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Pellagra, therapy

Pellagra is often characterized by mental abnormalities such as anxiety, irritability, and depression. The classic symptoms of pellagra are known as the 4 Ds -dementia, diarrhea, dermatitis, and death. Inflammation of mucosal surfaces, weakness, anorexia, and other gastrointestinal disturbances are also seen. Niacin (300 to 500 mg per day) is the definitive therapy. [Pg.297]

I.6. Various Diseases. Abbassy et al. (Al) observed in 12 cases of malnutrition (including kwashiorkor), toxic dyspepsia, 8 cases of acute nephritis, 8 cases of infective hepatitis, and muscular dystrophy an increased spontaneous excretion of xanthurenic acid, the amount of which was found to depend on the severity of the case. In all these cases, with the exception of acute nephritis and hepatitis, the amount of xanthurenic acid was restored to normal levels after vitamin Be therapy. In 8 children with mental retardation, cerebral palsy, recurrent convulsions, 5 with nephrotic syndrome, and 5 with pellagra the amount of xanthurenic acid spontaneously excreted was found to be within the normal range, indicating that pyridoxine is probably not concerned in these cases. [Pg.108]

Ishii N, Nishihara Y. Pellagra encephalopathy among tuberculous patients its relation to isoniazid therapy. J Neurol Neurosurg Psychiatry 1985 48(7) 628-34. [Pg.1928]

Dose for deficiency Thiamine 30-60 mg/d Riboflavin 5-25 mg/d Prophylactic 3 mg/d Nicotinic acid or niacin Prevention 5-20 mg/d Deficit 50-100 mg/d Pellagra 300-500 mg in three divided doses Hyperlipidemia 1-2 g/d in three divided doses Pyridoxine 25-100 mg/d Isoniazid therapy prophylaxis 25-20 mg/d Peripheral neuritis 50-200 mg/d... [Pg.93]

The only rational treatment of patients having pellagra-like symptoms is the administration of niacin (nicotinic acid) in oral doses up to 300 mg/day. Although the rash, ataxia, and neuropsychiatric manifestations of niacin deficiency may disappear, the hyperaminoaciduria and intestinal transport defect do not respond to this therapy. In addition to niacin, a high-protein diet may benefit some patients. [Pg.694]

Nicotinic acid is approved for the treatment of hyper-cholesterolemia, hypertriglyceridemia, and familial combined hyperlipidemia (Fredrickson s type lla, Mb, IV, and V) (Table 30.2) in patients who have not responded to diet, exercise, and other nonpharmacological methods. It also is approved for nutritional supplementation, the prevention of pellagra, and as adjunct therapy for peripheral vascular disease and circulatory disorders. It is contraindicated in patients with hepatic disease and peptic ulcer disease. Additionally, because of its ability to elevate glucose and uric acid levels, especially when taken in large doses, nicotinic acid should be used with caution in patients who have or are predisposed to diabetes mellitus and gout (15,20,21). [Pg.1204]

Nicotinic acid Supplement nicotinamide deficiency, impaired absorption, increased requirements Therapy pellagra, vasomotoric headache, migraine, schizophrenia... [Pg.662]

The question of vitamin supplementation obviously requires an affirmative answer when one considers therapy for overt, specific deficiency syndromes such as scurvy, rickets, beriberi, pellagra, megaloblastic anemia, ariboflavinosis, and convulsions due to pyridoxine deficiency. In some syndromes, biochemical evidence of deficiency occurring before overt symptoms is accepted as indication for general preventive supplementation. For example, the hydroxyphenyluria of premature infants and decreased serum phosphate and citrate, are taken as indications for early... [Pg.568]

The earliest neurologic symptoms of pellagra are reminiscent of neurasthenia, with insomnia, fatigue, nervousness, irritability, and depression with memory loss (Victor et al, 1971). A progressive dementia can develop, but this seems unlikely to be caused solely by the absence of niacin. An acute confusional syndrome also occurs in human pellagra, and this is reversible with niacin therapy. A central neuritis is prominent in the large motor cortex cells (the Betz cells). This is not a demyelinating process like Bj2 deficiency but a primary involvement of the whole neuron. [Pg.84]

Therapy. A true deficiency of vitamin B5 is rare. Neurological symptoms associated with pellagra and beri-beri seem to be improved with pyridoxine. Doses of pyridoxine (40-150 mg daily) are used for the peripheral neuritis due to treatment with isoniazid and related compounds. Pyridoxine has also been used for nausea and vomiting due to a variety of conditions. It has been recommended for the treatment of agranulocytosis and seborrhoeic dermatitis (Marks, 1975). [Pg.192]

Tuscan oncologist noted for having studied immune mechanisms implicated in the pathogenesis, diagnosis, and therapy of infectious and neoplastic diseases. He was certairrly one of the first to assert that pellagra was caused by a diet deficiency. He was President of the National Tumor Institute from 1935-56... [Pg.82]


See other pages where Pellagra, therapy is mentioned: [Pg.1459]    [Pg.1459]    [Pg.229]    [Pg.169]    [Pg.11]    [Pg.541]    [Pg.546]    [Pg.570]    [Pg.271]    [Pg.84]    [Pg.713]    [Pg.190]    [Pg.178]    [Pg.243]   
See also in sourсe #XX -- [ Pg.11 ]




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