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Alcoholic neuropathy

Neuropathy can result from deficiency of vitamins or hormones. Alcoholics often obtain a large proportion of their caloric needs from ethanol, and hence become thiamine-deficient. Alcoholic neuropathy results from a combination of thiamine deficiency, which impairs... [Pg.623]

Koike, H., Iijima, M., Sugiura, M. et al. Alcoholic neuropathy is clinicopathologically distinct from thiamine-deficiency neuropathy. Ann. Neurol. 54 19-29,2003. [Pg.627]

Chronic use of alcohol may lead to nerve damage. The clinical picture is similar to that seen in other neuropathies but in patients with alcoholic neuropathy, tendon reflexes are often preserved. [Pg.245]

Drug-induced Antihypertensives, antiandrogens, antidepressants, alcohol abuse, cigarette smoking Central suppression, decreased libido, alcoholic neuropathy, vascular insufficiency... [Pg.18]

The reported risk factors for HIV-associated sensory neuropathy are varied and may have changed since the availability of HAART. In the pre-HAART era, age, nutritional deficiencies, alcohol exposure, higher HIV viral load, and low CD4 counts (Moyle and Sadler 1998 Childs et al. 1999), as well as mood, other neurologic disorders and functional abnormalities (Schifitto et al. 2002) were neuropathy risk factors. In the HAART era, the use of NRTI (Cherry et al. 2006 Pettersen et al. 2006) and exposure to protease inhibitor (PI) medication (Pettersen et al. 2006 Smyth et al. 2007) are considered additional risk factors. Although hepatitis C mono-infection has been associated with peripheral nerve disease, and there is... [Pg.55]

Pregnant women, alcoholics, and patients with poor diets who are treated with INH should receive pyridoxine, 10 to 50 mg daily, to reduce the incidence of CNS effects or peripheral neuropathies. [Pg.548]

Therapy with INH results in a transient elevation in serum transaminases in 12% to 15% of patients and usually occurs within the first 8 to 12 weeks of therapy. Risk factors for hepatotoxicity include patient age, preexisting liver disease, and pregnancy or postpartum state. INH also may result in neurotoxicity, most frequently presenting as peripheral neuropathy or, in overdose, seizures, and coma. Patients with pyridoxine deficiency, such as alcoholics, children, and the malnourished, are at increased risk, as are patients who are slow acetylators of INH and those predisposed to neuropathy, such as those with diabetes. [Pg.555]

Thiamine deficiency is commonly seen in alcoholics, who may develop a complex of symptoms associated with Wernicke peripheral neuropathy and Korsakoff psychosis. Alcohol interferes with thiamine absorption from the intestine. Symptoms include ... [Pg.175]

So-called peripheral neuropathies can result from excessive exposure to certain industrial solvents such as carbon disulfide (CS2, used in the rubber and rayon industries) and hexane (CgHn, once used in certain glues and cleaning fluids). Over-exposure to acrylamide, an important industrial chemical, and chronic alcohol abuse can also induce this effect. As the name implies, it involves attack of the chemical on and damage to axonal portions of neurons. Typical symptoms of peripheral neuropathies include weakness or numbness in the limbs, which are more or less reversible depending upon the specific agent and the intensity of exposure. [Pg.123]

Toxicology. Methyl alcohol causes optic neuropathy, metabolic acidosis, and respiratory depression. [Pg.453]

Adverse reactions may include acneiform eruptions allergic dermatitis arthropathy multiple cases of cholestatic and fulminant hepatitis drowsiness fatigue headache hepatotoxicity resembling viral or alcoholic hepatitis impotence metallic or garlic-like aftertaste peripheral neuropathy polyneuritis optic or retrobulbar neuritis restlessness occasional skin eruptions. [Pg.1325]

Isoniazid (child 10 mg/kg up to) 300 mg orally, for 6 months 15 mg/kg orally, for 6 months 15 mg/kg orally, for 6 months Hepatic enzyme elevation Hepatitis Peripheral neuropathy CNS (mild) Drug interactions Hepatitis risk increases with age and alcohol consumption. Pyridoxine can prevent peripheral neuropathy... [Pg.565]

A. Ethambutol is associated with retrobulbar neuritis, resulting in loss of central vision and impaired red-green discrimination. Ethionamide (B) is an analogue of isonicotinic acid and is associated with GI intolerance and peripheral neuropathy, but not the optic neuritis or color vision discrimination problems. Aminosalicylic acid (C) can cause GI irritation and bleeding problems, so caution is required in peptic ulcer patients. It has no neurological side effects. Rifampin (D) is associated with red-orange discoloration of saliva, tears, and urine but not the color vision problems. Isoniazid (E) is associated with peripheral neuritis in chronic alcoholics and malnourished individuals and requires pyridoxine supplements. It is not associated with optic neuritis. [Pg.565]

Peripheral neuropathy occurs in up to 50% of patients taking zalcitabine. Stomatitis, esophageal ulceration, hepatotoxicity, rash, and pancreatitis may occur. Zalcitabine should be used with caution in individuals with a history of pancreatitis, liver disease, or alcohol abuse. Dosage adjustment is necessary for individuals with renal impairment. Zalcitabine should not be used in combination with didanosine, lamivudine, or stavudine. [Pg.588]

A. The NRTIs can produce a potentially fatal syndrome of lactic acidosis and severe hepatomegaly with hepatic steatosis. Risk factors associated with the development of this syndrome include female sex, obesity, alcoholism, and prolonged exposure to NRTIs. Peripheral neuropathy is a common side effect of some NRTIs (e.g., stavudine., didanosine, and zalcitabine) but not associated with these risk factors. Stevens-Johnson syndrome is rarely associated with NNRTIs, such as nevirapine, and not with these risk factors. Hyperuricemia is not associated with these risk factors. Hypersensitivity reaction may oc-... [Pg.594]

Unlabeled Uses Treatment of alcohol abuse, dementia, diabetic neuropathy, obsessive-compulsive disorder, panic disorder, smoking cessation... [Pg.272]

Assess the patient for burning, numbness, and tingling of the extremities. Be aware that patients at risk for neuropathy, such as alcoholics, those with chronic hepatic disease, diabetics, the elderly, and malnourished individuals, may receive pyridox-ine prophylactically... [Pg.651]

Another complication of diabetes is blindness, which is due to blood vessel damage at the back of the eye (proliferative retinopathy), this accounts for about 12% of all blindness. In hyperglycemia, fructose is only slowly metabolized, and sorbitol accumulates in tissues. Because aldose reductase is found in kidneys, optic nerve, and peripheral neurons, retinopathy and painful neuropathies develop in poorly controlled or long-standing diabetes as a result of sugar alcohol (sorbitol) accumulation. Aldose reductase inhibitors, such as tokestat (5.129) or sorbinil (5.130), have been evaluated as agents to ameliorate these additional symptoms of diabetes. [Pg.370]

Peripheral neuropathy is observed in 10-20% of patients given dosages greater than 5 mg/kg/d, but it is infrequently seen with the standard 300-mg adult dose. Peripheral neuropathy is more likely to occur in slow acetylators and patients with predisposing conditions such as malnutrition, alcoholism, diabetes, AIDS, and uremia. Neuropathy is due to a relative pyridoxine deficiency. Isoniazid promotes excretion of pyridoxine, and this toxicity is readily reversed by administration of pyridoxine in a dosage as low as 10 mg/d. Central nervous system toxicity, which is less common, includes memory loss, psychosis, and seizures. These may also respond to pyridoxine. [Pg.1045]

Didanosine (ddl) NRTT1 Tablets, 400 mg daily,3 adjusted for weight. 30 min before or 2 h after meals. Separate dosing from fluoroquinolones and tetracyclines by 2 h Peripheral neuropathy, pancreatitis, diarrhea, nausea, hyperuricemia. Possible increase in myocardial infarction Avoid concurrent neuropathic drugs (eg, stavudine, zalcitabine, isoniazid), ribavirin, and alcohol. Do not administer with tenofovir... [Pg.1074]

Adverse effects include nausea, diarrhea, stomatitis, and peripheral neuropathy with prolonged use. Metronidazole has a disulfiram-like effect, and patients should be instructed to avoid alcohol. Although teratogenic in some animals, metronidazole has not been associated with this effect in humans. Other properties of metronidazole are discussed in Chapter 52. [Pg.1092]

Aliphatic hydroxylation. As well as unsaturated aliphatic compounds such as vinyl chloride mentioned above, which are metabolized by epoxidation, saturated aliphatic compounds also undergo oxidation. The initial products will be primary and secondary alcohols. For example, the solvent n-hexane is known to be metabolized to the secondary alcohol hexan-2-ol and then further to hexane-2,5-dione (Fig. 4.9) in occupationally exposed humans. The latter metabolite is believed to be responsible for the neuropathy caused by the solvent. Other toxicologically important examples are the nephrotoxic petrol constituents, 2,2,4- and 2,3,4-trimethylpentane, which are hydroxylated to... [Pg.86]

Coma was independently related to neuropathy, beta-blockers, and alcohol. [Pg.396]


See other pages where Alcoholic neuropathy is mentioned: [Pg.20]    [Pg.581]    [Pg.160]    [Pg.241]    [Pg.245]    [Pg.186]    [Pg.537]    [Pg.884]    [Pg.20]    [Pg.581]    [Pg.160]    [Pg.241]    [Pg.245]    [Pg.186]    [Pg.537]    [Pg.884]    [Pg.146]    [Pg.544]    [Pg.173]    [Pg.187]    [Pg.210]    [Pg.189]    [Pg.258]    [Pg.328]    [Pg.1732]    [Pg.269]    [Pg.484]    [Pg.419]    [Pg.559]    [Pg.608]    [Pg.1077]    [Pg.1135]    [Pg.300]    [Pg.304]   
See also in sourсe #XX -- [ Pg.245 ]




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