SEARCH · Search PubMed

Results for “PELLAGRA”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

SourceResearch connectionFrom yearThrough year

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 37 records · Page 2Linked to original sources

PubMed2000

Pellagra in the United States: a historical perspective.

Pellagra was in existence for nearly two centuries in Europe before being recognized in the United States, where it was first reported in 1902. Over the next two decades, pellagra occurred in epidemic proportions in the American South. Poverty and consumption of corn were the most frequently observed risk factors. Since the exact cause and cure of pellagra was not known, a culture of "pellagraphobia" formed among the public. Patients were shunned and ostracized. The medical community implicated spoiled corn as the cause of pellagra, which had economic repercussions for agriculturists. Joseph Goldberger, MD, of the United States Public Health Service eventually solved the secret of the malady: faulty diet. Goldberger was able to prevent and induce pellagra by dietary modification, a landmark event in the annals of medicine, nutrition, and epidemiology. His work and the social history of that period are reviewed.

Disease Outbreaks↗

PubMed1982

Pellagra: "A reappraisal".

A brief review of the epidemiological history of pellagra is attempted. In Europe and North America Pellagra is practically eradicated at the present time. However, in mediterranean countries, with much sunlight, cases of the disease are sporadically seen. Nevertheless, in countries with a low nutritional level Pellagra still exists as endemic form. In Athens, Greece, the last decade 1971-1981, 56 new cases of Pellagra were studied. A short analysis of the above cases concerning mainly the real cause of the disease is presented. Moreover, the more recent aspects concerning the aetiological factors responsible for the appearance of Pellagra, with special emphasis to vitamins, is reported.

Alcoholism↗

PubMed1993

Pellagra--increased viscosity of extracellular matrix.

Pellagra is the result of increased viscosity of extracellular matrix (ECM). The skin changes in pellagra localize at sites of sun exposure or trauma because the mediators which are released cannot diffuse from the area. Edema is reported as the first clinical and microscopic change. Changes in the ECM are not directly visible. Increased viscosity of ECM in the gastrointestinal tract would decrease absorption of fluid and nutrients from the bowel resulting in diarrhea. In the tongue the excess ECM viscosity holds water producing swelling. The effect of climate and seasons relates to the increased demand for ECM repair on sunlight exposed areas. Infections increase the severity of pellagra by requiring increased tissue repair. Local infections are often unusually severe. Infections have a greater inflammatory component at sites of high ECM viscosity. Nicotinic acid reverses the neurologic and gastrointestinal changes of pellagra in 24 h. This suggests a simple rapid mode of action. Nicotinic acid plays a major role in tissue respiration which is essential for tissue repair and degradation of glycosaminoglycans. Altering ECM viscosity is a method of modulating inflammation, immunity, and normal tissue physiology.

Central Nervous System↗

PubMed2004

Niacin metabolite excretion in alcoholic pellagra and AIDS patients with and without diarrhea.

OBJECTIVE: Malnourished patients with the acquired immunodeficiency syndrome (AIDS) can develop pellagra-like manifestations such as dermatitis, diarrhea, and dementia; therefore, we tested the hypothesis that patients with AIDS and diarrhea would have niacin depletion. This study compared 24-h urine excretion of N1-methyl-nicotinamide (N1MN) among patients with pellagra and patients with AIDS who did and did not have diarrhea. METHODS: Three groups were studied: G1 (patients with AIDS and diarrhea, n = 5); G2 (patients with AIDS and no diarrhea, n = 7), and G3 (patients with alcoholic pellagra and without the human immunodeficiency virus, n = 8). Diarrhea was defined as the production of at least three liquid stools per day over 3 to 5 d. Studies included mucosal intestinal biopsy, malabsorption tests, detection of parasites in stool, and serum albumin measurements. Semiquantitative food-frequency questionnaire, anthropometry, and daily urinary N1MN excretion were also determined. Groups were matched in relation to age, sex, presence of parasites in stool, and intestinal absorption results. RESULTS: G1 had normal intestinal examination by light microscopy and no parasites in stools. G2 group showed lower levels of serum albumin (2.6 +/- 0.3 g/dL) when compared with G1 (3.4 +/- 0.3 g/dL) and G3 (3.1 +/- 0.7 g/dL). Except for patients with pellagra, groups met their energy requirements. Patients in G3 (0.013, 0.01-0.081 mg/dL) and G1 (0.062, 0.001-0.33 mg/dL) excreted smaller amounts of N1MN in urine than did those in G2 (0.63, 0.02-2.9 mg/dL). CONCLUSIONS: Patients with AIDS and diarrhea excreted less N1MN in urine than did those without diarrhea. These patients may have an impaired niacin nutritional status, possibly associated with increased metabolic needs.

Acquired Immunodeficiency Syndrome↗

PubMed1988

The clinical spectrum of alcoholic pellagra encephalopathy. A retrospective analysis of 22 cases studied pathologically.

A retrospective clinical study of 22 heavy alcohol drinkers is reported in which postmortem study showed diffuse chromatolysis of neurons identical to that found in neurological pellagra, associated in 13 cases with Marchiafava-Bignami disease and/or Wernicke-Korsakoff disease. The clinical features included confusion and/or clouding of consciousness, marked oppositional hypertonus ('gegenhalten') and myoclonus. Because of the frequent coexistence of other alcoholic encephalopathies in the same patient, alcoholic pellagra was often unrecognized. Fifteen patients received thiamine and pyridoxine therapy without niacin. It appeared to aggravate the neurological state or to trigger the development of alcoholic pellagra encephalopathy in 9 cases. The relationship between pellagra occurring during thiamine and pyridoxine therapy and 'nicotinic acid deficiency' is discussed. Multiple vitamin therapy should be given in the treatment of undiagnosed encephalopathies in alcoholic patients.

Adult↗

PubMed1988

Chromatolysis in alcoholic encephalopathies. Pellagra-like changes in 22 cases.

In 22 patients with alcoholic encephalopathies, chromatolysis similar to that reported in endemic pellagra was found on postmortem examination. No gross macroscopic changes were seen in affected areas and only neurons were involved. The changes consisted of central chromatolysis, seen predominantly in the brainstem, especially in the pontine nuclei, where they were constant, and in the cerebellar dentate nuclei. Nuclei of cranial nerves (mainly the third, sixth, seventh and eighty), the reticular nuclei, arcuate nuclei and posterior horn cells, were also markedly affected. Changes were sometimes seen in the cerebral cortex, the interpeduncular nuclei, the central mesencephalic grey matter, the colliculi, the tenth and twelfth cranial nerve and perihypoglossal nuclei, the gracile and cuneate nuclei and anterior horn cells. This distribution was different from that reported in endemic and 'endogenous' pellagra or in isoniazid-induced pellagra encephalopathy. Central chromatolysis was the only pertinent finding of the CNS examination in 9 cases. In 8 cases, chromatolysis was associated with Marchiafava-Bignami encephalopathy, in 4 cases with Wernicke-Korsakoff encephalopathy, and in 1 other case with both. Mild degeneration of spinal cord tracts was seen in 3 cases. The chromatolysis of alcoholic pellagra did not appear to be a retrograde change related to axonal degeneration. Systemic examination showed liver changes in 15/16 cases. Treatment of these cases had not included niacin. No differences were found between cases given thiamine and pyridoxine and those which had not. Microscopic examination of the pons is essential in alcoholic encephalopathies.

Alcoholism↗

PubMed1985

A reexamination of the composition of diets associated with pellagra.

Diets described in historical studies of human pellagra, have been reexamined by using modern tables of nutrient composition. Five apparently pellagragenic diets from field studies were estimated to have niacin equivalents (NE) well in excess of the Recommended Dietary Allowance (RDA), i.e., 6.6 mg/1000 kcal. In these diets, the estimated contribution of riboflavin was below the RDA, i.e., 0.6 mg/1000 kcal. A series of trials of the pellagra-preventive value of different foods carried out by the U.S. Public Health Service from 1920 to 1936 used over 400 women subjects, of whom fifty developed signs of pellagra on diets now calculated to contribute 7.2-10.6 mg NE/1000 kcal. Most of these diets apparently had less than 60% of the RDA for riboflavin. Further calculations, assuming that the niacin in ordinary cereal foods has only 30% bioavailability, still left half of the pellagragenic diets apparently with more than the RDA for "available NE." Possible reasons for the apparent discrepancy between these results and the RDA's calculated from more recent controlled studies are discussed. It is suggested that the pellagra epidemic in the U.S.A. in the early 1900's has not yet been explained satisfactorily.

Biological Availability↗

PubMed1991

Plasma amino acid patterns in alcoholic pellagra patients.

Plasma amino acid concentrations in 33 male alcoholic patients with pellagra (age 20-68 years) were compared with those in 17 healthy male subjects (age 20-45 years). Pellagra diagnosis was made on the basis of the typical clinical skin picture, and low urinary excretion of N'methylnicotinamide and N'methyl-2-pyridone-5-carboxamide (reduced by 70 and 80%, respectively, compared with controls). There were significant differences in body mass index, creatinine/high index and serum albumin between the two groups, indicating that besides pellagra the alcoholic patients had some degree of malnutrition. Of 17 plasma amino acids measured, the following had significantly lower concentrations in the pellagrins: tryptophan (3.65 vs 5.93 mumol/dl, pellagrin vs control), isoleucine (6.31 vs 11.13), leucine (11.54 vs 24.19), lysine (16.25 vs 34.47), methionine (2.61 vs 4.22), phenylalanine (5.71 vs 9.23), threonine (13.29 vs 26.81), valine (17.60 vs 41.06), alanine (42.54 vs 70.87), arginine (5.87 vs 10.09), tyrosine (5.57 vs 9.30). Glutamic acid was significantly higher in the pellagrins (18.45 vs 9.49). There was no difference between the groups of aspartic acid, glycine, histidine, proline and serine concentrations. It is concluded that pellagra is an important factor influencing the amino acid profiles in these patients. This finding should be taken into account when using plasma amino acid levels to assess the clinical status of the pellagrin.

Alcoholism↗

PubMed1993

Pellagra secondary to 5-fluorouracil.

The development of pellagra in a patient treated with 5-fluorouracil for malignant disease is reported. The aetiology of pellagra in this patient is discussed, and the reasons for possible under-diagnosis of pellagra in association with malignant disease considered. We report a patient who presented with the typical skin changes of pellagra. The rash, and an associated acute deterioration in cerebral function, were exacerbated by treatment with 5-fluorouracil. The importance of considering nicotinic-acid deficiency in patients with malignant disease has not been emphasized in the literature.

Aged↗

PubMed1981

Pellagra among chronic alcoholics: clinical and pathological study of 20 necropsy cases.

Twenty cases of pellagra, diagnosed on neuropathological grounds, were found amont 74 necropsy cases of chronic alcoholism. Although these patients had presented with various mental, neurological and gastrointestinal symptoms, the diagnosis of pellagra had not been established clinically because, in the majority, there were no skin lesions. It is emphasised that whenever chronic alcoholics exhibit certain mental, neurological or gastrointestinal symptoms, one should strongly suspect pellagra even in the absence of skin lesions (pellagra sine pelle agra).

Adult↗

PubMed2003

A case of pellagra and a South Carolina history of the disorder.

This case raises many questions about pellagra in the 21st century. Why are so few cases diagnosed in industrialized societies? Are physicians and other health care providers overlooking many cases? Should we treat any "sick" person and those with unexplained skin, mental status changes or gastrointestinal complaints with safe, inexpensive doses of niacin? Should an inexpensive, reliable laboratory test for pellagra be developed? Clearly the quote, "if you keep pellagra in mind, you will recognize it when you see it" is valid. But perhaps that is not sufficient and pellagra is frequently invisible.

Aged↗

PubMed2006

[A suspected case of alcoholic pellagra encephalopathy with marked response to niacin showing myoclonus and ataxia as chief complaints].

We report a 47-year-old alcoholic man with alcoholic pellagra encephalopathy (APE) showing myoclonus and ataxia as chief complaints. He had been a heavy drinker for 30 years. He had noticed appetite loss and subsequently showed a subacutely progressive gait disturbance. He had no history of diarrhea, dementia, or dermatitis. On admission, he showed severe alcoholic liver cirrhosis with a large amount of ascites, limbs and truncal ataxia, myoclonus of the limbs and areflexia, although his consciousness was alert and there were no sign of dermatitis. Though the plasma level of ammonia was normal, we started administration of amino acids suspecting hepatic encephalopathy. Symptoms showed no improvement, and subsequent administration of thiamine was also ineffective. A decreased serum level of niacin was demonstrated. After administration of nicotinamide, the symptoms improved gradually. This patient received a diagnosis of APE. Endemic pellagra, characterized by the classical triad of dermatitis, diarrhea and dementia, is known to be caused by a dietary deficiency of the niacin, and has now become very rare in developed countries. At present, pellagra is encountered most often in patients with chronic alcoholism, which is called APE. APE patients often show only disturbance of consciousness. Although several reports has described ataxia and myoclonus in patients with APE, APE patients with myoclonus and ataxia as chief complaints have not previously been reported. On autopsy cases, central chromatolysis of neurons in the dentate nucleus of the cerebellum, gracile and cuneate nuclei, and the Clarke's column has been demonstrated. The APE patients would show myoclonus and ataxia as their first symptoms. In conclusion, we would like to emphasize that administration of niacin should be started for the treatment of chronic alcoholic patients showing myoclonus and ataxia even without the classical triads found in endemic pellagra patients.

Alcoholism↗

PubMedDate not supplied

Lack of relationship between sorghum consumption, mycotoxin contamination and pellagra in a traditionally sorghum eating population.

Traditionally, the disease pellagra has been associated with corn consumption and niacin deficiency, and has presently been recognised as a multiple factor nutritional syndrome. In the recent past, it has been suggested that consumption of mycotoxin contaminated sorghum/corn may be involved in the development of pellagra in a sorghum/corn eating population. The present study relates to the assessment of levels of mycotoxins (aflatoxin B1 and T-2 toxin) in sorghum collected from a traditionally sorghum eating population. Despite 25% fungal contamination in the sorghum samples collected, the levels of mycotoxins were minimal (1.4%) and there was no incidence of pellagra in the survey area. The absence of pellagra in the survey areas may be attributed to the changing dietary pattern.

Edible Grain↗

PubMed1991

Pellagra and pellagralike dermatoses: etiology, differential diagnosis, dermatopathology, and treatment.

Clinical pellagra is a multiple vitamin-deficiency disease. The clinical manifestations include dermatitis, diarrhea, and dementia; the result is often death. Photosensitivity has also been associated with pellagra. Other clinical findings may depend on the nutritional status of the patient. Pellagrins may not have specific cutaneous pathological findings, although necrolytic migratory erythema has been reported in clinical pellagra. Most pellagrins respond to niacin combined with a high-protein diet, although other concomitant vitamin deficiencies may prevent the use of niacin. Clinical pellagra should be considered in the differential diagnosis of patients with chronic alcoholism, malnutrition, and amino acid imbalance.

Humans↗

PubMed1998

[Pellagra (deficiency of vitamin B3 or of the amino acid tryptophan): a disease still extant in the Netherlands].

Pellagra was diagnosed in a 48-year-old female patient with a bullous skin disease. The skin disease with purple/red sharply demarcated spots on hands and feet had worsened after sun exposure. She was a chronic alcoholic and for the last few months she had had diarrhoea. The treatment included vitamin B3, vitamin B complex and a high-quality protein diet. Within three days her skin disease improved. Pellagra is caused by a deficiency of nicotinamide or of its precursor tryptophan. It may occur in patients with dietary deficiency diseases (e.g. chronic alcoholics), carcinoid syndrome, HIV infections and drugs: fluorouracil, isoniazid, chloramphenicol and mercaptopurine. Pellagra leads to the triad: dermatitis, diarrhoea and dementia, eventually followed by death. The skin changes are characteristic and pathognomonic. Recognition of pellagra is important; the prognosis is good after treatment.

Alcoholism↗

PubMed2006

Intestinal permeability and oxidative stress in patients with alcoholic pellagra.

BACKGROUND & AIMS: Increased intestinal permeability is one of the grastointestinal changes observed in alcoholic patients. However, there are no objective definitions as yet of how alcohol induces pathological changes in the various organs. The action of oxygen-free radicals during ethanol metabolism has been considered a determinant factor of these alterations. The present study was undertaken to determine the effect of niacin supplementation on intestinal permeability and oxidative stress in patients with alcoholic pellagra. METHODS: The study was divided into two phases: in Phase 1 we studied ten patients with pellagra before treatment with niacin, and in Phase 2 we studied the same patients after 27 days of treatment with niacin. Intestinal permeability was assessed by the (51)CrEDTA test and the antioxidant action of niacin supplementation was assessed by the determination of lipid peroxidation (plasma malondialdehyde, MDA), protein oxidation (plasma carbonyl group) and of the antioxidants plasma vitamin E and erythrocyte glutathione peroxidase. RESULTS: Comparison of intestinal permeability by the (51)CrEDTA test before and after niacin treatment showed a significant decrease in permeability from 4.29+/-1.92% to 1.90+/-1.19% (P<0.05). Assessment of oxidative stress showed a significant decrease (P<0.05) in lipid and protein peroxidation (MDA: 1.19+/-0.40-0.89+/-0.27 micromol/l; carbonyl groups: 2.22+/-0.36-1.84+/-0.40 nmol/mg protein). CONCLUSIONS: The results suggest that niacin and vitamin E deficiency in patients with pellagra could be important factors in increased intestinal permeability and decreased antioxidant conditions, recovering to normal values after treatment with niacin, associated to alcohol abstinence and a balanced diet.

Alcoholism↗

PubMed1999

Isoniazid induced pellagra despite pyridoxine supplementation.

Although pellagra is a recognized complication of isoniazid therapy, the diagnosis may be overlooked or delayed--sometimes with life-threatening consequences. We report a case of isoniazid-induced pellagra which occurred despite pyridoxine supplementation. Drug withdrawal and supplementation with niacin led to a rapid and sustained clinical improvement. The possible mechanisms of isoniazid induced pellagra are discussed.

Anti-Inflammatory Agents↗

PubMed1984

Inhibition of tryptophan metabolism by oestrogens in the rat: a factor in the aetiology of pellagra.

The effect of the administration of oestrone sulphate on tryptophan metabolism has been assessed in rats in order to determine whether and to what extent inhibition of tryptophan metabolism by oestrogens may be a factor in the aetiology of pellagra, and might explain the reported twofold excess of females over males in many outbreaks of pellagra. Feeding ovariectomized rats for 1 week on a diet containing 15 mg oestrone sulphate/kg led to significant inhibition of kynurenine hydroxylase (EC 1.14.13.9), kynureninase (EC 3.7.1.3) and 3-hydroxyanthranilate oxidase (EC 1.13.11.6). There was also a significant increase in plasma tryptophan, suggesting decreased activity of tryptophan oxygenase (EC 1.13.11.11). This inhibition of tryptophan metabolism will result in a considerable reduction in the synthesis of the nicotinamide nucleotide coenzymes (NAD and NADP) from tryptophan. When ovariectomized rats were maintained for 4 weeks on a diet providing no preformed niacin and only a marginally adequate amount of tryptophan (1030 mg/kg), the addition of sulphate to the diet led to a significant reduction in the liver content of nicotinamide nucleotides and the urinary excretion of the end-product of NAD metabolism, N1-methyl nicotinamide. It is suggested that when the diet is only marginally adequate in tryptophan and niacin, inhibition of tryptophan metabolism by endogenous or administered oestrogens may be an additional factor in the development of pellagra.

Animals↗