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)

In the civilized world the traditional causes of pellagra such as hunger, malnutrition are disappeared, but the disease has not disappeared after all. In the well developed countries the current etiologic causes are the following: alcoholism, psychiatric disorders, diseases causing cachexy, malabsorption and some drugs. In the case reported by the authors the malnutrition, accompanying the chronic alcoholism was the cause of the diarrhoea, dementia and dermatitis. The correct diagnosis was established after four years of repeated psychiatrical and medical treatment.
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PMID:[Pellagra--a forgotten disease]. 834 32

In approximately 2 to 4 percent of patients, laboratory evidence of macrocytosis is found. Macrocytic anemias are classified as those resulting from disorders of DNA synthesis of erythrocyte precursors in bone marrow (megaloblastic anemias) or those caused primarily by alcoholism, liver disease and hypothyroidism (nonmegaloblastic anemias). A blood smear should be performed to differentiate the two forms. Neutrophil hypersegmentation is one of the most sensitive and specific signs of megaloblastic anemia. Other testing should include vitamin B12 and red blood cell folate levels, reticulocyte count, and thyroid and liver function tests. The Schilling test can determine if B12 can be absorbed and, if not, whether adding intrinsic factor corrects the malabsorption. The most common form of nonmegaloblastic macrocytic anemia results from alcoholism. Nonmegaloblastic macrocytic anemias may be accompanied by increased reticulocyte counts (hemolysis, hemorrhage) or by normal or decreased reticulocyte counts (alcoholism, liver disease, hypothyroidism and various bone marrow disorders).
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PMID:Macrocytic anemia. 870 32

There is some controversy as to the effect of ethanol on body weight and alcohol energy contribution to body mass. The aim of this study was to evaluate the effect of alcohol addiction on resting energy expenditure (REE) and body composition. Twelve patients with current alcoholism (A) without severe liver disease or lipid and carbohydrate malabsorption were compared with a group of healthy social drinkers (B) matched for sex, age, and height. Their caloric intake was computed on the basis of a food diary. REE was measured with indirect calorimetry, and body composition was assessed by both anthropometry and bioimpedance. A significant decrease in fat mass in A compared with B was found (14.8 +/- 5.39 vs. 19.0 +/- 3.50 kg; p < 0.05). No significant differences were observed in fat-free mass (FFM) or in total body water between the two groups. A showed higher REE values normalized by FFM than B (35.5 +/- 2.97 vs. 33.0 +/- 2.95 kcal/kgFFM; p < 0.05). The nonprotein respiratory quotient was significantly lower in A than in B (0.76 +/- 0.03 vs. 0.86 +/- 0.03; p < 0.001), and A showed significantly higher lipid oxidation and lower carbohydrate oxidation than B (p < 0.05). The daily caloric intake provided only by food ingestion was found to be significantly higher in controls, but because the percentage of alcohol calories of total energy intake was 46.3 +/- 6.80 in alcoholics and 13.6 +/- 3.59 in controls (p < 0.0001), the total caloric intake, computed as food intake plus alcohol intake, was higher in alcoholics than in control subjects. No statistical differences were found in urinary nitrogen excretion and fecal loss between groups. Patients with alcoholism showed an increased REE over predicted values and a preferential lipid oxidation with respect to controls; these findings could be related to induction of microsomal ethanol oxidizing system and to mitochondrial function adaptation secondary to chronic alcohol abuse. In either case, the effects of such changes in energy metabolism may contribute to alcohol associated hepatic injury.
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PMID:Energy expenditure, substrate oxidation, and body composition in subjects with chronic alcoholism: new findings from metabolic assessment. 930 2

Hip fractures in men account for one third of all hip fractures and have a higher mortality than in women. The public health burden will increase as the increase in the numbers of elderly men in the community increases. In addition, the age-specific incidence of hip fractures may be increasing in some, but not all, countries. Vertebral fractures may be a public health problem as recent studies suggest that the prevalence in the community is 20-30%, similar to that reported in women. Forearm fractures should probably not be regarded as a public health problem. Peak bone mass is higher in men than women because men have bigger bones. Peak bone mineral density is the same. The amount of trabecular bone lost at the spine and iliac crest during ageing is similar in men and women. Cortical bone loss is less in men because endocortical resorption is less and periosteal formation is greater. Bone loss accelerates in elderly men because endocortical resorption and increasing cortical porosity increase the surface available for resorption. Bone fragility is less in men than women because: (a) the cross-sectional surface of the bone is larger; (b) trabecular bone loss is less as a percentage of the higher peak bone mass; (c) trabecular bone loss occurs by thinning rather than perforation; and (d) periosteal appositional growth compensates for endocortical resorption by maintaining the bending strength of bone. Reduced BMD in men with fractures may be due to reduced peak bone size and mass, and bone loss. Bone loss occurs by reduced bone formation. Whether men with fractures have increased bone fragility due to reduced periosteal appositional growth during ageing is unknown. The age-related decline in testosterone, adrenal androgens, growth hormone, and insulin-like growth factor 1 may contribute to reduced bone formation and bone loss. Men with vertebral fractures often have hypogonadism or illnesses with few clinical features that should be considered with a high index of suspicion (alcoholism, myeloma, malabsorption, primary hyperparathyroidism, haemochromatosis, Cushing's disease). Secondary hyperparathyroidism may contribute to bone loss by activating bone turnover and so increasing the number of bone remodelling units with impaired bone formation in each. There is no proven treatment for osteoporosis in men because there have been no trials using anti-fracture efficacy as an end point. Testosterone replacement should be considered in men with proven hypogonadism and vitamin D deficiency should be corrected if present. Calcium supplements and bisphosphonates are reasonable options given the lack of information.
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PMID:Osteoporosis in men. 936 40

Azathioprine is employed for its immunosuppressive properties, as a steroid-sparing agent or as monotherapy. Its most traditional clinical indications are connective tissue diseases, vasculitis, post-transplant, and immunobullous dermatoses. The main disadvantages of azathioprine therapy are a delayed onset of action (6-8 weeks), and rare profound bone marrow toxicity. Susceptibility to bone marrow toxicity is due to a genetically determined metabolic defect (1 in 300). Patients at risk of such toxicity may be identified by a Thiopurine methyltransferase enzyme assay. We have undertaken a retrospective study, looking at the use of azathioprine as monotherapy for non-bullous inflammatory dermatoses. We studied a total of 24 patients (10 male, 14 female). The dermatoses comprised: atopic eczema (10), pompholyx (6), plaque psoriasis (6), and chronic actinic dermatitis (2). All patients had severe refractory disease warranting systemic second line therapy. The mean age was 49.4 years (range 17-86 years). The starting dose of azathioprine was 100-150 mg/day, and the maintenance dose 50-100 mg/day. The mean duration of treatment was 33.5 months(range 1-132 months). Eighteen patients (75%) showed a good to excellent sustained clinical response to azathioprine. This response rate was evenly represented in the 4 dermatoses studied. The adverse reactions encountered were raised MCV (6), leucopenia (2), raised hepatic enzymes (6), and dyspepsia (4). Azathioprine had to be discontinued due to adverse reactions in 2 patients (dyspepsia, raised hepatic enzymes) followed by normalization. Other factors that potentially contributed to the observed adverse events were present in 5 patients: alcoholism (2), erythromycin toxicity (1), and malabsorption (2). Our study demonstrates the efficacy of azathioprine monotherapy for severe atopic eczema, pompholyx, plaque psoriasis, and chronic actinic dermatitis. Furthermore, azathioprine is a low cost and generally well tolerated drug.
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PMID:Azathioprine in dermatological practice. An overview with special emphasis on its use in non-bullous inflammatory dermatoses. 1059 68

Magnesium deficiency is a common clinical condition that may exist despite a normal serum magnesium concentration. Patients with chronic pancreatitis could develop magnesium deficiency due to either malabsorption, diabetes mellitus, or chronic alcoholism. Since serum levels of magnesium are a poor indicator of magnesium deficiency, the retention of a low-dose intravenous magnesium load (0.1 mmol/kg body weight) was determined in 13 patients with chronic pancreatitis (10 due to alcoholism) and eight healthy controls. Percentage magnesium retention was greater in patients with chronic pancreatitis than controls (59.8+/-37.3% S.D. versus 22.0+/-38.2% S. D.: P=0.038), and 10 of 13 patients showed evidence of magnesium deficiency. Routine evaluation of magnesium status could allow appropriate supplementation and conceivably symptomatic improvement in patients with severe chronic pancreatitis.
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PMID:Magnesium deficiency in patients with chronic pancreatitis identified by an intravenous loading test. 1107 71

A component of ATP, phosphate is at the hub of the energy-related mechanisms operative in muscle cells. Together with calcium, phosphate is involved in bone tissue mineralization: thus, a chronic alteration in the metabolism of phosphate can induce bone and joint disorders. Diagnosis of chronic hypophosphatemia. Serum phosphate, calcium, and creatinine should be assayed simultaneously. Serum calcium is increased in hypophosphatemia caused by hyperparathyroidism and decreased in osteomalacia. Urinary phosphate excretion should be measured in patients with a normal serum calcium level and a serum phosphate level lower than 0.80 mmol/L. A decrease in urinary phosphate excretion to less than 10 mmol/24 h strongly suggests a gastrointestinal disorder, such as malabsorption, antacid use, or chronic alcohol abuse. In patients with a urinary phosphate excretion greater than 20 mmol/24 h, the maximal rate of tubular reabsorption of phosphate (TmPO4) and the ratio of TmPO4 over glomerular filtration rate (GFR) should be determined to look for phosphate diabetes. Manifestations and causes of phosphate diabetes in adults. Moderately severe phosphate diabetes in adults manifests as chronic fatigue, depression, spinal pain, and polyarthralgia, with osteoporosis ascribable to increased bone resorption. Although many cases are idiopathic, investigations should be done to look for X-linked vitamin D-resistant rickets missed during childhood, a mesenchymatous tumor, or Fanconi's syndrome with renal wasting of phosphate, glucose, and amino acids. Management of phosphate diabetes. Phosphate supplementation and, in patients with normal urinary calcium excretion, calcitriol produce some improvement in the symptoms and increase the bone mineral density. Whether dipyramidole is clinically effective remains unclear.
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PMID:Phosphate, the renal tubule, and the musculoskeletal system. 1139 20

There are various potential explanations for weight-loss and poor physical performance in patients with chronic pancreatitis: In severe chronic pancreatitis the decline in enzyme secretion is an important cause for the malassimilation syndrome frequently seen in these patients. Occasionally, difficulties may arise in establishing this decline and in quantifying the secretory capacity of the gland. Many patients limit their food intake because of the pain caused by eating. In untreated patients with diabetes, glucosuria may contribute to their malnutrition. Insufficient funds for food due to alcoholism and anorexia may also be of some significance. Concomitant gastrointestinal diseases and malabsorption following gastrointestinal surgery are frequently found in patients with chronic pancreatitis. Neurological complications and traumatic lesions after accidents - often in connection to the underlying alcoholism - are joined by physical inactivity and thus contribute to the development of muscular atrophy and decreased physical performance. Consequently, rehabilitation of patients with chronic pancreatitis is challenging: They not only need expert medical treatment of both the symptoms of chronic pancreatitis and the concomitant disorders. Therapy must also include dietary support, careful physical training, and - in cases caused by alcoholism - psycho-social support. So far, the multi-professional competence required for these purposes can only be expected in a specialized rehabilitation centre.
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PMID:[Chronic pancreatitis: weight loss and poor physical performance - experience from a specialized rehabilitation centre]. 1174 23

Chronic alcoholism is a medical, economical and social problem. Motility and mental function disorders are among the complications of chronic alcoholism and have been known for more than two centuries as "alcoholic paralysis", and are caused by alcoholic neuropathy. The pathogenesis of alcoholic neuropathy does not appear to be identical with central nervous system disorders which are caused by chronic alcoholism and it seems that it results from a failure of the protection barrier systems in the peripheral nervous system. To the pathogenesis of alcoholic neuropathy includes: 1. direct toxic effects of alcohol on the cellular population of the central nervous system and other tissues, especially of parenchymatous organs (in particular of the liver), 2. indirect metabolic and exotoxic changes mediated by malabsorption, maldigestion and secondary caloric and energy deprivation, 3. effects of genetic factors. (Fig. 2, Ref. 23.)
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PMID:Pathogenesis of alcoholic neuropathy. 1206 Oct 83

The goals and objectives of these studies, conducted over the past 30 y, were to determine: a) how chronic alcoholism leads to folate deficiency and b) how folate deficiency contributes to the pathogenesis of alcoholic liver disease (ALD). The intestinal absorption of folic acid was decreased in binge drinking alcoholics and, prospectively, in volunteers fed alcohol with low folate diets. Monkeys fed alcohol for 2 y developed decreased hepatic folate stores, folic acid malabsorption and decreased hepatic uptake but increased urinary excretion of labeled folic acid. Micropigs fed alcohol for 1 y developed features of ALD in association with decreased translation and activity of intestinal reduced folate carrier. Another study in ethanol-fed micropigs demonstrated abnormal hepatic methionine and DNA nucleotide imbalance and increased hepatocellular apoptosis. When alcohol feeding was combined with folate deficiency, micropigs developed typical histological features of ALD in 14 wk, together with elevated plasma homocysteine levels, reduced liver S-adenosylmethionine and glutathione and increased markers for DNA and lipid oxidation. In summary, chronic alcohol exposure impairs folate absorption by inhibiting expression of the reduced folate carrier and decreasing the hepatic uptake and renal conservation of circulating folate. At the same time, folate deficiency accelerates alcohol-induced changes in hepatic methionine metabolism while promoting enhanced oxidative liver injury and the histopathology of ALD.
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PMID:Metabolic interactions of alcohol and folate. 1216 94


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