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)

Hypophosphatemia is common in hospitalized patients and occurs under a variety of circumstances other than parathyroid hormone excess. Charts of 100 inpatients with hypophosphatemia were reviewed and the patients divided into five groups on the basis of serum phosphate level: 18, 2.1 to 2.4 mg/dL; 49, 1.6 to 2.0 mg/dL; 20, 1.1 to 1.5 mg/dL; 12, 0.6 to 1.0 mg/dL; 1, 0.1 to 0.5 mg/dL. The effect of glucose ingestion on serum phosphate level was shown in one normal patient. Whenever carbohydrate was administered intravenously (45 cases), this was considered the primary cause of the hypophosphatemia. Other causes were as follows: diuretics, hyperalimentation, alcoholism, respiratory alkalosis, dialysis, insulin, corticosteroids, diabetic ketoacidosis, vomiting, phosphate-binding antacid, Gram-negative sepsis, primary hyperparathyroidism, saline, epinephrine, gastrointestinal malabsorption, and unknown. Hypophosphatemia in hospitalized patients may have multiple causes.
JAMA 1979 Jul 13
PMID:Hypophosphatemia in hospitalized patients. 44 90

Chronic renal failure is accompanied by secondary hyperparathyroidism. Inhibition of parathyroid hormone secretion has been reported to be induced by hypomagnesemia in conditions other than chronic renal failure, since severe hypomagnesemia is rare in chronic renal failure. In the case reported here, the patient had chronic renal failure and malabsorption-induced hypomagnesemia; she exhibited hypoparathyroidism while hypomagnesemic, and hyperparathyroidism after magnesium was replaced. Hypomagnesemia induced parathyroid hormone suppression in this patient with chronic renal failure, despite the presence of chronic hyperfunctioning parathyroid cells.
JAMA 1979 Feb 16
PMID:Hypomagnesemia. Suppression of secondary hyperparathyroidism in chronic renal failure. 76 31

Many manifestations following jejunoileal bypass are due to chronic inflammation of the excluded bowel rather than short bowel malabsorption. Diarrhea, abdominal distention, and gas-fluid levels were common diagnostic features of "bypass enteropathy." Exploration showed the bypassed bowel to be dilated, with serosal inflammation and pneumatosis cystoides intestinalis. The bypassed loops contained a fecal flora and the mucosa demonstrated nonspecific chronic inflammatory changes. Exudative protein losses were noted. Systemic complications of bypass enteropathy were similar to other inflammatory diseases of the bowel. Improvement following treatment with metronidazole or after dismantling of the bypass suggested that bacterial byproducts originating in the excluded bowel were causally related.
JAMA 1976 Jul 19
PMID:Bypass enteropathy. Intestinal and systemic manifestations following small-bowel bypass. 94 28

A study was conducted on 7 fertile women (ages 19-44) after end-side jejunoileostomy for obesity. The peak plasma norethindrone (norethisterone) and levonorgestrel (formerly known as d-norgestrel) levels were measured during separate 24-hour norethindrone or levonorgestrel loads using conventional oral contraceptives (OCs). Compared to normal control patients, the intestinal bypass patients had severely reduced mean levels. The levels were 5.0 versus 20.8 ng/ml for norethindrone and the levels were 1.63 versus 4.25 ng/ml for levonorgestrel. Investigation of the patients' sex steroid binding globulin levels showed markedly reduced levels, implying a defective hepatic synthesis of this globulin rather than malabsorption as the most important factor. The data shows a reduced plasma level of OC in patients operated in this way, and OCs cannot be considered safe after intestinal bypass.
JAMA 1976 Dec 20
PMID:Oral contraceptives after intestinal bypass operations. 103 86

Malnutrition is common among alcoholics because alcohol displaces protein-, vitamin-, and mineral-containing foods in the diet, and chronic alcohol consumption results in maldigestion and malabsorption of essential nutrients. In addition, alcohol exerts direct toxic effects on both the liver and gut, resulting in structural alterations in the intestine and the development of fatty liver, alcoholic hepatitis, and cirrhosis. Liver injury is preceded by an adaptive phase characterized by accelerated metabolism of drugs (including ethanol), and hyperlipemia, secondary to hypertrophy and hyperactivity of the smooth endoplasmic reticulum. Side effects include enhanced hepatotoxicity of CCI4 and possibly energy wastage. Alcoholics should not be led to beleive that correction or prevention of nutritional deficiency will prevent liver damage in the face of continued alcohol abuse.
JAMA 1975 Sep 08
PMID:Alcohol and malnutrition in the pathogenesis of liver disease.. 117 54

Idiopathic late-onset immunoglobulin deficiency in a young man was associated with achlorhydria and a severe intestinal malabsorption syndrome that did not respond to conventional therapy. Combined therapy with high doses of prednisone and tetracycline hydrochloride resulted in weight gain, cessation of diarrhea, improved absorption of water, fat, and vitamin B12, and production of gastric acid after stimulation with histamine. Serum immunoglobulin levels, however, did not increase.
JAMA 1975 Sep 15
PMID:Gastrointestinal dysfunction in immunoglobulin deficiency. Effect of corticosteroids and tetracycline. 117 74

This report deals with the onset of Giardia-induced, primary malabsorption in patients with chronic pancreatitis. To our knowledge, this association has been reported only once previously. A further review of the literature suggests that malnourished patients with chronic pancreatitis may be susceptible to G lamblia infection. Therapy for giardiasis rapidly reverses the diarrhea, malabsorption, and edema seen in these patients.
JAMA 1975 Sep 29
PMID:Giardia-induced malabsorption in pancreatitis. 117 10

Pancreatic enzyme products are formulated, manufactured, and sold without submitting efficacy or bioavailability data to the Food and Drug Administration because of a quirk in the law. We documented therapeutic failures in three patients with cystic fibrosis after pharmacists substituted generic pancrelipase capsules for the Pancrease brand. Gastrointestinal symptoms and fat malabsorption rapidly resolved after therapy was reinstituted with brand name products. In vitro analysis indicated that after 1 hour of exposure to simulated gastric fluid, lipase activity was less than 200 U per capsule from all three generic capsules dispensed to the patients compared with 6820 U per capsule from Pancrease. These data indicate that the enteric coating of the generic product was defective and that the substituted product was not bioequivalent to the prescribed brand. We conclude that the Food and Drug Administration should institute regulations over this group of products.
JAMA 1990 May 09
PMID:Treatment failure after substitution of generic pancrelipase capsules. Correlation with in vitro lipase activity. 232 38

We describe a patient with refractory sprue with malabsorption, a flat small-bowel biopsy specimen unresponsive to a gluten-free diet, and colonic biopsy specimens consistent with lymphocytic (microscopic) colitis. To investigate further the relation between celiac disease and lymphocytic or collagenous colitis (a similar and possibly related entity), we examined colorectal and small-bowel biopsy specimens in patients indexed histologically as having celiac disease who have been seen at The Johns Hopkins Hospital since 1958. Of 135 indexed patients, 21 had colorectal biopsies. Colorectal biopsy specimens were abnormal in 7 of the 21 patients. Four patients had biopsy specimens resembling lymphocytic colitis, 2 patients had acute colitis, and another patient had both lymphocytic and acute colitis. No patients had collagenous colitis. Three of the patients with lymphocytic colitis and celiac-like changes of the small bowel never responded to a gluten-free diet and may represent a distinctive panintestinal disease for which the term "lymphocytic enterocolitis" with malabsorption is proposed.
JAMA 1989 Aug 18
PMID:Lymphocytic enterocolitis in patients with 'refractory sprue'. 275 95

A coagulopathy due to vitamin K deficiency was discovered in 42 hospitalized patients, most of whom had been misdiagnosed as having disseminated intravascular coagulation. Factors contributing to vitamin deficiency included inadequate diet, malabsorption, failure of physicians to prescribe vitamin K supplements, antibiotic therapy, renal insufficiency, hepatic dysfunction, recent major surgery, and possibly pregnancy. Sixteen patients (34%) bled sufficiently to need red blood cell transfusions and ten patients (24%) ultimately died. Of 18 patients who also had thrombocytopenia, three did have disseminated intravascular coagulation. The deficiency, a contributor to morbidity and mortality, can be prevented by prophylactic administration of vitamin K to severely ill patients who are eating inadequately and receiving antibiotics.
JAMA 1987 Oct 09
PMID:Coagulopathy caused by vitamin K deficiency in critically ill, hospitalized patients. 365 2


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