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Query: UMLS:C0024523 (malabsorption)
 7,319 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Serum alpha-tocopherol, lipids, potassium, and creatine phosphokinase levels were measured in 20 adult male control patients and eight malabsorption patients. The malabsorption group had significantly lower serum alpha-tocopherol levels than the control group. This change was independent of serum total lipid levels that were not significantly different among the two groups. Serum potassium and creatine phosphokinase levels that are normally used to assess muscle pathology in man did not correlate with serum alpha-tocopherol levels in either the control of the malabsorption groups. Body mass indices that are directly related to adiposity of the individuals were calculated. Among the control patients, there was a significant increase in serum alpha-tocopherol and serum total lipids with increase in body mass index. Similar correlations did not exist in the malabsorption group. In the latter group serum alpha-tocopherol levels may have reached low enough levels to be independent of factors such as adiposity and serum total lipids.
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PMID:Serum alpha-tocopherol, lipids, potassium, and creatine phosphokinase in normal and malabsorption patients. 48 25

Although a neuromuscular syndrome has been induced experimentally by vitamin E deficiency, a human syndrome has not yet been documented. This report describes a 7-year-old boy with severe malabsorption since birth who presented with progressive external ophthalmoplegia, proximal muscle weakness, peripheral neuropathy, hyporeflexia, and bilateral Babinski signs. Abnormalities on neurologic examination included elevated creatine phosphokinase and aldolase, slowed distal sensory latencies, type II muscle fiber atrophy, and a plasma vitamin E level of 8 microgram per deciliter (normal, 550-1500 microgram per deciliter). Treatment with oral water-solubilized vitamin E (400 IU daily; greater than 50 times the normal daily intake) was begun, with repeat laboratory studies at 3-month intervals. Over a 16-month period, plasma vitamin E content gradually increased to 350 microgram per deciliter, associated with declining sarcoplasmic enzyme activities and clinical improvement.
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PMID:Reversibility of human myopathy caused by vitamin E deficiency. 57 10

Ten patients, aged 39-61 years, with hypomagnesaemia due to chronic alcoholism (7 cases) or malabsorption (3 cases), have been investigated by assessing the maximum isometric voluntary contraction force (MVC) of the quadriceps femoris muscle (7 cases), laboratory screening (9 cases) and estimating the electrolyte and metabolite content of biopsy specimens from the quadriceps femoris muscle. The MVC ranged from 0.5 to 34 kp and was significantly lower than in 12 apparently healthy normomagnesaemic controls (p is less than 0.001). The results of the laboratory screening, apart from a significant lowering of the serum magnesium concentration (p is less than 0.01), were mainly within the range of normal values, apart from signs of liver damage, such as an elevated activity of S-OCT (3 cases), alkaline phosphatease(3 cases), S-ALAT (1 case) and an elevation of bilirubin and blood ammonia (2 cases). Low serum iron-binding capacity occurred in 4 cases, a finding reported in protein-calorie malnutrition. Muscle magnesium content was significantly lower than in healthy controls (p is less than 0.001). Muslce sodium and chloride contents were significantly increased (p is less than 0.05). Total H2O content and the extracellular H2O content were both significantly increased (p is less than 0.05). Pyruvate and lactate values were within the normal range. The apparent equilibrium constant for creatine kinase differed significantly ( is less than 0.01). ATP values were within the normal range, but there were slight decreases for ADP (p is less than 0.05) and creatine phosphate ( is less than 0.01), whcih is of interest in view of the lowering of the MVC and the diminished capacity for sustained muscular effort in hypomagnesaemic patients reported earlier.
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PMID:Hypomagnesaemia and muscle electrolytes and metabolites. 85 Oct 37

Two IgA-deficient children with inflammatory myopathy and intestinal malabsorption were evaluated. The myopathy was characterized by weakness of facial and proximal limb muscles, increased serum concentrations of lactic dehydrogenase and creatine phosphokinase, and histologic evidence of inflammation and degeneration of muscle fibers. Features of the intestinal abnormality were blunted villi, interstitial inflammation, and reduction in IgA-containing plasma cells and IgA content of epithelial cells. The myopathy and malabsorption improved with corticosteroid treatment. Circulating antibodies to striated muscle could not be demonstrated in either patient, but one had antibodies to milk and chicken serum proteins. We speculate that IgA deficiency may predispose to the development of inflammatory myopathy.
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PMID:Inflammatory myopathy, IgA deficiency, and intestinal malabsorption. 94 14

Three cases of Crohn's disease (CD) which showed an elevation of creatine phosphokinase (CPK) during the course were reported. In two cases, elevations of serum myoglobin and aldolase were also observed which indicated rhabdomyolysis. Rhabdomyolysis occurred unrelated to the activity of CD and it was asymptomatic. It was unable to identify an apparent known cause for rhabdomyolysis. All three cases were under elemental diet (ED) but the causality of ED for rhabdomyolysis was uncertain. So far as we know, there is no report on rhabdomyolysis during ED treatment and there are only two reports in which rhabdomyolysis was documented in CD. The latter was rhabdomyolysis due to electrolyte depletion secondary to malabsorption in CD which was not encountered in our cases. Our department dealt only three cases of CD and all of them had an elevation of CPK which had been measured as one of routine blood chemistry in our hospital. These observations led to a following conclusion that subclinical rhabdomyolysis may be one of extra-intestinal complications of CD.
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PMID:Rhabdomyolysis associated with Crohn's disease. 362 67

Serum alpha-tocopherol, lipids, potassium and creatine phosphokinase levels we-remeasured in 20 adult male control patients and 120 malabsorption patients. The malabsorption group had significantly lower serum alpha-tocopherol levels than the control group. The change was independent of serum total lipid levels that were not significantly different among the two groups. Serum potassium and creatine phosphokinase did not correlate with serum alpha-tocopherol levels in either control and malabsorption group. Body mass indices that are directly relate to adiposity increased with increase of serum alpha-tocopherol and total lipids of serum.
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PMID:Serum alpha-tocopherol, lipids, potassium and creatine phosphokinase in normal and patients with malabsorption. 724 3

Plasma chemistry and haematological studies were conducted on chickens with coccidiosis. Male White Leghorn chickens, of two weeks old, were inoculated with 5 x 10(4) Eimeria tenella sporulated oocysts or with 1 x 10(6) E acervulina sporulated oocysts. Blood samples were taken four, seven and 11 days after inoculation. A wet chemistry system was applied to measure the plasma activities of aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase, gamma glutamyltransferase, creatine kinase, amylase and lactate dehydrogenase and the concentrations of creatine, total bilirubin, urate, total cholesterol, total protein, albumin, glucose and triglycerides. A dry chemistry system was applied to measure sodium, potassium, chloride and calcium. The number of red blood cells and packed cell volume were determined by a micro cell counter and blood pH was measured with a blood gas analyser. The erythrocyte count, packed cell volume, sodium and chloride levels in the chickens infected with E tenella were significantly (P < 0.05) lower than those of the uninfected controls. The significant decrease in blood pH of the chickens infected with E acervulina suggests malabsorption associated with duodenal lesions induced by the infection.
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PMID:Evaluation of plasma chemistry and haematological studies on chickens infected with Eimeria tenella and E acervulina. 925 31

Skeletal muscle disorders manifested by muscle pain, fatigue, proximal weakness, and serum creatine kinase (CK) elevation have been reported in patients with selenium deficiency. The object of this report was to review the conditions in which selenium deficiency is associated with human skeletal muscle disorders and to evaluate the importance of mitochondrial alterations in these disorders. A systematic literature review using the Medline database and Cochrane Library provided 38 relevant articles. The main conditions associated with selenium deficiency fell into three categories: (1) insufficient selenium intake in low soil-selenium areas; (2) parenteral or enteral nutrition, or malabsorption; and (3) chronic conditions associated with oxidative stress, such as chronic alcohol abuse and human immunodeficiency virus (HIV) infection. In low soil-selenium areas, reversibility of muscle symptoms was similar after selenium supplementation and placebo administration, suggesting a role for other factors in the development of disease. In parenteral or enteral nutrition, or malabsorption, muscle symptoms improved after selenium supplementation in 18 of 19 patients (median delay: 4 weeks). The reason that only a minority of selenium-deficient patients present with skeletal muscle disorders is unclear and is possibly related to cofactors, such as viral infections and drugs. Prospective studies of selenium-deficient myopathies would be useful in critically ill patients, alcohol abusers, and HIV-infected patients.
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PMID:Skeletal muscle disorders associated with selenium deficiency in humans. 1276 76

Anderson's disease (AD) or chylomicron retention disease (CMRD) is a rare hereditary lipid malabsorption syndrome linked to SARA2 gene mutations. We report in this study a novel mutation in two sisters for which the Sar1b protein is predicted to be truncated by 32 amino acids at its carboxyl-terminus. Because the SARA2 gene is also expressed in the muscle, heart, liver and placenta, extraintestinal clinical manifestations may exist. For the first time, we describe in this study in the two sisters muscular as well as cardiac abnormalities that could be related to the reported expression of SARA2 in these tissues. We also evaluated six other patients for potential manifestations of the SARA2 mutation. The creatine phosphokinase levels were increased in all patients [1.5-9.4 x normal (N)] and transaminases were moderately elevated in five of the eight patients (1.2-2.6 x N), probably related to muscle disease rather than to liver dysfunction. A decreased ejection fraction occurred in one patient (40%, N: 60%). The muscle, liver and placental tissues that were examined had no specific abnormalities and, in particular, no lipid accumulation. These results suggest that myolysis and other extraintestinal abnormalities can occur in AD/CMRD and that the clinical evaluation of patients should reflect this.
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PMID:Anderson's disease (chylomicron retention disease): a new mutation in the SARA2 gene associated with muscular and cardiac abnormalities. 1878 34

Neuroacanthocytosis (NA) syndromes are a group of genetically defined diseases characterized by the association of red blood cell acanthocytosis and progressive degeneration of the basal ganglia. NA syndromes are exceptionally rare with an estimated prevalence of less than 1 to 5 per 1'000'000 inhabitants for each disorder. The core NA syndromes include autosomal recessive chorea-acanthocytosis and X-linked McLeod syndrome which have a Huntington's disease-like phenotype consisting of a choreatic movement disorder, psychiatric manifestations and cognitive decline, and additional multi-system features including myopathy and axonal neuropathy. In addition, cardiomyopathy may occur in McLeod syndrome. Acanthocytes are also found in a proportion of patients with autosomal dominant Huntington's disease-like 2, autosomal recessive pantothenate kinase-associated neurodegeneration and several inherited disorders of lipoprotein metabolism, namely abetalipoproteinemia (Bassen-Kornzweig syndrome) and hypobetalipoproteinemia leading to vitamin E malabsorption. The latter disorders are characterized by a peripheral neuropathy and sensory ataxia due to dorsal column degeneration, but movement disorders and cognitive impairment are not present. NA syndromes are caused by disease-specific genetic mutations. The mechanism by which these mutations cause neurodegeneration is not known. The association of the acanthocytic membrane abnormality with selective degeneration of the basal ganglia, however, suggests a common pathogenetic pathway. Laboratory tests include blood smears to detect acanthocytosis and determination of serum creatine kinase. Cerebral magnetic resonance imaging may demonstrate striatal atrophy. Kell and Kx blood group antigens are reduced or absent in McLeod syndrome. Western blot for chorein demonstrates absence of this protein in red blood cells of chorea-acanthocytosis patients. Specific genetic testing is possible in all NA syndromes. Differential diagnoses include Huntington disease and other causes of progressive hyperkinetic movement disorders. There are no curative therapies for NA syndromes. Regular cardiologic studies and avoidance of transfusion complications are mandatory in McLeod syndrome. The hyperkinetic movement disorder may be treated as in Huntington disease. Other symptoms including psychiatric manifestations should be managed in a symptom-oriented manner. NA syndromes have a relentlessly progressive course usually over two to three decades.
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PMID:Neuroacanthocytosis syndromes. 2202 13


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