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)

Plasma carnitine levels were determined in 17 patients maintained on long-term total parenteral nutrition (TPN) for a mean (+/- SEM) period of 69 +/- 11 months (range 12-196). All had severe malabsorption and were dependent on intravenous feeding. Plasma carnitine was determined by a modified Cederblad enzymatic method. Mean plasma carnitine was significantly below the mean normal for females (p less than 0.02) and borderline low for males (p = 0.07). In six patients the levels were below the low normal range, and in five others they were at the lowest levels of normal. Of the six patients with normal levels, three had elevated serum creatinine, indicating renal dysfunction which may by itself elevate plasma carnitine. In 10 patients the plasma levels of lysine (a carnitine precursor) were determined and found to be lower than normal (p less than 0.05). Plasma carnitine levels correlated positively with serum albumin (r = 0.62, p less than 0.05), and negatively with serum alkaline phosphatase (r = -0.64, p less than 0.05). Thus, patients maintained on long-term TPN may have low plasma carnitine, which could represent carnitine deficiency. The low plasma carnitine may be related to a deficiency of the carnitine precursor lysine. Further studies are required to determine the significance of the low plasma carnitine and whether carnitine supplementation should be required in long-term TPN.
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PMID:Low plasma carnitine in patients on prolonged total parenteral nutrition: association with low plasma lysine. 211 37

110 children suffering from malabsorption underwent several biopsies of the gut to confirm coeliac disease (CD) following the ESPGAN criteria. We studied the values for alkaline phosphatase (AP) in the intestinal mucosa after gluten challenge. In 42 patients the after challenge biopsy was normal, thus excluding coeliac disease. In 68 children the mucosa was severely damaged confirming CD. In all biopsy specimens lactase, invertase, maltase and alkaline phosphatase were measured. We found a good correlation between PA values and severity of mucosal damage, showing that measurement of PA in the mucosa is helpful in assessing the degree of mucosal atrophy in children suffering from malabsorption.
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PMID:[Alkaline phosphatase in the intestinal mucosa of children with the malabsorption syndrome]. 250 30

In a retrospective study, jejunal mucosal disaccharidase and alkaline phosphatase activities have been investigated in 40 controls and patients with proven celiac sprue (n = 26), lactase deficiency (n = 26), osteoporosis or osteomalacia (n = 16), chronic pancreatitis (n = 12), giardiasis (n = 7), or Crohn's disease (n = 7). Apart from a nonselective reduction of mucosal enzyme activities in the sprue syndrome and a selective reduction of lactase activity in the patients with primary lactase deficiency, assays of mucosal disaccharidases revealed only inconstant or slight deviations from the control group and were not of diagnostic significance for any of the above-mentioned disorders. Isolated forms of enzyme deficiencies other than lactase deficiency, such as sucrase-isomaltase or trehalase deficiency were not present among 168 investigations carried out from 1972-1982. It is concluded that assay of small intestinal disaccharidase or alkaline phosphatase activities does not expand the diagnostic impact of morphological examination of small bowel biopsy specimens and modern noninvasive methods for the detection of carbohydrate malabsorption. Thus, the method does not appear a necessary or relevant investigation in routine clinical practice.
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PMID:Is the assay of disaccharidase activity in small bowel mucosal biopsy relevant for clinical gastroenterologists? 274 34

We studied intestinal absorption of vitamin E in 26 adults with primary biliary cirrhosis (PBC) and 6 control subjects. Seven (27%) PBC patients were vitamin E-deficient based on the ratio of serum vitamin E to serum total lipid concentrations. An oral vitamin E tolerance test was performed in all patients and control subjects using a loading dose of 2000 IU alpha-tocopheryl acetate with measurement of serial serum vitamin E concentrations over 24 h. Vitamin E absorption was expressed as the maximal rise in serum vitamin E above baseline, the area under the oral tolerance test curve, and these two values divided by the fasting total serum lipid concentration. Absorption of vitamin E was significantly impaired in all PBC patients vs. control subjects (p less than 0.01), in vitamin E-deficient vs. vitamin E-sufficient PBC patients (p less than 0.05 to p less than 0.01), and in PBC patients with serum vitamin E levels below 10 micrograms/ml vs. those with serum vitamin E levels above 10 micrograms/ml (p less than 0.01). Vitamin E absorption was inversely related to stage of PBC, serum cholylglycine, total bilirubin, cholesterol, alkaline phosphatase, aspartate aminotransferase, and prothrombin time. Patients with serum vitamin E below 10 micrograms/ml, serum total bilirubin above 3 mg/dl, serum cholylglycine above 600 micrograms/dl, or serum alkaline phosphatase above 1000 IU/L had severe malabsorption of vitamin E and would be at high risk for the development of vitamin E deficiency. Therefore, vitamin E supplementation should be considered not only in patients in whom overt vitamin E deficiency is present, but also in PBC patients meeting these criteria.
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PMID:Intestinal malabsorption of vitamin E in primary biliary cirrhosis. 291 Jul 63

Fifty-one adult patients with coeliac disease, verified by a proximal small-intestinal biopsy, were investigated. Before treatment with a gluten-free and low-lactose diet 52% showed a slight rise in blood glucose during the lactose tolerance test. Seventy-nine per cent of these patients had watery stools, and 88% had three or more bowel movements a day--statistically significantly different from the coeliac patients with a normal lactose tolerance test. After treatment 12% had a flat lactose tolerance curve. Half of them (6%) had specific lactase deficiency. This is approximately the incidence of lactose malabsorption in the general Danish population. The small-intestinal disaccharidases and alkaline phosphatase levels were severely depressed before treatment. After treatment the activities increased, but not to normal. We conclude that lactose malabsorption is a clinically important condition in many patients with untreated coeliac disease, giving rise to more frequent and more watery stools. In well-treated coeliac disease lactose malabsorption is not commoner than in the general population. The lactose activity in a proximal intestinal biopsy specimen was found to be an unreliable indicator of lactose malabsorption in coeliac disease.
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PMID:Incidence and clinical significance of lactose malabsorption in adult coeliac disease. 313 38

We examined the zinc status of 80 children with sickle cell disease (SCD) and 44 disease-free sibling controls aged 3 to 18 years. For both patients and controls, variations in serum zinc by age, type of hemoglobinopathy, and growth status were measured. The mean serum zinc concentration of patients was significantly lower than for controls (77.8 +/- 9.9 vs. 82.2 +/- 9.8 micrograms/dl, mean +/- 1SD, P less than .05). Serum levels of alkaline phosphatase (AP) and retinol-binding protein (RBP), two zinc-dependent proteins, were also lower among patients (AP: 171 +/- 66 vs. 243 +/- 97 IU/L, P less than .001; RBP: 1.92 +/- .9 vs. 2.77 +/- .9 mg/dl, P less than .001). Patients greater than or equal to 12 years of age (n = 34) had significantly lower zinc levels than those less than 12 years (74.5 +/- 8.4 vs. 80.3 +/- 10.3 micrograms/dl, P less than .01), and children with homozygous SCD (Hb SS, n = 55) had a more pronounced deficiency than those with a variant hemoglobinopathy (76.3 +/- 8.9 vs. 81.5 +/- 11.5, micrograms/dl, P less than .05). Patients classified as having "poor" growth (height-for-age less than 5th percentile, n = 24) had a lower serum zinc level than those with "normal" growth (72.8 +/- 8.0 vs. 79.8 +/- 10.0 micrograms/dl, P less than .01). Dietary intake data, body mass index, and serum total protein and albumin levels were similar for patients and controls, suggesting that zinc deficiency in SCD does not relate to inadequate dietary intake. The origin of low serum zinc levels in children with SCD is more likely to relate to factors such as increased urinary zinc excretion, chronic intravascular hemolysis, and/or zinc malabsorption.
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PMID:Zinc status of children with sickle cell disease: relationship to poor growth. 318 4

NMRI mice immunosuppressed with dexamethasone followed by challenge intraesophageally with axenic Giardia lamblia (Portland I) trophozoites had severe infection in terms of the trophozoite counts in the jejunum. Although the immunosuppressive treatment with cortisone itself resulted in a deleterious effect on brush border membrane enzymes, the decline in disaccharidases (sucrase, maltase, and lactase) and alkaline phosphatase was highly significant (P less than 0.001) following G. lamblia infection. The alterations in enzymatic activity in immune intact but infected animals demonstrated the potential of the parasite itself to cause damage to the brush border membrane. We believe that individuals with underlying immunodeficiency, upon infection with G. lamblia, may have increased damage of the brush border membrane, leading to severe malabsorption.
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PMID:Giardia lamblia infection in immunosuppressed animals causes severe alterations to brush border membrane enzymes. 276 19

As part of a randomised controlled study to assess the effect of pasteurization of breast milk on the growth of very-low-birth-weight infants, the longitudinal changes in serum calcium, phosphorus, alkaline phosphatase, 25-hydroxyvitamin D, and bone-gla-protein concentrations were investigated. Infants fed untreated own mother's milk grew more rapidly than those fed pasteurized pooled preterm milk and had higher serum alkaline phosphatase and lower phosphorus values. Serum calcium and 25-hydroxyvitamin D (25-OHD) concentrations were similar in the two groups. Despite the provision of 750 IU vitamin D daily from the 2nd week of life, serum 25-OHD values remained low in a number of infants in both groups, suggesting that either malabsorption of vitamin D or hepatic immaturity might be responsible for the persistently low values. Bone-gla-protein rose significantly after birth and was correlated with alkaline phosphatase values, but not with 25-OHD or phosphorus values. The study supports previous work that indicates that the low phosphorus content of breast milk is probably responsible for biochemical evidence of inadequate bone mineralization and that despite vitamin D supplementation, 25-OHD values do not rise adequately. Thirty-six infants were reexamined between 4 and 11 months after birth. The 25-OHD values had risen significantly in all infants except one who had vitamin D deficiency rickets.
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PMID:Mineral homeostasis in very low birth weight infants fed either own mother's milk or pooled pasteurized preterm milk. 351 33

Thirty-three patients with alcoholic cirrhosis (AC), selected on widely recognized criteria (16, 57), were investigated prospectively for cutaneous manifestations of zinc deficiency. The patients were divided into 3 groups: group A (n = 12): AC without skin lesions; group B (n = 12): AC with skin lesions responsive to a zinc-free topical treatment or resistant to enteral zinc sulfate intake; group C (n = 9): AC with skin lesions cured by oral zinc replacement therapy alone. The lesions observed in group C were studied microscopically. Data concerning zinc metabolism (Zn concentrations in plasma, red cells, urine and hair; alkaline phosphatase values), biochemical criteria of AC (plasma serum-albumin concentration, IgA/transferrin ratio) and a malabsorption test (xylosemia 120 min after oral absorption of D-xylose 25 g) were compared by the variance analysis method. A control group (D, n = 12) was used as reference. Few cases of cutaneous manifestations of zinc deficiency in AC patients have been published. In more than one half of the 15 or so we found in the literature, an aggravating factor (total parenteral nutrition, digestive tract surgery) had to be taken into account. In this prospective study 9 new cases in which AC was the only cause of zinc deficiency are reported. A clinical picture similar to acrodermatitis enteropathica with peribuccal bullous lesions was observed in only one patient. In all other cases the patients presented with a cracked and reticulated eczema on the extensor aspect of the limbs and (often erosive) in the perianal and genital regions. The eczema was associated with cheilitis, glossitis, stomatitis, alopecia and, seldom, ungual Beau's lines. Disorders of behaviour, diarrhoea and bouts of lever regressing under zinc replacement therapy were frequent. Histology was not very specific, except for the presence of necrotic areas in the stratum germinativum, sometimes associated with small subcorneal pustules containing altered polymorphonuclears. In every case, it was the rapid regression of symptoms under zinc sulfate treatment that confirmed the diagnosis. Plasma zinc concentrations were most significantly decreased in all AC groups as compared to controls (61.2 +/- 19.4 vs 97.8 +/- 10.4 micrograms/100 ml) and also in AC patients with skin manifestations of zinc deficiency as compared to the other AC patients (44.4 +/- 9.2 vs 66.5 +/- 18.8 micrograms/100 ml) table V). Changes in serum-albumin levels and in hepatocellular function were parallel to changes in plasma zinc concentrations.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Cutaneous manifestations of zinc deficiency in ethylic cirrhosis]. 357 31

Juvenile rickets or osteopenia in rural black children is thought to be due to low calcium intake. Characteristic findings include mild calcium deficiency, normal serum phosphate levels, increased alkaline phosphatase concentrations and normal plasma vitamin D levels. The present series consisted of 62 black children (average age 6.82 years), 41 males and 21 females. Low levels of serum calcium and phosphate were present in 34 (54%) and 18 (29%) of the patients respectively. Alkaline phosphatase concentrations were raised (greater than 350 IU/l) in 38 (61%). Serum sodium, potassium, chloride, total bicarbonate, magnesium, ceruloplasmin and albumin levels were generally within normal limits. Urinary acidification was normal and barium studies were reported as normal in all but 4 children. Malabsorption was not an important feature. Serum vitamin D levels were not determined. All 18 patients with hypophosphataemia improved. Eleven children showed no clear response after at least 8 weeks in hospital--8 remained hypocalcaemic and 2 of the 3 patients with normal biochemical values showed no radiological improvement of osteopenia after 2 and 4 months in hospital, while the 3rd showed only very slight improvement after 7 months in hospital. It is not clear why these patients did not respond and whether even longer hospitalisation would have been effective.
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PMID:[Aspects of juvenile rickets/osteopenia in black children]. 360 15


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