Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0024523 (malabsorption)
 7,319 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A toxic effect of alcohol is the principal cause of the development of liver disease in alcoholism. Fatty infiltration of the liver is a consequence of ethanol metabolism due mainly to an increased synthesis and decreased degradation of fatty acids. Mechanisms that have been suggested for ethanol-induced hepatocellular necrosis include centrolobular hypoxia due to an increased oxygen requirement and intracellular accumulation of protein, fat, and water which results in increased cell size. Hepatocellular necrosis, however, may not be a necessary stage in the development of cirrhosis. Chronic ethanol administration increases hepatic collagen deposition, and acute and chronic ethanol administration inhibit liver cell regeneration. Increased humoral and cellular immunological activity to liver tissue and its components may contribute to the persistence of liver disease in the alcoholic. However, only a small proportion of alcoholics and baboons fed alcohol develop cirrhosis, suggesting that other factors, either genetic, environmental, or nutritional, play a role. Malnutrition is common in alcoholics. Liver disease is more common in some malnourished populations, and has been produced by nutrient deficiencies. Decreased dietary intake, as well as malabsorption and alterations in the metabolism of nutrients, are causes of nutrient deficiencies in alcoholism. Some of the effects of alcohol on the liver may be mediated by its actions on nutrient absorption and metabolism.
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PMID:Alcoholic liver disease: roles of alcohol and malnutrition. 700 89

Magnesium deficiency may complicate many diseases. The causes include the following: inadequate intake during starvation or increased requirement during early childhood, pregnancy, or lactation; excessive losses of magnesium as a result of malabsorption from the gastrointestinal tract or from the kidneys during use of diuretics; and to a combination of the two, as in alcoholism. Most often the etiological factors have been operative for a month or more. Acute hypomagnesemia can occur without previous Mg deficiency after epinephrine, cold stress and stress of serious injury or extensive surgery. The clinical manifestations depend on the age of the patient and may begin insidiously or with dramatic suddenness, or there may be no overt symptoms or signs. The manifestations can be divided into the following categories: totally non-specific symptoms and signs ascribable to the primary disease; neuromuscular hyperactivity including tremor, myoclonic jerks, convulsions, Chvostek sign, Trousseau sign (rarely), spontaneous carpopedal spasm (rarely), ataxia, nystagmus and dysphagia; psychiatric disturbances from apathy and coma to some of all facets of delirium; cardiac arrhythmias including ventricular fibrillation and sudden death; hypocalcemia which is responsive only to Mg therapy; and hypokalemia which is not easily nor completely corrected without Mg therapy. The diversity of etiologies and the multiplicity of manifestations result in confusion and controversy. The documentation of normal renal function is absolutely necessary for maximum doses. The order of magnitude of dose is 1.0 meq Mg/kg on day 1, and 0.3 to 0.5 mEq/kg per day for 3 to 5 days. In emergencies such as convulsions or ventricular arrhythmias, a bolus injection of 1.0 gm (8.1 meq) of MgSO4 is indicated. Therapy of Mg deficiency in the presence of renal insufficiency requires smaller doses and frequent monitoring. Complete repletion occurs slowly.
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PMID:Magnesium deficiency. Etiology and clinical spectrum. 702 Mar 47

In three different groups of patients presenting severe folate deficiency (purely nutritional folate deficiency, chronic alcoholism or various intestinal diseases), vitamin B12 absorption has been tested by Schilling test in order to investigate the possible effect of folate deficiency on B12 absorption. Following this study, it appears that folate deficiency in itself, even severe, cannot induce vitamin B12 malabsorption, since in the first group, consisting of malnourished old people, the Schilling test was always normal even in those who presented a lowered B12 serum level; in the group of patients with intestinal disease, the Schilling test was abnormal as expected in some patients; 3 alcoholics out of 12 presented a malabsorption of B12 on the Schilling test; the follow-up of 2 of them exhibited complete correction after normal diet and alcohol suppression. Consequently, folate deficiency does not seem responsible for a secondary B12 malabsorption unless another etiological factor is present, such as alcohol or ileopathy.
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PMID:Effect of folate deficiency on vitamin B12 absorption. 714 39

The high incidence of megaloblastic anemia observed at our institution (2.1% of hospital admissions) prompted us to analyze the causes of cobalamin and/or folate deficiency in 30 patients admitted during the period 1983-1991 to the Medical Department of Locarno District Hospital. The study population includes 19 women and 11 men with a mean age of 69 years (range 28-91 years). All patients had severe macrocytic anemia (mean hemoglobin 74 +/- 23 g/l, MCV 121 +/- 12 fl), striking megaloblastic changes in aspirated marrow, and an elevated serum level of LDH (2170 +/- 2150 U/l). 19 patients had associated thrombocytopenia, 12 leukopenia and 11 both thrombocytopenia and leukopenia. Treatment led to prompt reticulocytosis and correction of megaloblastic changes in all patients, as well as to nearly complete resolution of the neurologic disorder in a patient with severe spastic ataxia. In 15 patients, megaloblastic anemia was caused by folate deficiency related to alcoholism (n = 6, mean age 55 years) and old age or poverty (n = 9, mean age 73 years). Cobalamin deficiency was present in 9 patients (mean age 69 years); it was due to pernicious anemia in 6 patients and to malabsorption in 2, while the cause remained unexplained in 1. The last patients (mean age 76 years) had deficiency of both cobalamin and folate, related to alcoholism (n = 3) or poverty (n = 3).
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PMID:[Megaloblastic anemia: 30 cases in a district hospital]. 787 99

Chronic ethanol consumption produces nutrient malabsorption. The mechanisms by which this occurs are poorly understood. One potential mechanism is an alteration in microvillus membrane (MVM) composition and fluidity. The effects of in vivo ethanol exposure on MVM lipid composition and fluidity were determined in rats fed either a standard diet or 15% ethanol in water for 2 months. Acute jejunal exposure to 4% ethanol was also performed in vivo in each feeding group. Acute exposure to ethanol produced an increase in static and dynamic membrane fluidity associated with a decrease in MVM cholesterol regardless of prior ethanol exposure. Chronic ethanol feeding alone did not alter membrane fluidity. Changes in membrane fatty acid composition were minor and variable after both acute and chronic ethanol exposure. Prior chronic ethanol feeding did not prevent the acute effects of ethanol on MVM composition or fluidity. These data support the theory that ethanol acutely disrupts nutrient transport by changing MVM lipid fluidity. The absence of adaptive changes in membrane composition and fluidity may also explain the persistent absorptive defects seen with chronic alcoholism.
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PMID:Effects of acute and chronic ethanol exposure on intestinal microvillus membrane lipid composition and fluidity. 794 55

Wernicke's encephalopathy (WE) is a thiamine deficiency disorder and is characterized clinically by the triad of ocular abnormalities, ataxia and disturbances of consciousness. We report on 3 patients with WE, of whom 2 had insufficient thiamine substitution. In the first patient symptoms disappeared during thiamine substitution. In the second patient acute WE was the terminating event in the sequence of parenteral nutrition, lactic acidosis and cardio-pulmonary decompensation. Possibly due to hereditary deficits WE developed in the third patient despite sufficient thiamine substitution. Attention to thiamine deficiency should be paid in all patients with history of alcoholism, malnutrition, malabsorption, tumors, inflammation, other severe diseases and in parenteral hyperalimentation. In order to prevent WE thiamine should be substituted with at least 100 mg/day i.v. or i.m.
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PMID:Wernicke's encephalopathy--causes to consider. 804 22

Mucocutaneous changes occur in vitamin deficiency states and may be helpful in clinical diagnosis of the underlying disease. Substitution and therapy with vitamins can also cause skin problems, which may be of allergic of nonallergic origin. The skin and mucosal changes in pellagra and scurvy can be diagnostic; however, in other vitamin deficiencies, skin signs are rather unspecific. In most cases combined vitamin deficiencies occur that result in polymorphic and nonspecific mucocutaneous signs. Vitamin deficiencies are due to malnutrition, malabsorption or genetic defects. In industrialized countries alcoholism and gastrointestinal disorders are the main cause of vitamin deficiencies. Alcoholics or patients with malabsorption syndrome suffering from seborrheic dermatitis-like or ichthyosiform-like eruptions should be investigated for vitamin deficiency. Laboratory analysis of blood and urine vitamin levels can be misleading because of the poor correlation with tissue vitamin concentrations. Rapid clinical improvement following vitamin substitution frequently confirms the clinical diagnosis. In this overview we describe mucocutaneous signs of vitamin deficiencies. Excellent reviews of this topic are recommended for further reading [1-5].
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PMID:[Vitamins and skin]. 807 86

A 32-year-old man with chronic alcoholism over 10 years developed skin eruptions, dark-red tongue and severe watery diarrhea, followed by weakness of bilateral lower extremities. Physical examination revealed hyperpigmented skin eruptions with scales on the dorsa of his hands and extensor aspects of his forearms. Neurological examination showed proximal muscle weakness of both lower extremities, hyperactive knee and ankle jerks, positive Chaddock reflexes and stocking type sensory disturbances. Laboratory data revealed elevation of myolytic enzyme, hypokalemia and decrease of niacin level in the blood. Diagnosis of hypokalemic myopathy and pellagra was made. With the correction of serum potassium level, muscle weakness improved rapidly and with the supplement of niacin, other physical signs and symptoms improved. In this case hypokalemic myopathy could be attributed to the alcoholic malnutritional state such as pellagrous diarrhea, malnutrition, malabsorption and others.
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PMID:[A case of alcoholism presenting pellagra and hypokalemic myopathy]. 812 77

Hypophosphatemia due to parenteral nutrition has been described frequently. It was attributed to the lack of phosphorus content in parenteral nutrition solutions. With modern parenteral nutrition regimens containing phosphorus, this problem has been virtually eliminated. Enteral nutrition solutions contain adequate phosphate for patients with normal phosphate stores. Hypophosphatemia has therefore rarely been reported in enteral nutrition. We describe two patients with protein-energy malnutrition who developed severe hypophosphatemia during tube feeding with phosphorus-containing formula diets. Chronic alcoholism and vitamin D deficiency due to malabsorption because of Crohn's disease were additional risk factors in these two patients. Patients with depleted phosphate stores and high metabolic demand have a higher daily requirement for phosphorus than is available in routine isotonic enteral formulas. This case report emphasizes the importance of monitoring serum phosphate concentration daily during the first week of refeeding.
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PMID:Enteral supplementation of phosphate does not prevent hypophosphatemia during refeeding of cachectic patients. 820 56

Until the 1960s, liver disease of the alcoholic patient was attributed exclusively to dietary deficiencies. Since then, however, our understanding of the impact of alcoholism on nutritional status has undergone a progressive evolution. Alcohol, because of its high energy content, was at first perceived to act exclusively as 'empty calories' displacing other nutrients in the diet, and causing primary malnutrition through decreased intake of essential nutrients. With improvement in the overall nutrition of the population, the role of primary malnutrition waned and secondary malnutrition was emphasized as a result of a better understanding of maldigestion and malabsorption caused by chronic alcohol consumption and various diseases associated with chronic alcoholism. At the same time, the concept of the direct toxicity of alcohol came to the forefront as an explanation for the widespread cellular injury. Some of the hepatotoxicity was found to result from the metabolic disturbances associated with the oxidation of ethanol via the liver alcohol dehydrogenase (ADH) pathway and the redox changes produced by the generated NADH, which in turn affects the metabolism of lipids, carbohydrates, proteins and purines. Exaggeration of the redox change by the relative hypoxia which prevails physiologically in the perivenular zone contributes to the exacerbation of the ethanol-induced lesions in zone 3. In addition to ADH, ethanol can be oxidized by liver microsomes: studies over the last twenty years have culminated in the molecular elucidation of the ethanol-inducible cytochrome P450IIE1 (CYP2E1) which contributes not only to ethanol metabolism and tolerance, but also to the selective hepatic perivenular toxicity of various xenobiotics. Their activation by CYP2E1 now provides an understanding for the increased susceptibility of the heavy drinker to the toxicity of industrial solvents, anaesthetic agents, commonly prescribed drugs, 'over the counter' analgesics, chemical carcinogens and even nutritional factors such as vitamin A. Ethanol causes not only vitamin A depletion but it also enhances its hepatotoxicity. Furthermore, induction of the microsomal pathway contributes to increased acetaldehyde generation, with formation of protein adducts, resulting in antibody production, enzyme inactivation and decreased DNA repair; it is also associated with a striking impairment of the capacity of the liver to utilize oxygen. Moreover, acetaldehyde promotes glutathione depletion, free-radical mediated toxicity and lipid peroxidation. In addition, acetaldehyde affects hepatic collagen synthesis: both in vivo and in vitro (in cultured myofibroblasts and lipocytes), ethanol and its metabolite acetaldehyde were found to increase collagen accumulation and mRNA levels for collagen. This new understanding of the pathogenesis of alcoholic liver disease may eventually improve therapy with drugs and nutrients.
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PMID:Aetiology and pathogenesis of alcoholic liver disease. 821 1


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