is increased, approximately two-fold, probably due to decreases in the first-pass metabolism and renal function in the elderly.
The plasma elimination half-life of acebutolol is approximately 3 to 4 hours, while that of its metabolite, diacetolol, is 8 to 13 hours. The time to reach peak concentration for acebutolol is 2.5 hours and for diacetolol, after oral administration of acebutolol hydrochloride, 3.5 hours.
Within the single oral dose range of 200 to 400 mg, the kinetics are dose proportional. However, this linearity is not seen at higher doses, probably due to saturation of hepatic biotransformation sites. In addition, after multiple dosing the lack of linearity is also seen by AUC increases of approximately 100% as compared to single oral dosing. Elimination via renal excretion is approximately 30% to 40% and by non-renal mechanisms 50% to 60%, which includes excretion into the bile and direct passage through the intestinal wall.
Acebutolol hydrochloride has a low binding affinity for plasma proteins (about 26%).
Acebutolol and its metabolite, diacetolol, are relatively hydrophilic and, therefore, only minimal quantities have been detected in the cerebrospinal fluid (CSF).
Drug interaction studies with tolbutamide and warfarin indicated no influence on the therapeutic effects of these compounds. Digoxin and hydrochlorothiazide plasma levels were not affected by concomitant acebutolol administration. The kinetics of acebutolol were not significantly altered by concomitant administration of hydrochlorothiazide, hydralazine, sulfinpyrazone, or oral contraceptives.
In patients with renal impairment, there is no effect on the elimination half-life of acebutolol, but there is decreased elimination of the metabolite, diacetolol, resulting in a two- to three-fold increase in its half-life. For this reason, the drug should be administered with caution in patients with renal insufficiency (see PRECAUTIONS). Acebutolol and its major metabolite are dialyzable.
Acebutolol crosses the placental barrier, and is secreted in breast milk.
In geriatric patients, the bioavailability of acebutolol and its metabolite is increased, approximately two-fold, probably due to decreases in the first-pass metabolism and renal function in the elderly.
INDICATIONS AND USAGE
Hypertension
Acebutolol hydrochloride capsules are indicated for the management of hypertension in adults. They may be used alone or in combination with other antihypertensive agents, especially thiazide-type diuretics.
Ventricular Arrhythmias
Acebutolol hydrochloride capsules are indicated in the management of ventricular premature beats; it reduces the total number of premature beats, as well as the number of paired and multiform ventricular ectopic beats, and R-on-T beats.
CONTRAINDICATIONS
Acebutolol hydrochloride capsules are contraindicated in: 1) persistently severe bradycardia; 2) second- and third-degree heart block; 3) overt cardiac failure; and 4) cardiogenic shock (see WARNINGS).
WARNINGS
Cardiac Failure
Sympathetic stimulation may be essential for support of the circulation in individuals with diminished myocardial contractility, and its inhibition by beta-adrenergic receptor blockade may precipitate more severe failure. Although beta blockers should be avoided in overt cardiac failure, acebutolol can be used with caution in patients with a history of heart failure who are controlled with digitalis and/or diuretics. Both digitalis and acebutolol impair AV conduction. If cardiac failure persists, therapy with acebutolol should be withdrawn.
In Patients Without a History of Cardiac Failure
In patients with aortic or mitral valve disease or compromised left ventricular function, continued depression of the myocardium with beta-blocking agents over a period of time may lead to cardiac failure. At the first signs of failure, patients should be digitalized and/or be given a diuretic and the response observed closely. If cardiac failure continues despite adequate digitalization and/or diuretic, acebutolol therapy should be withdrawn.
Exacerbation of Ischemic Heart Disease Following Abrupt Withdrawal
Following abrupt cessation of therapy with certain beta-blocking agents in patients with coronary artery disease, exacerbation of angina pectoris and, in some cases, myocardial infarction and death have been reported. Therefore, such patients should be cautioned against interruption of therapy without a physician's advice. Even in the absence of overt ischemic heart disease, when discontinuation of acebutolol is planned, the patient should be carefully observed, and should be advised to limit physical activity to a minimum while acebutolol is gradually withdrawn over a period of about two weeks. (If therapy with an alternative beta-blocker is desired, the patient may be transferred directly to comparable doses of another agent without interruption of beta-blocking therapy.) If an exacerbation of angina pectoris occurs, antianginal therapy should be restarted immediately in full doses and the patient hospitalized until his condition stabilizes.
Peripheral Vascular Disease
Treatment with beta-antagonists reduces cardiac output and can precipitate or aggravate the symptoms of arterial insufficiency in patients with peripheral or mesenteric vascular disease. Caution should be exercised with such patients, and they should be observed closely for evidence of progression of arterial obstruction.
Bronchospastic Diseases
PATIENTS WITH BRONCHOSPASTIC DISEASE SHOULD, IN GENERAL, NOT RECEIVE A BETA BLOCKER. Because of its relative β1-selectivity, however, low doses of acebutolol may be used with caution in patients with bronchospastic disease who do not respond to, or who cannot tolerate, alternative treatment. Since β1-selectivity is not absolute and is dose-dependent, the lowest possible dose of acebutolol should be used initially, preferably in divided doses to avoid the higher plasma levels associated with the longer dose-interval. A bronchodilator, such as a theophylline or a β2-stimulant, should be made available in advance with instructions concerning its use.
Anesthesia and Major Surgery
The necessity, or desirability, of withdrawal of a beta-blocking therapy prior to major surgery is controversial. Beta-adrenergic receptor blockade impairs the ability of the heart to respond to beta-adrenergically mediated reflex stimuli. While this might be of benefit in preventing arrhythmic response, the risk of excessive myocardial depression during general anesthesia may be enhanced and difficulty in restarting and maintaining the heart beat has been reported with beta blockers. If treatment is continued, particular care should be taken when using anesthetic agents which depress the myocardium, such as ether, cyclopropane and trichlorethylene, and it is prudent to use the lowest possible dose of acebutolol. Acebutolol, like other beta blockers, is a competitive inhibitor of beta-receptor agonists, and its effect on the heart can be reversed by cautious administration of such agents (e.g., dobutamine or isoproterenol-see OVERDOSAGE).
Manifestations of excessive vagal tone (e.g., profound bradycardia, hypotension) may be corrected with atropine 1 to 3 mg IV in divided doses.
Manifestations of excessive vagal tone (e.g., profound bradycardia, hypotension) may be corrected with atropine 1 to 3 mg IV in divided doses.
Diabetes and Hypoglycemia
Beta blockers may potentiate insulin-induced hypoglycemia and mask some of its manifestations such as tachycardia; however, dizziness and sweating are usually not significantly affected. Diabetic patients should be warned of the possibility of masked hypoglycemia.
Thyrotoxicosis
Beta-adrenergic blockade may mask certain clinical signs (tachycardia) of hyperthyroidism. Abrupt withdrawal of beta blockade may precipitate a thyroid storm; therefore, patients suspected of developing thyrotoxicosis from whom acebutolol therapy is to be withdrawn should be monitored closely.
PRECAUTIONS
Risk of Anaphylactic Reaction
While taking beta-blockers, patients with a history of severe anaphylactic reaction to a variety of allergens may be more reactive to repeated challenge, either accidental, diagnostic, or therapeutic. Such patients may be unresponsive to the usual doses of epinephrine used to treat allergic reaction.
Impaired Renal or Hepatic Function
Studies on the effect of acebutolol in patients with renal insufficiency have not been performed in the United States. Foreign published experience shows that acebutolol has been used successfully in chronic renal insufficiency. Acebutolol is excreted through the G.I. tract, but the active metabolite, diacetolol, is eliminated predominantly by the kidney. There is a linear relationship between renal clearance of diacetolol and creatinine clearance. Therefore, the daily dose of acebutolol should be reduced by 50% when the creatinine clearance is less than 50 mL/min and by 75% when it is less than 25 mL/min. Acebutolol should be used cautiously in patients with impaired hepatic function.
Acebutolol has been used successfully and without problems in elderly patients in the U.S. clinical trials without specific adjustment of dosage. However, elderly patients may require lower maintenance doses because the bioavailability of both acebutolol and its metabolite are approximately doubled in this age group.
Acebutolol has been used successfully and without problems in elderly patients in the U.S. clinical trials without specific adjustment of dosage. However, elderly patients may require lower maintenance doses because the bioavailability of both acebutolol and its metabolite are approximately doubled in this age group.
Information for Patients
Patients, especially those with evidence of coronary artery disease, should be warned against interruption or discontinuation of acebutolol therapy without a physician's supervision. Although cardiac failure rarely occurs in properly selected patients, those being treated with beta-adrenergic blocking agents should be advised to consult a physician if they develop signs or symptoms suggestive of impending CHF, or unexplained respiratory symptoms.
Patients should also be warned of possible severe hypertensive reactions from concomitant use of alpha-adrenergic stimulants, such as the nasal decongestants commonly used in OTC cold preparations and nasal drops.
Patients should also be warned of possible severe hypertensive reactions from concomitant use of alpha-adrenergic stimulants, such as the nasal decongestants commonly used in OTC cold preparations and nasal drops.
Clinical Laboratory Findings
Acebutolol, like other beta-blockers, has been associated with the development of antinuclear antibodies (ANA). In prospective clinical trials, patients receiving acebutolol had a dose-dependent increase in the development of positive ANA titers and the overall incidence was higher than that observed with propranolol. Symptoms (generally persistent arthralgias and myalgias) related to this laboratory abnormality were infrequent (less than 1% with both drugs). Symptoms and ANA titers were reversible upon discontinuation of treatment.
Drug Interactions
Catecholamine-depleting drugs, such as reserpine, may have an additive effect when given with beta-blocking agents. Patients treated with acebutolol plus catecholamine depletors should, therefore, be observed closely for evidence of marked bradycardia or hypotension which may present as vertigo, syncope/presyncope, or orthostatic changes in blood pressure without compensatory tachycardia. Exaggerated hypertensive responses have been reported from the combined use of beta-adrenergic antagonists and alpha-adrenergic stimulants, including those contained in proprietary cold remedies and vasoconstrictive nasal drops. Patients receiving beta-blockers should be warned of this potential hazard.
Blunting of the antihypertensive effect of beta-adrenoceptor blocking agents by non-steroidal anti-inflammatory drugs has been reported.
No significant interactions with digoxin, hydrochlorothiazide, hydralazine, sulfinpyrazone, oral contraceptives, tolbutamide, or warfarin have been observed.
Blunting of the antihypertensive effect of beta-adrenoceptor blocking agents by non-steroidal anti-inflammatory drugs has been reported.
No significant interactions with digoxin, hydrochlorothiazide, hydralazine, sulfinpyrazone, oral contraceptives, tolbutamide, or warfarin have been observed.
Carcinogenesis, Mutagenesis, Impairment of Fertility
Chronic oral toxicity studies in rats and mice, employing dose levels as high as 300 mg/kg/day, which is equivalent to 15 times the maximum recommended (60 kg) human dose, did not indicate a carcinogenic potential for acebutolol. Diacetolol, the major metabolite of acebutolol in man, was without carcinogenic potential in rats when tested at doses as high as 1800 mg/kg/day. Acebutolol and diacetolol were also shown to be devoid of mutagenic potential in the Ames Test. Acebutolol, administered orally to two generations of male and female rats at doses of up to 240 mg/kg/day (equivalent to 12 times the maximum recommended therapeutic dose in a 60-kg human) and diacetolol, administered to two generations of male and female rats at doses of up to 1000 mg/kg/day, had no significant impact on reproductive performance or fertility.
Pregnancy
Teratogenic Effects
Labor And Delivery
The effect of acebutolol on labor and delivery in pregnant women is unknown. Studies in animals have not shown any effect of acebutolol on the usual course of labor and delivery.
Nursing Mothers
A-METHAPREDMethylprednisolone SodiumSuccinate for Injection, USP
A-METHAPREDMethylprednisolone SodiumSuccinate for Injection, USP
Rx only
For Intravenous or Intramuscular Administration
For Intravenous or Intramuscular Administration
DESCRIPTION
A-Methapred (methylprednisolone sodium succinate for injection, USP) sterile powder contains methylprednisolone sodium succinate as the active ingredient. Methylprednisolone sodium succinate, USP, occurs as a white, or nearly white, odorless hygroscopic, amorphous solid. It is very soluble in water and in alcohol; it is insoluble in chloroform and is very slightly soluble in acetone.
The chemical name for methylprednisolone sodium succinate is pregna-1,4-diene-3,20-dione,21-(3-carboxy-1-oxo-propoxy)-11,17-dihydroxy-6-methyl-monosodium salt, (6α, 11β), and the molecular weight is 496.53.
The structural formula is represented below:
Methylprednisolone sodium succinate is so extremely soluble in water that it may be administered in a small volume of diluent and is especially well suited for intravenous use in situations in which high blood levels of methylprednisolone are required rapidly.
A-Methapred is available in several strengths and packages for intravenous or intramuscular administration.
40 mg Single-Dose Vial− Each mL (when mixed) contains methylprednisolone sodium succinate equivalent to 40 mg methylprednisolone; also 1.6 mg monobasic sodium phosphate anhydrous; 17.46 mg dibasic sodium phosphate anhydrous; 25 mg lactose anhydrous; 8.8 mg benzyl alcohol added as preservative.
125 mg Single-Dose Vial− Each 2 mL (when mixed) contains methylprednisolone sodium succinate equivalent to 125 mg methylprednisolone; also 1.6 mg monobasic sodium phosphate anhydrous; 17.4 mg dibasic sodium phosphate anhydrous; 17.6 mg benzyl alcohol added as preservative.
When necessary, the pH of each formula was adjusted with sodium hydroxide so that the pH of the reconstituted solution is within the USP specified range of 7 to 8 and the tonicities are, for the 40 mg per mL solution, 0.50 osmolar; for the 125 mg per 2 mL, 0.40 osmolar; (Isotonic saline = 0.28 osmolar).
IMPORTANT− Use only Bacteriostatic Water For Injection with Benzyl Alcohol when reconstituting A-Methapred.
Use within 48 hours after mixing.
The chemical name for methylprednisolone sodium succinate is pregna-1,4-diene-3,20-dione,21-(3-carboxy-1-oxo-propoxy)-11,17-dihydroxy-6-methyl-monosodium salt, (6α, 11β), and the molecular weight is 496.53.
The structural formula is represented below:
Methylprednisolone sodium succinate is so extremely soluble in water that it may be administered in a small volume of diluent and is especially well suited for intravenous use in situations in which high blood levels of methylprednisolone are required rapidly.
A-Methapred is available in several strengths and packages for intravenous or intramuscular administration.
40 mg Single-Dose Vial− Each mL (when mixed) contains methylprednisolone sodium succinate equivalent to 40 mg methylprednisolone; also 1.6 mg monobasic sodium phosphate anhydrous; 17.46 mg dibasic sodium phosphate anhydrous; 25 mg lactose anhydrous; 8.8 mg benzyl alcohol added as preservative.
125 mg Single-Dose Vial− Each 2 mL (when mixed) contains methylprednisolone sodium succinate equivalent to 125 mg methylprednisolone; also 1.6 mg monobasic sodium phosphate anhydrous; 17.4 mg dibasic sodium phosphate anhydrous; 17.6 mg benzyl alcohol added as preservative.
When necessary, the pH of each formula was adjusted with sodium hydroxide so that the pH of the reconstituted solution is within the USP specified range of 7 to 8 and the tonicities are, for the 40 mg per mL solution, 0.50 osmolar; for the 125 mg per 2 mL, 0.40 osmolar; (Isotonic saline = 0.28 osmolar).
IMPORTANT− Use only Bacteriostatic Water For Injection with Benzyl Alcohol when reconstituting A-Methapred.
Use within 48 hours after mixing.
CLINICAL PHARMACOLOGY
Methylprednisolone is a potent anti-inflammatory steroid with greater anti-inflammatory potency than prednisolone and even less tendency than prednisolone to induce sodium and water retention.
Methylprednisolone sodium succinate has the same metabolic and anti-inflammatory actions as methylprednisolone. When given parenterally and in equimolar quantities, the two compounds are equivalent in biologic activity. The relative potency of A-Methapred sterile powder and hydrocortisone sodium succinate, as indicated by depression of eosinophil count, following intravenous administration, is at least four to one. This is in good agreement with the relative oral potency of methylprednisolone and hydrocortisone.
Methylprednisolone sodium succinate has the same metabolic and anti-inflammatory actions as methylprednisolone. When given parenterally and in equimolar quantities, the two compounds are equivalent in biologic activity. The relative potency of A-Methapred sterile powder and hydrocortisone sodium succinate, as indicated by depression of eosinophil count, following intravenous administration, is at least four to one. This is in good agreement with the relative oral potency of methylprednisolone and hydrocortisone.
INDICATIONS AND USAGE
When oral therapy is not feasible, and the strength, dosage form and route of administration of the drug reasonably lend the preparation to the treatment of the condition, A-Methapred sterile powder is indicated for intravenous or intramuscular use in the following conditions:
- Endocrine Disorders
• Primary or secondary adrenocortical insufficiency (hydrocortisone or cortisone is the drug of choice; synthetic analogs may be used in conjunction with mineralocorticoids where applicable; in infancy, mineralocorticoid supplementation is of particular importance)
• Acute adrenocortical insufficiency (hydrocortisone or cortisone is the drug of choice; mineralocorticoid supplementation may be necessary, particularly when synthetic analogs are used)
• Preoperatively and in the event of serious trauma or illness, in patients with known adrenal insufficiency or when adrenocortical reserve is doubtful
• Shock unresponsive to conventional therapy if adrenocortical insufficiency exists or is suspected
• Congenital adrenal hyperplasia
• Hypercalcemia associated with cancer
• Nonsuppurative thyroiditis - Rheumatic Disorders
As adjunctive therapy for short-term administration (to tide the patient over an acute episode or exacerbation) in:
• Post-traumatic osteoarthritis
• Synovitis of osteoarthritis
• Rheumatoid arthritis, including juvenile rheumatoid arthritis (selected cases may require low-dose maintenance therapy)
• Acute and subacute bursitis
• Epicondylitis
• Acute nonspecific tenosynovitis
• Acute gouty arthritis
• Psoriatic arthritis
• Ankylosing spondylitis - Collagen Diseases
During an exacerbation or as maintenance therapy in selected cases of:
• Systemic lupus erythematosus
• Systemic dermatomyositis (polymyositis)
• Acute rheumatic carditis - Dermatologic Diseases
• Pemphigus
• Severe erythema multi-forme (Stevens-Johnson syndrome)
• Exfoliative dermatitis
• Bullous dermatitis herpetiformis
• Severe seborrheic dermatitis
• Severe psoriasis
• Mycosis fungoides - Allergic States
Control of severe or incapacitating allergic conditions intractable to adequate trials of conventional treatment in:
• Bronchial asthma
• Contact dermatitis
• Atopic dermatitis
• Serum sickness
• Seasonal or perennial allergic rhinitis
• Drug hypersensitivity reactions
• Urticarial transfusion reactions
• Acute noninfectious laryngeal edema (epinephrine is the drug of first choice) - Ophthalmic Diseases
Severe acute and chronic allergic and inflammatory processes involving the eye, such as:
• Herpes zoster ophthalmicus
• Iritis, iridocyclitis
• Chorioretinitis
• Diffuse posterior uveitis and choroiditis
• Optic neuritis
• Sympathetic ophthalmia
• Anterior segment inflammation
• Allergic conjunctivitis
• Allergic corneal marginal ulcers
• Keratitis - Gastrointestinal Diseases
To tide the patient over a critical period of the disease in:
• Ulcerative colitis (systemic therapy)
• Regional enteritis (systemic therapy) - Respiratory Diseases
• Symptomatic sarcoidosis
• Berylliosis
• Fulminating or disseminated pulmonary tuberculosis when used concurrently with appropriate antituberculous chemotherapy
• Loeffler’s syndrome not manageable by other means
• Aspiration pneumonitis - Hematologic Disorders
• Acquired (autoimmune) hemolytic anemia
• Idiopathic thrombocytopenic purpura in adults (IV only; IM administration is contraindicated)
• Secondary thrombocytopenia in adults
• Erythroblastopenia (RBC anemia)
• Congenital (erythroid) hypoplastic anemia - Neoplastic Diseases
For palliative management of:
• Leukemias and lymphomas in adults
• Acute leukemia of childhood - Edematous States
• To induce diuresis or remission of proteinuria in the nephrotic syndrome, without uremia, of the idiopathic type or that due to lupus erythematosus - Nervous System
• Acute exacerbations of multiple sclerosis - Miscellaneous
• Tuberculous meningitis with subarachnoid block or impending block when used concurrently with appropriate antituberculous chemotherapy
• Trichinosis with neurologic or myocardial involvement
CONTRAINDICATIONS
The use of A-Methapred sterile powder is contraindicated in premature infants because the reconstitution diluent contains benzyl alcohol. Benzyl alcohol has been reported to be associated with a fatal “Gasping Syndrome” in premature infants. A-Methapred sterile powder is also contraindicated in systemic fungal infections and patients with known hypersensitivity to the product and its constituents.
WARNINGS
While on corticosteroid therapy patients should not be vaccinated against smallpox. Other immunization procedures should not be undertaken in patients who are on corticosteroids, especially on high dose, because of possible hazards of neurological complications and a lack of antibody response.
In patients on corticosteroid therapy subjected to any unusual stress, increased dosage of rapidly acting corticosteroids before, during, and after the stressful situation is indicated.
Corticosteroids may mask some signs of infection, and new infections may appear during their use. There may be decreased resistance and inability to localize infection when corticosteroids are used.
A study has failed to establish the efficacy of Methylprednisolone Sodium Succinate for Injection, USP in the treatment of sepsis syndrome and septic shock. The study also suggests that treatment of these conditions with Methylprednisolone Sodium Succinate for Injection, USP may increase the risk of mortality in certain patients (ie, patients with elevated serum creatinine levels or patients who develop secondary infections after Methylprednisolone Sodium Succinate for Injection, USP.
Prolonged use of corticosteroids may produce posterior subcapsular cataracts, glaucoma with possible damage to the optic nerves, and may enhance the establishment of secondary ocular infections due to fungi or viruses.
Usage in pregnancy. Since adequate human reproduction studies have not been done with corticosteroids, the use of these drugs in pregnancy, nursing mothers, or women of child-bearing potential requires that the possible benefits of the drug be weighed against the potential hazards to the mother and embryo or fetus. Infants born of mothers who have received substantial doses of corticosteroids during pregnancy should be carefully observed for signs of hypoadrenalism.
Average and large doses of cortisone or hydrocortisone can cause elevation of blood pressure, salt and water retention, and increased excretion of potassium. These effects are less likely to occur with the synthetic derivatives except when used in large doses. Dietary salt restriction and potassium supplementation may be necessary. All corticosteroids increase calcium excretion.
While on corticosteroid therapy patients should not be vaccinated against smallpox. Other immunization procedures should not be undertaken in patients who are on corticosteroids, especially on high dose, because of possible hazards of neurological complications and a lack of antibody response.
The use of Methylprednisolone Sodium Succinate for Injection, USP sterile powder in active tuberculosis should be restricted to those cases of fulminatingor disseminated tuberculosis in which the corticosteroid is used for the management of the disease in conjunction with appropriate antituberculous regimen.
If corticosteroids are indicated in patients with latent tuberculosis or tuberculin reactivity, close observation is necessary as reactivation of the disease may occur. During prolonged corticosteroid therapy, these patients should receive chemoprophylaxis.
Because rare instances of anaphylactic (eg, bronchospasm) reactions have occurred in patients receiving parenteral corticosteroid therapy, appropriate precautionary measures should be taken prior to administration, especially when the patient has a history of allergy to any drug.
There are reports of cardiac arrhythmias and/or circulatory collapse and/or cardiac arrest following the rapid administration of large IV doses of Methylprednisolone Sodium Succinate for Injection, USP (greater than 0.5 gram administered over a period of less than 10 minutes). Bradycardia has been reported during or after the administration of large doses of Methylprednisolone sodium succinate, and may be unrelated to the speed or duration of infusion.
Persons who are on drugs which suppress the immune system are more susceptible to infections than healthy individuals. Chicken pox and measles, for example, can have a more serious or even fatal course in non-immune children or adults on corticosteroids. In such children or adults who have not had these diseases, particular care should be taken to avoid exposure. How the dose, route and duration of corticosteroid administration affects the risk of developing a disseminated infection is not known. The contribution of the underlying disease and/or prior corticosteroid treatment to the risk is also not known. If exposed to chicken pox, prophylaxis with varicella zoster immune globulin (VZIG) may be indicated. If exposed to measles, prophylaxis with pooled intramuscular immunoglobulin (IG) may be indicated. (See the respective package inserts for complete VZIG and IG prescribing information.) If chicken pox develops, treatment with antiviral agents may be considered.
In patients on corticosteroid therapy subjected to any unusual stress, increased dosage of rapidly acting corticosteroids before, during, and after the stressful situation is indicated.
Corticosteroids may mask some signs of infection, and new infections may appear during their use. There may be decreased resistance and inability to localize infection when corticosteroids are used.
A study has failed to establish the efficacy of Methylprednisolone Sodium Succinate for Injection, USP in the treatment of sepsis syndrome and septic shock. The study also suggests that treatment of these conditions with Methylprednisolone Sodium Succinate for Injection, USP may increase the risk of mortality in certain patients (ie, patients with elevated serum creatinine levels or patients who develop secondary infections after Methylprednisolone Sodium Succinate for Injection, USP.
Prolonged use of corticosteroids may produce posterior subcapsular cataracts, glaucoma with possible damage to the optic nerves, and may enhance the establishment of secondary ocular infections due to fungi or viruses.
Usage in pregnancy. Since adequate human reproduction studies have not been done with corticosteroids, the use of these drugs in pregnancy, nursing mothers, or women of child-bearing potential requires that the possible benefits of the drug be weighed against the potential hazards to the mother and embryo or fetus. Infants born of mothers who have received substantial doses of corticosteroids during pregnancy should be carefully observed for signs of hypoadrenalism.
Average and large doses of cortisone or hydrocortisone can cause elevation of blood pressure, salt and water retention, and increased excretion of potassium. These effects are less likely to occur with the synthetic derivatives except when used in large doses. Dietary salt restriction and potassium supplementation may be necessary. All corticosteroids increase calcium excretion.
While on corticosteroid therapy patients should not be vaccinated against smallpox. Other immunization procedures should not be undertaken in patients who are on corticosteroids, especially on high dose, because of possible hazards of neurological complications and a lack of antibody response.
The use of Methylprednisolone Sodium Succinate for Injection, USP sterile powder in active tuberculosis should be restricted to those cases of fulminatingor disseminated tuberculosis in which the corticosteroid is used for the management of the disease in conjunction with appropriate antituberculous regimen.
If corticosteroids are indicated in patients with latent tuberculosis or tuberculin reactivity, close observation is necessary as reactivation of the disease may occur. During prolonged corticosteroid therapy, these patients should receive chemoprophylaxis.
Because rare instances of anaphylactic (eg, bronchospasm) reactions have occurred in patients receiving parenteral corticosteroid therapy, appropriate precautionary measures should be taken prior to administration, especially when the patient has a history of allergy to any drug.
There are reports of cardiac arrhythmias and/or circulatory collapse and/or cardiac arrest following the rapid administration of large IV doses of Methylprednisolone Sodium Succinate for Injection, USP (greater than 0.5 gram administered over a period of less than 10 minutes). Bradycardia has been reported during or after the administration of large doses of Methylprednisolone sodium succinate, and may be unrelated to the speed or duration of infusion.
Persons who are on drugs which suppress the immune system are more susceptible to infections than healthy individuals. Chicken pox and measles, for example, can have a more serious or even fatal course in non-immune children or adults on corticosteroids. In such children or adults who have not had these diseases, particular care should be taken to avoid exposure. How the dose, route and duration of corticosteroid administration affects the risk of developing a disseminated infection is not known. The contribution of the underlying disease and/or prior corticosteroid treatment to the risk is also not known. If exposed to chicken pox, prophylaxis with varicella zoster immune globulin (VZIG) may be indicated. If exposed to measles, prophylaxis with pooled intramuscular immunoglobulin (IG) may be indicated. (See the respective package inserts for complete VZIG and IG prescribing information.) If chicken pox develops, treatment with antiviral agents may be considered.
PRECAUTIONS
General Precautions
Drug-induced secondary adrenocortical insufficiency may be minimized by gradual reduction of dosage. This type of relative insufficiency may persist for months after discontinuation of therapy; therefore, in any situation of stress occurring during that period, hormone therapy should be reinstituted. Since mineralocorticoid secretion may be impaired, salt and/or a mineralocorticoid should be administered concurrently.
There is an enhanced effect of corticosteroids on patients with hypothyroidism and in those with cirrhosis.
Corticosteroids should be used cautiously in patients with ocular herpes simplex because of possible corneal perforation.
The lowest possible dose of corticosteroid should be used to control the condition under treatment, and when reduction in dosage is possible, the reduction should be gradual.
Psychic derangements may appear when corticosteroids are used, ranging from euphoria, insomnia, mood swings, personality changes, and severe depression, to frank psychotic manifestations. Also, existing emotional instability or psychotic tendencies may be aggravated by corticosteroids.
Aspirin should be used cautiously in conjunction with corticosteroids in hypoprothrombinemia.
Steroids should be used with caution in nonspecific ulcerative colitis, if there is a probability of impending perforation, abscess or other pyogenic infection; diverticulitis; fresh intestinal anastomoses; active or latent peptic ulcer; renal insufficiency; hypertension; osteoporosis; and myasthenia gravis.
Growth and development of infants and children on prolonged corticosteroid therapy should be carefully observed.
Although controlled clinical trials have shown corticosteroids to be effective in speeding the resolution of acute exacerbations of multiple sclerosis, they do not show that corticosteroids affect the ultimate outcome or natural history of the disease. The studies do show that relatively high doses of corticosteroids are necessary to demonstrate a significant effect. (See DOSAGE AND ADMINISTRATION.)
Since complications of treatment with glucocorticoids are dependent on the size of the dose and duration of treatment, a risk/benefit decision must be made in each individual case as to dose and duration of treatment and as to whether daily or intermittent therapy should be used.
There is an enhanced effect of corticosteroids on patients with hypothyroidism and in those with cirrhosis.
Corticosteroids should be used cautiously in patients with ocular herpes simplex because of possible corneal perforation.
The lowest possible dose of corticosteroid should be used to control the condition under treatment, and when reduction in dosage is possible, the reduction should be gradual.
Psychic derangements may appear when corticosteroids are used, ranging from euphoria, insomnia, mood swings, personality changes, and severe depression, to frank psychotic manifestations. Also, existing emotional instability or psychotic tendencies may be aggravated by corticosteroids.
Aspirin should be used cautiously in conjunction with corticosteroids in hypoprothrombinemia.
Steroids should be used with caution in nonspecific ulcerative colitis, if there is a probability of impending perforation, abscess or other pyogenic infection; diverticulitis; fresh intestinal anastomoses; active or latent peptic ulcer; renal insufficiency; hypertension; osteoporosis; and myasthenia gravis.
Growth and development of infants and children on prolonged corticosteroid therapy should be carefully observed.
Although controlled clinical trials have shown corticosteroids to be effective in speeding the resolution of acute exacerbations of multiple sclerosis, they do not show that corticosteroids affect the ultimate outcome or natural history of the disease. The studies do show that relatively high doses of corticosteroids are necessary to demonstrate a significant effect. (See DOSAGE AND ADMINISTRATION.)
Since complications of treatment with glucocorticoids are dependent on the size of the dose and duration of treatment, a risk/benefit decision must be made in each individual case as to dose and duration of treatment and as to whether daily or intermittent therapy should be used.
DRUG INTERACTIONS
The pharmacokinetic interactions uled below are potentially clinically important. Mutual inhibition of metabolism occurs with concurrent use of cyclosporin and methylprednisolone; therefore, it is possible that adverse events associated with the individual use of either drug may be more apt to occur. Convulsions have been reported with concurrent use of methylprednisolone and cyclosporin.
Information for the Patient
Persons who are on immunosuppressant doses of corticosteroids should be warned to avoid exposure to chicken pox or measles. Patients should also be advised that if they are exposed, medical advice should be sought without delay.
ADVERSE REACTIONS
Fluid and Electrolyte Disturbances
Sodium retention, Fluid retention, Congestive heart failure in susceptible patients, Potassium loss, Hypokalemic alkalosis, Hypertension
Musculoskeletal
Muscle weakness, Steroid myopathy, Loss of muscle mass, Severe arthralgia, Vertebral compression fractures, Aseptic necrosis of femoral and humeral heads, Pathologic fracture of long bones, Osteoporosis
Gastrointestinal
Peptic ulcer with possible perforation and hemorrhage, Pancreatitis, Abdominal distention, and Ulcerative esophagitis
Dermatologic
Impaired wound healing, Thin fragile skin, Petechiae and ecchymoses, Facial erythema, Increased sweating, May suppress reactions to skin tests
Neurological
Increased intracranial pressure with papilledema (pseudo-tumor cerebri) usually after treatment, Convulsions, Vertigo, Headache
Endocrine
Development of Cushingoid state, Suppression of growth in children, Secondary adrenocortical and pituitary unresponsiveness, particularly in times of stress, as in trauma, surgery or illness, Menstrual irregularities, Decreased carbohydrate tolerance, Manifestations of latent diabetes mellitus, Increased requirements for insulin or oral hypoglycemic agents in diabetics
Ophthalmic
Posterior subcapsular cataracts, Increased intraocular pressure, Glaucoma, Exophthalmos
Metabolic
Negative nitrogen balance due to protein catabolism
The following additional adverse reactions are related to parenteral corticosteroid therapy: Hyperpigmentation or hypopigmentation, Subcutaneous and cutaneous atrophy, Sterile abscess, Anaphylactic reaction with or without circulatory collapse, cardiac arrest, bronchospasm, Urticaria, Nausea and vomiting, Cardiac arrhythmias; hypotension or hypertension
Sodium retention, Fluid retention, Congestive heart failure in susceptible patients, Potassium loss, Hypokalemic alkalosis, Hypertension
Musculoskeletal
Muscle weakness, Steroid myopathy, Loss of muscle mass, Severe arthralgia, Vertebral compression fractures, Aseptic necrosis of femoral and humeral heads, Pathologic fracture of long bones, Osteoporosis
Gastrointestinal
Peptic ulcer with possible perforation and hemorrhage, Pancreatitis, Abdominal distention, and Ulcerative esophagitis
Dermatologic
Impaired wound healing, Thin fragile skin, Petechiae and ecchymoses, Facial erythema, Increased sweating, May suppress reactions to skin tests
Neurological
Increased intracranial pressure with papilledema (pseudo-tumor cerebri) usually after treatment, Convulsions, Vertigo, Headache
Endocrine
Development of Cushingoid state, Suppression of growth in children, Secondary adrenocortical and pituitary unresponsiveness, particularly in times of stress, as in trauma, surgery or illness, Menstrual irregularities, Decreased carbohydrate tolerance, Manifestations of latent diabetes mellitus, Increased requirements for insulin or oral hypoglycemic agents in diabetics
Ophthalmic
Posterior subcapsular cataracts, Increased intraocular pressure, Glaucoma, Exophthalmos
Metabolic
Negative nitrogen balance due to protein catabolism
The following additional adverse reactions are related to parenteral corticosteroid therapy: Hyperpigmentation or hypopigmentation, Subcutaneous and cutaneous atrophy, Sterile abscess, Anaphylactic reaction with or without circulatory collapse, cardiac arrest, bronchospasm, Urticaria, Nausea and vomiting, Cardiac arrhythmias; hypotension or hypertension
DOSAGE AND ADMINISTRATION
When high dose therapy is desired, the recommended dose of A-Methapred sterile powder is 30 mg/kg administered intravenously over at least 30 minutes. This dose may be repeated every 4 to 6 hours for 48 hours.
In general, high dose corticosteroid therapy should be continued only until the patient’s condition has stabilized; usually not beyond 48 to 72 hours.
Although adverse effects associated with high dose short-term corticoid therapy are uncommon, peptic ulceration may occur. Prophylactic antacid therapy may be indicated.
In other indications initial dosage will vary from 10 to 40 mg of methylprednisolone depending on the clinical problem being treated. The larger doses may be required for short-term management of severe, acute conditions. The initial dose usually should be given intravenously over a period of several minutes. Subsequent doses may be given intravenously or intramuscularly at intervals dictated by the patient’s response and clinical condition. Corticoid therapy is an adjunct to, and not replacement for conventional therapy.
Dosage may be reduced for infants and children but should be governed more by the severity of the condition and response of the patient than by age or size. It should not be less than 0.5 mg/kg every 24 hours.
Dosage must be decreased or discontinued gradually when the drug has been administered for more than a few days. If a period of spontaneous remission occurs in a chronic condition, treatment should be discontinued. Routine laboratory studies, such as urinalysis, two-hour postprandial blood sugar, determination of blood pressure and body weight, and a chest X-ray should be made at regular intervals during prolonged therapy. Upper GI X-rays are desirable in patients with an ulcer history or significant dyspepsia.
A-Methapred may be administered by intravenous or intramuscular injection or by intravenous infusion, the preferred method for initial emergency use being intravenous injection. To administer by intravenous (or intramuscular) injection, prepare solution as directed. The desired dose may be administered intravenously over a period of several minutes.
To prepare solutions for intravenous infusion, first prepare the solution for injection as directed. This solution may then be added to indicated amounts of 5% dextrose in water, isotonic saline solution or 5% dextrose in isotonic saline solution.
Multiple Sclerosis
In treatment of acute exacerbations of multiple sclerosis, daily doses of 200 mg of prednisolone for a week followed by 80 mg every other day for 1 month have been shown to be effective (4 mg of methylprednisolone is equivalent to 5 mg of prednisolone).
Directions for Reconstitution
Protect from light.
Store unreconstituted product at 20 to 25°C (68 to 77°F). [See USP Controlled Room Temperature.]
Store solution at 20 to 25°C (68 to 77°F). [See USP Controlled Room Temperature.]
Use solution within 48 hours after mixing.
In general, high dose corticosteroid therapy should be continued only until the patient’s condition has stabilized; usually not beyond 48 to 72 hours.
Although adverse effects associated with high dose short-term corticoid therapy are uncommon, peptic ulceration may occur. Prophylactic antacid therapy may be indicated.
In other indications initial dosage will vary from 10 to 40 mg of methylprednisolone depending on the clinical problem being treated. The larger doses may be required for short-term management of severe, acute conditions. The initial dose usually should be given intravenously over a period of several minutes. Subsequent doses may be given intravenously or intramuscularly at intervals dictated by the patient’s response and clinical condition. Corticoid therapy is an adjunct to, and not replacement for conventional therapy.
Dosage may be reduced for infants and children but should be governed more by the severity of the condition and response of the patient than by age or size. It should not be less than 0.5 mg/kg every 24 hours.
Dosage must be decreased or discontinued gradually when the drug has been administered for more than a few days. If a period of spontaneous remission occurs in a chronic condition, treatment should be discontinued. Routine laboratory studies, such as urinalysis, two-hour postprandial blood sugar, determination of blood pressure and body weight, and a chest X-ray should be made at regular intervals during prolonged therapy. Upper GI X-rays are desirable in patients with an ulcer history or significant dyspepsia.
A-Methapred may be administered by intravenous or intramuscular injection or by intravenous infusion, the preferred method for initial emergency use being intravenous injection. To administer by intravenous (or intramuscular) injection, prepare solution as directed. The desired dose may be administered intravenously over a period of several minutes.
To prepare solutions for intravenous infusion, first prepare the solution for injection as directed. This solution may then be added to indicated amounts of 5% dextrose in water, isotonic saline solution or 5% dextrose in isotonic saline solution.
Multiple Sclerosis
In treatment of acute exacerbations of multiple sclerosis, daily doses of 200 mg of prednisolone for a week followed by 80 mg every other day for 1 month have been shown to be effective (4 mg of methylprednisolone is equivalent to 5 mg of prednisolone).
Directions for Reconstitution
- Remove protective cap.
- Cleanse stopper with suitable germicide.
- Aseptically add 1 mL Bacteriostatic Water for Injection, USP (with benzyl alcohol) for the 40 mg vial or 2 mL Bacteriostatic Water for Injection, USP (with benzyl alcohol) for the 125 mg vial.
- Agitate to effect solution.
- Invert vial. Insert needle through target area of stopper until tip is just visible. Withdraw dose.
Protect from light.
Store unreconstituted product at 20 to 25°C (68 to 77°F). [See USP Controlled Room Temperature.]
Store solution at 20 to 25°C (68 to 77°F). [See USP Controlled Room Temperature.]
Use solution within 48 hours after mixing.
HOW SUPPLIED
A-Methapred sterile powder is available in the following packages:
Rev: October, 2005
©Hospira 2005EN-1059Printed in USA
HOSPIRA, INC., LAKE FOREST, IL 60045 USA
| List | Container | Concentration |
| 3217 | Single-Dose Vial | 40 mg/vial |
| 3218 | Single-Dose Vial | 125 mg/vial |
©Hospira 2005EN-1059Printed in USA
HOSPIRA, INC., LAKE FOREST, IL 60045 USA
Doctor Says Surgery May Relieve Pain Of Neuropathy
Now a doctor in Colorado is one of just a few surgeons in the country offering another alternative.Gregory Garland says he has a tremendous amount of pain in his foot and leg and is going under the knife to treat it.
Howdy Folks:) Sue Relays Asked Me to Post My Results Here
I got to know Sue when she visited the Colorectal Board - she's been a good friend and terrific supporter to me. And since she does not get over to our side very much anymore, she asked me if I would post my results over here so she could see them. I hope you don't mind.
From Sue:
"Will be waiting to see your results. Will you post on the anal board as well??"
This is a long post but covers the past year of my fight, currently at 7-years, Stage IV.
Grab something to drink and you're welcome to read along with Sue. And maybe Joanne will show up here - I miss her to and met her on the other board when she first got here.
Ok, Sue and everybody here we go!
“SUNDANCE vs CANCER” – The Results Post
Faster than a speeding locomotive – Able to leap tall buildings in a single bound – Look! – Up in the air! – It’s a bird! – It’s a plane! – It’s…..it’s……awww $hit, it’s only Sundance:)
LOL:)
The “Betting Windows” are now officially closed, so I hope you got your wagers down – there was sure plenty of time:)
Well, this is finally the post that I have waited for and waited to write. And also the one that many of you have waited for as well. Almost a year in the making and through it all, it has been a “Watershed Moment” in my journey.
I suppose when I reflect back on it, we could say that it’s the most influential battle of my entire campaign. There was much at stake to be won or lost. It carried huge significance as I motored on toward my 7th year of this incredible saga. And all the time, never knowing exactly which way the battle was going to go. Would I win? Or would I begin to slip?
The stakes we were playing for was my very existence, which I believe we can all agree, is worth playing for. The difference is we had to fight like there was never going to be tomorrow – because that’s always in the cards and is the key component that weighs so heavily on all of our minds.
It’s a funny feeling looking back on this past year. In many ways, it still feels like yesterday – and then on the other side, it seems like a lifetime ago.
Cancer played a dirty little trick on me this time. We know he does not play fair and is a dirty fighter. He used the DaVinci tumors the time before, to lull us into a false sense of complacency while he stealthily hid behind my lungs and gathered his forces, before he could again announce his presence in my body for this last year’s fight.
When I was still in the hospital after this lung surgery, I remember a nurse bringing me my pathology report. Even dazed on morphine and with blurred eyesight, I could still make out the words…”Colorectal Mets to Lung.”
And I remember thinking, “Now, you’ve showed yourself, you SOB!” I sat up in bed and thought, “I’ve got you now.” You’ve just kicked the sleeping dog – you just woke up the Gentle Giant. So, once again, it’s “officially back on.”
Strangely though, I felt some sense of comfort in those words, in the fact that I again knew what I was going back up against….there was no guessing anymore, there it was in the report. It was time once more to “get my mind right to fight.”
Once I found out the surgery did not completely remove the malignant tumors, I knew it was going to a really long and hard road, with no shortcuts. I was going to have to go all in and gut this one out for the long haul, if I was to have a chance at any kind of victory.
You all know there were times when it looked like I was beaten. Down and out for the count is what’s ahead for our good old Sundance, folks were probably thinking – put a fork in him, he’s done. But then again, you don’t know Sundance:)
I’ve always said I may “bend or waver” during the fight, but that I would never “break.”
Maybe that’s not an entirely true statement. Perhaps, it depends on what your definition of “break” is. In fact, Cancer had me beaten and on my knees begging for either “Death or Mercy.” It had me beaten at the time, but not broken for the long haul of the fight.
“The CURE” had me beaten as well this time , but I stayed strong enough to complete the entire protocol “by the numbers.” It was really difficult this time to mentally and physically step through all the obstacles that stood in our way. As I’ve said before, it gets a little harder to keep taking the pounding, the longer you stay in the fight.
The mind and heart are still willing – but the body just doesn’t “bounce” like it used to. I think this is the biggest difference in an old veteran fighter vs the newly diagnosed.
While the surgeries and treatments have compromised our bodies, we learn we must adapt and use our experience and smarts to fight on, instead of relying on a new body that is just starting out.
My medical team continuously put the foot on the gas and we were very aggressive in our treatment plan and there was no time to rest. We relentlessly pursued our target and stayed in the attack mode the entire time.
Oh yes, I can be beaten – I can be hurt – I can bleed – I can hurt – I can suffer. I am just a mortal man, composed of blood & flesh..
However, on the other side of the coin, I can also be tenacious – persistent – stubborn – and relentless in my own pursuit. My horoscope is “Cancer, the Crab.” I’m a “July Baby.”
We’re loveable, friendly, and loyal – but when fuc*ed with, we raise our pinschers and will snap you. We’re a very formidable force to reckon with. When we hit back, it hurts too, just like we were hurt. We only fight when provoked though and let’s face it, Cancer does provoke us, doesn’t it?
Here’s the last topic I wanted to discuss. Let’s talk about our roommate – HOPE.
What an interesting fella’ this guy is, am I right?
He’s very elusive and if we’re not real careful, he can just slip out of our fingertips and just be gone. And when he goes, he’s sometimes hard to find again. And when Hope moves out, Depression can move in – then he invites Despair, Hopelessness and Loneliness to the party, and from there our lives can disappear and become nothing but existence.
And that’s a very bad place to be – especially for too long. I know, because I spent 9-months with all of these guys this year. They are not nice “house guests.” They try to rob you of that thing that we call “Our Lives.”
And then it becomes up to us to take back back what was so wrongly taken from us. Each of us must do that and find a way to get Hope moved back in with us, so we can flourish and feel optimism.
What is my definition of Hope?
I’ve come to think of Hope as that “Intangible element of humanity that we cannot see, but one that we feel.”
It’s the single common denominator that every single one of us has inside. It’s the driving force behind our individualism and more importantly, the one thing that we “Cling To” and “Reach For” in times of dire circumstances that beset each of us, somewhere in our lifetime.
As the old saying goes, “Let’s Keep Hope Alive!”
Hey, let’s go down to ringside right now, looks like Michael Buffer is about to announce “The Decision.” Who came out on top? Sundance or Cancer?
“Ladies and Gentlemen! The Winner by KO and still the Undefeated Cancer Champion of the World, with a 3-0 title defense, is……….your very own…….SUNDANCE! “
LOL:)
And the crowd goes WILD……….:) !!!
For any of you that bet against me…….”Suckerzzzz!” LOL:)
That’s right folks – 3 recurrences Up and 3 recurrences Down – just like in baseball, huh?
We did it again. We knocked Cancer “Back into the Shadows” once more. He’s gone back into hiding, licking his wounds, while I lick mine. But, we got Him down right now. You read the BAD in my other post…….and now for something completely different, here is the GOOD:
1. Colon and Rectum = Clear
2. Liver = Clear
3. Lungs = All Clear:)
Many of you might recall in my Thanksgiving Message to my Cancer, that I said, “I am down right now – but when I get up, I’m coming – and He11 was coming with me.
Well, with Big Billy by my side, we “Huffed and we Puffed”…and we “Blew the Doors to the Gates of He11 Wide Open!”
What looked like a highly improbable, if not impossible mission at the beginning of this fight, has come to a successful conclusion. I know how fortunate I am to be on the “positive side of the ledger” right now. It sure could have gone either way, but somehow we are on top right now.
We’re officially back to “Watching and Waiting.” I’ll talk to NED, if I make it “clean” for 5-years, with no further recurrences….. (June 2016).
So, it does not get much better than this….am I right?
I thought the balloons were supposed to fall out of the ceiling about now? Why isn’t the band playing? Where’s the cake and ice cream? Where is Jennie with my margaritas?
LOL:)
Since I can’t get to any of you right now…we’ll just have to have a “Cyber Celebration!” I need some folks to share in this joy with me. It will mean more if I have all of you around me in the “same room.”
So, what’s next for Sundance?
I’m going to Disneyworld!...................................Not!
I’ll be lucky to get to Chicago for CP9 – with this very meaningful victory, it is my sincerest hope that I can make it there and get some lovin’ from my honeys:)
What’s next is instead of escaping Cancer, I’m going to jump back into the deep end of the pool and go back to the beginning of the journey – first chapter titled “The Diagnosis.”
I want to jump on getting this written now, while the wounds are fresh and the feelings raw. I’m excited about making this a reality – now publishing will be another story – coming to an Amazon Kindle near you?
I’ll close this post with these final thoughts…..
On the day that Donna (Shayenne) aka “My Chicky” passed away, I posted on that thread that Her Lion had roared for the final time.
A beautiful chapter in my life and on this board and a real life story of friendship had come to a tragic and painful end. On this day a part of me died with her –Her Lion was dead and gone, and yet the memories still remained, but were now forever buried deep within the archives of the CSN posts.
This is a day where I wished Chicky were still here with us – certainly a story she would have loved to hear about and rejoice in. I will miss not seeing her post in this thread.
In honor of her memory and to bookmark this momentous occasion, Donna’s Lion “ROARZZZZ” one more time:) Miss you, Chicky.
This one was for myself, but also for the Semi;Colon Nation. I stand before you as a living testimony to what Cancer “Can and Cannot” do to us. It will never be easy, but you too can do this. I’ll stand proudly beside each one of you and be with you for each stop in your journey. Don’t be afraid – get mad – get even – and get out there and fight!
I understand less and less as time goes by – have no idea of why I’m still here after 7 years of battling this stuff. Don’t understand why my friends did not make it, but I am still here. I suppose I’ll never know.
And Cancer may indeed catch me one day – but guess what? It won’t be TODAY!!!
All of you know that Sundance is not the kind of guy that “Goes Quietly into the Night.”
I carry all of your hopes and dreams with me in my heart. I have the deepest respect and admiration for each one of you here – both past and present. You are the finest group of people I know and I’m proud to know you all.
All of you are Winners – and Cancer will never, ever take that away from you! With all of the love I can muster, I thank you for staying with me and you are all in my thoughts, in my heart, and in my dreams. Semi;Colons Rock!
I SALUTE YOU!!!
Craig and Big Billy
“Team Sundance
Medifocus Guidebook on Peripheral Neuropathy
What is Peripheral Neuropathy?
The nervous system controls the smooth functioning of all systems in the body as well as all interactions between the human being and the environment. The nervous system is comprised of millions of neurons that are interconnected and form a communications network within the body that governs many vital functions including:
- The five senses (sight, hearing, touch, smell, and taste)
- Voluntary functions (e.g. walking, holding an object)
- Involuntary functions (e.g. breathing, blood pressure)
- Cognitive reasoning
- Central nervous system - includes the brain and spinal cord
- Peripheral nervous system - includes the nerves that lead from the brain and spinal cord to all parts of the body. An extensive system of specialized nerves makes up the peripheral nervous system which is responsible for a variety of important functions. These specialized nerves include:
- motor nerves which carry messages from the brain to the body and are responsible for the ability to move any part of the body (e.g., hands, feet)
- sensory nerves which carry information from organs to the central nervous system where it is processed into sensation (e.g., touch, temperature changes, and vibrations)
- nerves that control autonomic (involuntary) functions including heart rate, blood pressure, breathing, digestion, and bladder function
The incidence of peripheral neuropathy is not known with any degree of certainty. It has been estimated that approximately 2 to 3 million Americans have some form of peripheral neuropathy. The prevalence of peripheral neuropathy worldwide has been estimated to range from 2% to 8% of the population. Peripheral neuropathy affects both genders at all ages but symptoms are unique to each individual in terms of frequency, quality, and severity of pain. Idiopathic peripheral neuropathy typically affects adults over the age of 50. Peripheral neuropathy can significantly impact an individual's quality of life and daily activities by causing major disruptions including:
- Sleep disturbances
- Mood changes
- Impairment of social, occupational, and recreational functioning
If you or a loved one has been diagnosed with peripheral neuropathy, it's critical to learn everything you possibly can about this condition so that you can make informed decisions about your treatment. That's why we created the Medifocus Guidebook on Peripheral Neuropathy, a comprehensive 187 page patient Guidebook that contains vital information about peripheral neuropathy that you won't find anywhere in a single source.
The Medifocus Guidebook on Peripheral Neuropathy starts out with a detailed overview of the condition and quickly imparts fundamentally important information about peripheral neuropathy, including:
- The underlying causes and risk factors for developing peripheral neuropathy, which include:
- Diabetes
- Autoimmune disorders
- Metabolic disorders
- Hereditary disorders
- Infectious diseases
- Alcohol abuse
- Trauma
- Cancer chemotherapy
- The different types of peripheral neuropathy that can occur based on the pattern of nerve involvement and the distribution of pain, which include:
- Mononeuropathy
- Mononeuropathy multiplex
- Polyneuropathy
- The signs and symptoms associated with peripheral neuropathy based on the specific underlying cause, when known.
- How peripheral neuropathy is diagnosed based on a variety of factors and diagnostic tests including:
- Signs and symptoms
- Patient history and physical examination
- Pattern of distribution of pain along sensory or motor nerves
- Special electrodiagnostic studies, such as nerve conduction tests and electromyography (a test which measures the response of muscles to electrical stimulation)
The primary goals of treatment for peripheral neuropathy include accomplishing the following objectives:
- Determining and treating the underlying cause of the condition, if possible.
- Controlling and alleviating pain and other bothersome symptoms associated with the condition.
- Preserving function of the affected limbs, such as the hands and/or feet.
- Preventing a significant decrease in the patient's quality of life.
- The management of peripheral neuropathy in patients where the underlying cause can be identified, such as diabetes, autoimmune disorders, infectious diseases, nerve compression, and cancer chemotherapy.
- The major types of medications that are often prescribed to relieve pain associated with peripheral neuropathy, which include:
- Antidepressants
- Anticonvulsants
- Selective serotonin reuptake inhibitors
- Narcotic analgesics
- Topical agents such as capsaicin and lidocaine patches
- The treatment options that are available for controlling pain that does not adequately respond to drug therapy, including nerve blocks with local anesthetics and spinal cord stimulation.
- The role of physical and occupational therapy in functional rehabilitation of patients with peripheral neuropathy.
- The role of complementary and alternative therapies in the management of peripheral neuropathy.
- The impact of peripheral neuropathy on the patient's psychological well-being and quality of life, including aspects such as:
- Anxiety and depression
- Social relationships
- Activities of daily living
- Employment issues
- Sleep disturbances
- Recreational activities
- Feelings of self-worth
- Practical tips and suggestions for how to minimize the negative impact of peripheral neuropathy on your quality of life and learn how to better cope with the condition.
- Important questions to ask your doctor about peripheral neuropathy.
Since 1996, when Medifocus was founded, we've learned that many people with Peripheral Neuropathy are seeking more specific information that goes beyond the fundamentals, such as the causes, diagnosis, standard treatments, and treatment options. That's why we developed a "one-of-a-kind" reference Guidebook that goes way beyond the basics and also includes the following sections:
- A Guide to Recent Medical Literature on Peripheral Neuropathy - This section of the Guidebook contains an extensive bibliography of over 100 references to recently published articles about Peripheral Neuropathy in authoritative, peer-reviewed medical journals with links to the absracts (summaries) of the articles. These articles represent the latest advances in the field and focus on cutting-edge research, new developments, and the lessons learned from recently published clinical trials involving patients with Peripheral Neuropathy. This is the same level of that is used by doctors who treat people with Peripheral Neuropathy to keep abreast of the latest developments and breakthroughs in this specialized field of medicine.
- Centers of Research for Peripheral Neuropathy - We've compiled a unique directory of doctors, hospitals, medical centers, and research institutions with special interest and, in many cases, clinical expertise in managing people with Peripheral Neuropathy. The "Centers of Research" directory is a valuable resource for quickly identifying and locating leading medical authorities and medical institutions both within the United States and other countries who are considered to be at the forefront in clinical research and treatment of Peripheral Neuropathy. You'd have to spend days - or even weeks - attempting to compile your own list of doctors and medical centers but, with the "Centers of Research" directory, the information is already right at your fingertips. All you have to do is act on the information by selecting and contacting the experts or medical institutions listed in the directory by state and country.
- Organizations and Support Groups for Peripheral Neuropathy - The Guidebook also includes a directory of organizations and support groups whose goal is to help people with Peripheral Neuropathy by providing access to information, resources, and services. Many of these organizations can answer your specific questions, enable you to "network" with other patients, and provide guidance in areas such as financial, social, or medical-legal issues. This valuable directory of organizations and support groups includes complete contact information, including phone numbers and E-mail addresses.
Still not sure if you'll benefit from the Medifocus Guidebook on Peripheral Neuropathy? Still not convinced that the information included in the Guidebook is worth the minimal cost? If that's the case, then please consider the following value-added proposition that comes standard with your purchase of the Guidebook:
- Free Updates for One Year - With your initial purchase of the Guidebook, you also receive access to free updates for one-full year. The Guidebook is updated with new information every 4 to 6 months, so that you will be able to access the updated information several times during the course of a year for up to one full year after the date of your initial purchase.
- Free Digest E-Mail Alerts - When you purchase the Guidebook, you will also automatically receive a free subscription to our monthly newsletter - the Medifocus Digest Alert for Peripheral Neuropathy. This is an expertly selected listing of the latest articles published in the medical literature about Peripheral Neuropathy with convenient links to the abstracts of the articles that focus on cutting-edge research, clinical trials, and the latest treatment advances. The Medifocus Digest Alert for Peripheral Neuropathy is automatically delivered straight to your "inbox" monthly and is a valuable resource for keeping up with the latest developments in Peripheral Neuropathy almost as soon as the new information is published in the medical literature.
- 10% Discount - For a limited time, you can purchase the Medifocus Guidebook on Peripheral Neuropathy at a special 10% discount off the regular list price. Your 10% discount will automatically be applied when you go to "Checkout".
- Risk-Free Satisfaction Guarantee - Your purchase comes with our RISK-FREE satisfaction guarantee. If, for whatever reason, you are not totally satisfied with the content of your Guidebook, simply contact us within 30-days of your purchase for a prompt, full refund. We are so confident that you will be satisfied with your Guidebook that we offer this RISK-FREE satisfaction guarantee unconditionally - no questions and no hassles
Retinal - Vitamin A
Overview & Description
Vitamin A is a fat-soluble vitamin which means it can be dissolved in fat. Vitamin A is carried through the body by fat. The body can store this type of vitamin in fat tissue. Getting too much can be harmful.
Vitamin A can be stored in the fat tissues of the body. This can pose a problem for people taking extra doses of vitamin A. High doses can be toxic and cause symptoms such as the following:
headaches
dry and scaly skin
liver damage
bone and joint pain
vomiting or lack of appetite
abnormal bone growth
nerve damage
birth defects
In most cases, only levels 10 times the RDA (far more than a person could get through diet alone) have been linked with these symptoms. Vitamin A cannot reach toxic levels unless a person is taking extra doses. Carotenoids are not converted to vitamin A fast enough to increase the amount of vitamin A stored in the body. Beta-carotene is NOT toxic to the body.
Getting too little vitamin A can cause side effects too. Symptoms of significant deficiency include:
lowered resistance to infections
problems with getting pregnant
poor growth
improper tooth formation
rough, dry, and pimply skin
digestive problems
night blindness
eye disease, including xerophthalmia (zear-off-thal-me-ah), a condition in which the clear covering of the eye known as the cornea becomes dry and dull
Vitamin A is an important fat-soluble vitamin. Eat a variety of fruits, vegetables, lean meats, and fortified dairy products to ensure optimal intake of vitamin A. Read food labels to help choose foods with vitamin A content.
Information
Vitamin A is usually measured in retinol equivalents, also called RE. The Recommended Dietary Allowance, called RDA, for vitamin A for adult men, from age 11 on, is 1,000 RE per day. Women, from age 11 on, should get 800 RE per day. There is no increase of vitamin A requirements during pregnancy but lactating women need about 500 RE or more per day.Vitamin A can be stored in the fat tissues of the body. This can pose a problem for people taking extra doses of vitamin A. High doses can be toxic and cause symptoms such as the following:
In most cases, only levels 10 times the RDA (far more than a person could get through diet alone) have been linked with these symptoms. Vitamin A cannot reach toxic levels unless a person is taking extra doses. Carotenoids are not converted to vitamin A fast enough to increase the amount of vitamin A stored in the body. Beta-carotene is NOT toxic to the body.
Getting too little vitamin A can cause side effects too. Symptoms of significant deficiency include:
Vitamin A is an important fat-soluble vitamin. Eat a variety of fruits, vegetables, lean meats, and fortified dairy products to ensure optimal intake of vitamin A. Read food labels to help choose foods with vitamin A content.
Functions and Sources
What food source is the nutrient found in?
Vitamin A can come from animal sources such as:This form of Vitamin A is called retinal or retinol.
Vitamin A is also found in plants. This form is called carotenoids. Substances such as beta-carotene are converted from carotenoids into vitamin A in the body. Beta-carotene is one of the most common carotenoids. Carotenoids are pigments found in deep orange, red, and yellow fruits and vegetables. They are also found in many dark-green leafy vegetables, such as:
How does the nutrient affect the body?
Vitamin A helps develop and maintain healthy growth in the cells and almost all the parts of the body. It is especially key for proper night vision, but is also needed for the health of a person's:Vitamin A plays a key role in the immune system by helping protect from infections. Beta-carotene is an antioxidant. It has been studied for its role in cancer and heart disease protection. Antioxidants help fight free radicals. Free radicals are oxygen by-products produced when body cells burn oxygen. A build up of free radicals can damage body cells and tissues.
Attribution
Author:Clare Armstrong, MS, RDDate Written:
Editor:Crist, Gayle P., MS, BA
Edit Date:09/27/02
Reviewer:Kathleen A. MacNaughton, RN, BSN
Date Reviewed:09/26/02
Sources
Mahan, K, MS, RD, CDE & Escott-Stump, S., MA, RD, LDN. (2000). Krause's Food, Nutrition, & Diet Therapy (10th ed.). Pennsylvania: W.B. Saunders Company.Somer, E., MA, RD. & Health Media of America. (1995). The Essential Guide To Vitamins and Minerals (2nd ed.). New York: HarperCollins Publishers, Inc.
Duyff, R., MS, RD, CFCS. (1996). The American Dietetic Association's Complete Food & Nutrition Guide. Minnesota: Chronimed Publishing
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