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Pellagra is a nutritional disorder due to deficiency of vitamin niacin (vitamin-B3) or its precursor tryptophan, which was first described by a Spanish physician Gaspar Casal (1735AD). Classically, it manifests with triad of diarrhea, dermatitis and dementia and if not treated in time leading to death. Thus, it´s a disorder affecting the skin, nerv...
In developing countries like India, nutritional deficiencies are prevalent and hyperpigmentation due to protein energy malnutrition, zinc deficiency and pellagra are common. Indian women, especially vegetarian are prone to vitamin B12 deficiency. Vitamin B12 deficiency can present as anaemia, neurological defect, gastrointestinal symptoms or dement...
Pellagra is caused by an abnormal intake and/or use of niacin, but its phenotypes are diverse. The phenotypes of pellagra can also be atypical, such as nausea. We previously reported a mouse model of pellagra-related nausea. However, the mechanism of this model is unclear. In this study, we found that the gut microbiota, which is thought to be a so...
Pellagra is a forgotten disease, particularly in developed countries. It is a nutritional disorder characterized by 4 “Ds”: diarrhea, dermatitis, dementia, and death. Causes of pellagra are chronic alcoholism, inadequate diet, malabsorption, metabolic derangement and drugs. Half-and-half nail is an occasional but specific clinical finding in chroni...
Currently pellagra is usually the subject of dermatological or non-dermatological case reports. Since the first description of the disease, its cause has remained unknown for many years. There were no known methods of prevention and treatment. For two centuries, pellagra was an incurable disease and caused several hundred thousand deaths in Europe...
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... Thus, the potential antibacterial activity of the 4-INN product should be investigated. Pellagra is an infrequent side effect of long-term INH therapy that is believed to be due to competitive inhibition of NAD and NADP by INH (6,8,24). Based on the data presented, we can postulate that significant amounts of nicotinic acid can be lost through the excretion of 4-INN, resulting in nicotinic acid deficiency and the development of pellagra. ...
One of the most effective and widely used antituberculosis (anti-TB) drugs is isoniazid (INH), a prodrug activated via oxidation
that forms an adduct with NAD+ to inhibit NADH-dependent targets of Mycobacterium tuberculosis, such as enoyl-acyl carrier protein reductase (InhA). The metabolic by-products and potentially toxic intermediates resulting
from INH therapy have been identified through a large body of work. However, an INH-NAD adduct or structures related to this
adduct have not been identified in specimens from human TB patients or animal models of TB. Analyses by mass spectrometry
of urine collected from TB patients in a study conducted by the NIAID-funded Tuberculosis Research Unit identified 4-isonicotinoylnicotinamide
(C12H9N3O2) as a novel metabolite of INH therapy. This compound was formed by M. tuberculosis strains in a KatG-dependent manner but could also be produced by mice treated with INH independent of an M. tuberculosis infection. Thus, the 4-isonicotinoylnicotinamide observed in human urine samples is likely derived from the degradation of
oxidized INH-NAD adducts and provides direct evidence of host INH activation.
Antimicrobials are a widely used class of medications, but several of them are associated with neurological and psychiatric side effects. The exact incidence of neurotoxicity with anti-infectives is unknown, although it is estimated to be < 1%. Neurotoxicity occurs with all classes of antimicrobials, such as antibiotics, antimycobacterials, antivirals, antifungals and antiretrovirals, with side effects ranging from headaches, anxiety and depression to confusion, delirium, psychosis, mania and seizures, among others. It is important to consider these possible side effects to prevent misdiagnosis or delayed treatment as drug withdrawal can be associated with reversibility in most cases. This article highlights the different neurotoxic effects of a range of antimicrobials, discusses proposed mechanisms of onset and offers general management recommendations. The effects of antibiotics on the gut microbiome and how they may ultimately affect cognition is also briefly examined.
A Case of Pellagra Induced by Isoniazid during Treatment of Pulmonary Tuberculosis Pellagra is a disease caused by a deficiency of nicotinic acid or niacin. It is mostly found among people eating corn-based diets in parts of China, Africa and India. It is also induced by drugs, such as isoniazid or 5-fluorouracil. Isoniazid inhibits the conversion of tryptophan to niacin and may induce pellagra, particularly in poorly nourished patients. Pellagra should be suspected whenever tuberculous patients under the treatment with isoniazid develop mental, neurological or gastrointestinal symptoms, even in the absence of typical skin changes. Herein, our experienced of a case of pellagra induced by isoniazid during treatment of pulmonary tuberculosis is reported. The patient was referred due to a skin rash and drowsy mental status. Her skin lesion developed during treatment for pulmonary tuberculosis. Her symptoms were improved after discontinuation of antituberculous agents and on the administration of nicotinamide.
Background and aims This article reviews the published literature on the mechanisms by which drugs alter nutrient intake and the interactions between drugs and nutrients. We aimed to examine evidence of nutrient deficiencies caused by drug therapy, to indicate groups of ‘at-risk’ patients and suggestions made for practical methods of detection and intervention.
Methods Information was retrieved from a MEDLINE search of English language literature from 1963 to January 1999. Search terms included nutrient, deficiencies and interactions. Additional references were obtained from cross-referencing related review articles and from pharmacology textbooks relating to interactions and side-effects of drugs. All drugs are referred to by their generic names.
Results Drugs can reduce nutrient intake in several ways and can be broadly classified as: (i) drugs that reduce oral intake; (ii) drugs that alter nutrient absorption and (iii) drugs that affect nutrient metabolism. In this review the mechanisms by which drugs can alter nutritional status are discussed, with specific examples of drug therapy and associated symptoms of deficiencies.
Conclusions Patients at high risk of experiencing the effects of drug-induced nutrient deficiencies are the elderly and chronically ill. Recommendations made for methods of intervention include counselling and annotations on drug prescriptions.
The coenzyme functions of the B vitamins in intermediatry metabolism are well established; nevertheless, for none of them is it possible to determine precisely the connection between the biochemical lesions associated with deficiency and the neurological consequences. Although there is convincing evidence of a neurospecific role for thiamin and other B vitamins, in no case has this role been adequately described. Similarly, the neurochemical sequelae of intoxication by massive amounts of vitamins (so-called mega-vitamin therapy or orthomolecular medicine) remain largely unexplained.
Good clinical care extends beyond mere diagnosis and treatment of disease to appreciation that nutrient deficiencies can be the price of effective drug therapy. The major risk factors for developing drug-induced nutrient deficiencies are lack of awareness by the prescribing physician and long duration of drug therapy. The field of pharmacogenomics has potential to improve clinical care by detecting patients at risk for complications from drug therapy. Further improvements in patient safety rely on physicians voluntarily reporting serious suspected adverse drug reactions.
Refeeding syndrome (RFS) is the result of aggressive enteral or parenteral feeding in a malnourished patient, with hypophosphatemia being the hallmark of this phenomenon. Other metabolic abnormalities, such as hypokalemia and hypomagnesemia, may also occur, along with sodium and fluid retention. The metabolic changes that occur in RFS can be severe enough to cause cardiorespiratory failure and death. This article reviews the pathophysiology, the clinical manifestations, and the management of RFS. The key to prevention is identifying patients at risk and being aware of the potential complications involved in rapidly reintroducing feeds to a malnourished patient.
Malnutrition is common in infants and children with chronic liver disease (CLD) and may easily be underestimated by clinical appearance alone. The cause of malnutrition in CLD is multifactorial, although insufficient dietary intake is probably the most important factor and is correctable. Fat malabsorption occurs in cholestatic disorders, and one must also consider any accompanying fat-soluble vitamin and essential fatty acid deficiencies. The clinician should proactively evaluate, treat, and re-evaluate response to treatment of nutritional deficiencies. Because a better nutritional state is associated with better survival before and after liver transplantation, aggressive nutritional management is an important part of the care of these children.
Since the identification of cystic fibrosis (CF) in the 1940s, nutrition care of patients who have CF has been a challenge. Through optimal caloric intake and careful management of malabsorption, patients are expected to meet genetic potential for growth. Yet factors beyond malabsorption, including nutrient activity at the cellular level, may influence growth and health. This article reviews nutrition topics frequently discussed in relationship to CF and presents intriguing new information describing nutrients currently being studied for their impact on overall health of patients who have CF.
