Serum electrolytes in hospitalized pellagra alcoholics

Abstract

Background: Owing to high diarrhoea and protein malnutrition frequencies in pellagra, we hypothesised that pellagra patients would have higher electrolyte disturbances than non-pellagra alcoholics. Objective: To compare serum electrolytes of hospitalised alcoholics with or without pellagra. Design: Retrospective and descriptive case-control study. Setting: Internal Medicine wards at a University Hospital, Medical School of Uberaba, Brazil. Subjects: Medical records were reviewed to obtain relevant clinical details, main diagnosis and laboratory data, including serum electrolytes on hospital admission of pellagra patients (n 33) and a randomly chosen control group of alcoholics (n 37), matched in age, gender and socio-economic status. Anaemia was ascertained by haemoglobin`12.5 gadl (men) and 1.5 gadl (women), and hypoalbuminemia by serum albumin`3.3 gadl. Results: Pellagra and controls showed similar age (39.4 AE 13.1 vs 45.0 AE 11.4 years) and a male predominance of gender (69.7 vs 78.4%), and similar associated diagnoses, including high blood pressure (21.2 vs 16.2%), peripheral neuropathy (12.1 vs 13.5%), and pneumonia (9.1 vs 13.5%). Despite displaying similar serum sodium (136.6 AE 6.1 vs 137.8 AE 5.7 mEqaI), magnesium (1.72 AE 0.74 vs 1.62 AE 0.34 mgadl), phosphorus (3.79 AE 0.87 vs 3.87 AE 0.78 mEqa1) than controls,in addition to higher hypoalbuminemia (76.2 vs 33%) and anaemia (60.6 vs 35.1%) frequencies. Conclusions: Higher anaemia and hypoalbuminemia frequencies associated with lower serum potassium levels suggest increased protein malnutrition prevalence among pellagrins.

Magnesium, Calcium, Potassium, Sodium, Phosphorus, Selenium, Zinc, and Chromium Levels in Alcohol Use Disorder: A Review

“…However, clinical symptoms of chronic alcohol consumption are also decreased levels of phosphate, magnesium, potassium, sodium and calcium, and other elements in blood plasma [ 8 , 9 , 10 ]. Electrolyte abnormalities develop as a result of chronic alcohol consumption during acute alcohol intoxication, but they are particularly important during alcohol withdrawal [ 11 , 12 , 13 , 14 ]. It turns out that even during alcohol withdrawal, hypokalemia, hypomagnesemia, and hyponatremia are observed [ 15 , 16 ].…”

“…Alcohol is metabolized in three pathways, involving enzymes such as the alcohol dehydrogenase present in the cytosol, the Microsomal Ethanol Oxidizing System (MEOS), and the catalase (CAT) contained in peroxisomes (Figure 1). during acute alcohol intoxication, but they are particularly important during alcohol withdrawal [11][12][13][14]. It turns out that even during alcohol withdrawal, hypokalemia, hypomagnesemia, and hyponatremia are observed [15,16].…”

Alcohol as a toxic and disease‐forming agent: Not just the liver and brain and not every drinker

“…Another example is pellagra-associated neuropathy due to niacin deficiency [46]. In addition, deficiencies of riboflavin (B2), pyridoxine (B6) and cobalamin (B12) are also reported to cause neuropathy [46,47]. Foetal alcohol syndrome also causes neurological deficits.…”

“…For example, thiamine deficiency leading to damage of nervous tissues is particularly associated with alcoholism especially Wernicke encephalopathy or WernickeKorsakoff syndrome [45]. Another example is pellagra-associated neuropathy due to niacin deficiency [46]. In addition, deficiencies of riboflavin (B2), pyridoxine (B6) and cobalamin (B12) are also reported to cause neuropathy [46,47].…”

Toxic Effects of Alcohol on the Heart

“…126 Acute alcohol intoxication, acute withdrawal, and chronic alcohol abuse can all lead to SCD as a result of several overlapping mechanisms. 133 In chronic heavy drinkers, besides autonomic dysfunction due to vagal neuropathy, prolonged QTc, and dyselectrolytemia, increased QTc dispersion, steeper QT/RR slope, and the development of cardiomyopathy may all contribute to SCD. 127À129 Severe coronary vasospasm may be triggered by heavier doses of alcohol.…”