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

The endocrine abnormalities associated with acquired immunodeficiency syndrome (AIDS) are reviewed. These include adrenal insufficiency, hyporeninemic hypoaldosteronism, panhypopituitarism, hypogonadism, and alterations in thyroid function tests. AIDS-related infections or neoplasms may lead to hypercalcemia, whereas malabsorption may cause hypocalcemia. The possibility that AIDS-associated cachexia and hypertriglyceridemia may be caused by cachectin (tumor necrosis factor) is discussed, along with possible therapy for cachexia with megestrol acetate. Ketoconazole, sulfonamides, and pentamidine have specific, potentially deleterious metabolic effects when used in AIDS patients. Because treatment of endocrinological abnormalities of AIDS is often effective, improved diagnosis and appropriate therapy of these abnormalities will result in improved quality of life and, possibly, longer survival of patients with AIDS.
Mt Sinai J Med 1990 Sep
PMID:Endocrinologic and metabolic manifestations of the acquired immunodeficiency syndrome. 224 1

Sibling cases of familial vitamin E deficiency accompanied by ataxia, polyneuropathy and mental retardation were reported. Case 1 was a 37-year-old male who developed progressive gait disturbance, deformity of the feet and head tremor from childhood, after normal delivery and development of early childhood. On physical examination, he had cataract, high arched palate and pes cavus. Neurological examination revealed mental retardation (WAIS 68), scanning speech, muscular atrophy of the face and extremities with predominance in the lower limbs, absent Achilles tendon reflex, disturbance of superficial and deep sensation predominant in distal limbs, and marked gait ataxia. Ataxia was both cerebellar and sensory in nature. Laboratory data of the blood showed no significant abnormalities including blood glucose and vitamin B12 except a markedly low level of serum vitamin E. The brain CT scan revealed severe cerebellar atrophy and marked dilatation of the cisterna magna and the subarachnoid space around the cerebellum. Motor nerve conduction velocity in the leg was decreased. Biopsy specimen from the quadriceps muscle showed neurogenic atrophy. Sural nerve biopsy revealed decrease in large myelinated fibers with axonal degeneration and regeneration. Oral administration of alpha-tocopherol acetate, 600 mg per day, diminished ataxia significantly. Based on lysosomal enzyme activity in leukocytes, clinical and laboratory examination, lipidosis or spinocerebellar degeneration was excluded. Chronic lipid malabsorption or beta lipoprotein deficiency which can cause decrease in vitamin E absorption, was not recognized. On oral loading with 2 g of alpha-tocopherol acetate, the decrease rate of serum vitamin E was normal. Consequently the low vitamin E was considered to have resulted from selective impairment of vitamin E absorption.(ABSTRACT TRUNCATED AT 250 WORDS)
Rinsho Shinkeigaku 1990 Sep
PMID:[Familial idiopathic vitamin E deficiency associated with cerebellar atrophy]. 226 7

The meaning of a low serum cobalamin level when the classic findings of pernicious anemia are lacking is undergoing reevaluation. We therefore studied the neurologic status of 11 patients who had low cobalamin levels without definite hematologic evidence of deficiency. Neurologic evaluation included pattern-shift visual and median and posterior tibial nerve somatosensory evoked potentials. None of the patients had megaloblastic changes in the blood or bone marrow, although 7 of the 11 had subtle cellular cobalamin disturbances demonstrated by an abnormal deoxyuridine suppression test result. Seven patients had normal Schilling test results and 2 had borderline results; however, 2 of the 5 patients tested further had food-cobalamin malabsorption, while a third had prepernicious anemia. The patients displayed a variety of neurologic problems, including dementia, depression, myelopathy, neuropathy, and seizure disorder; 1 patient was neurologically normal by clinical criteria. Evoked potential abnormalities were demonstrable in 8 of the 9 patients with subtle cobalamin deficiency, and in at least 5 cases the disturbance was central. In contrast, both patients whose low serum cobalamin levels were found on evaluation to be spurious had normal evoked potentials. Evoked potential abnormalities improved in the one patient retested after cobalamin therapy. These findings demonstrate that neurologic deficits occur not only in classic cobalamin deficiency but also in subtle or atypical cobalamin deficiency states in which anemia is absent and Schilling test results are normal. Electrophysiologic evidence of neurologic impairment is often present, even in patients without obvious clinical neurologic abnormalities.
Arch Neurol 1990 Sep
PMID:Neurologic and evoked potential abnormalities in subtle cobalamin deficiency states, including deficiency without anemia and with normal absorption of free cobalamin. 239 29

Between January 1984 and March 1986, 10 children aged between 7 and 56 months were admitted to Queen Elizabeth Hospital for Children in London with chronic travellers' diarrhoea, after visiting the Indian subcontinent, France or Morocco. All the children were born in the United Kingdom and had been in good health before their journey abroad. On return to England most of these children were malnourished and two of them (twins) had a post-infective, tropical malabsorption-like syndrome. There was a high incidence of positive stool cultures and, on small intestinal biopsy, histological abnormalities were present in six. Children from the United Kingdom travelling abroad are at risk of developing severe travellers' diarrhoea, with serious consequences to their health and nutrition. There is a need for intensive parental education before travelling and this could be achieved through community health workers.
Ann Trop Paediatr 1988 Sep
PMID:Travellers' diarrhoea among children returning to the United Kingdom from visits abroad. 246 Nov 55

Nutritional support, whether enteral or parenteral, is an important part of the treatment of IBD. Inadequate oral intake, malabsorption, and increased gastrointestinal losses all contribute to malnutrition. Weight loss, cachexia, abnormal body composition, and multiple micronutrient deficiencies are common. Acute repletion of body weight and correction of specific nutrient deficiencies improve the patients' sense of well-being and decrease morbidity, especially in the perioperative period. If a short period of bowel rest (10 to 14 days) is part of the medical therapy of acute exacerbations of IBD, TPN should be administered to prevent further nutritional deficiencies. Chronic undernutrition, and growth failure in children, usually are best treated by intensive enteral supplementation. Prolonged bowel rest and TPN (4 to 6 weeks) have not been shown to improve outcome but may be appropriate in carefully selected patients. Long-term home TPN may be necessary for patients who have short gut syndrome. The mainstay of treatment for IBD is medical therapy including corticosteroids. Timely and appropriate surgery is equally important and should not be considered a last resort. Careful nutritional management is essential but is adjunctive rather than primary therapy.
Gastroenterol Clin North Am 1989 Sep
PMID:Nutrition and inflammatory bowel disease. 250 55

Selenium is the component of the glutationperoxidase one of the most important enzymes in the antioxidant protection of the organism. In preliminary studies the authors found in celiac children increased sensitivity to oxidative stress and biochemical changes referring to decreased activity of glutationperoxidase enzyme. Therefore the selenium content of washed erythrocytes has been determined with fluorimetry in 24 celiac children kept on gluten containing diet and 25 on gluten-free diet. In gluten loading the selenium level was significantly lower than in the healthy control group. The selenium value rose at a small degree in the erythrocytes of celiac children kept on gluten-free diet but did not reach the lower limit of the physiological value. On the basis of these results the malabsorption of selenium was found to play also an important role in the decreased protecting capacity against oxidative stress effects in celiac diseases of childhood. The necessity of supplementing the trace element is raised.
Orv Hetil 1989 Sep 24
PMID:[Selenium levels in erythrocytes of children with celiac disease]. 267 9

The term "malabsorption" is generally used to indicate any defect in absorption; strictly speaking, however, it is a defect in the mucosal phase of absorption. Defects in the intraluminal phase are termed "maldigestion." This distinction is essential when considering the pathophysiology to apply diagnostic tests in the evaluation of malabsorption. This article first discusses the signs and symptoms associated with malabsorption, the disorders associated with malabsorption, normal intestinal absorption, and, finally, the diagnostic test used to investigate absorption.
Gastroenterol Clin North Am 1989 Sep
PMID:Evaluation of the patient with suspected malabsorption. 268 Sep 65

After acute gastroenteritis, delayed recovery and protracted diarrhoea may occur, particularly in very young infants, in bottle-fed malnourished infants, and after rota virus infection. Monosaccharide and disaccharide malabsorption have been demonstrated to contribute to postenteritis problems in these children. The contribution of secondary food protein intolerance to the perpetuation of diarrhoea after gastroenteritis is less well understood. Secondary sugar intolerance is diagnosed by estimation of stool pH, Clinitest, H2 breath testing and, in some cases, direct enzyme determination from biopsy material. Diagnosis of secondary cow's milk or soy-protein intolerance has to be done by clinical challenge. Dietary therapy consists of elimination of the malabsorbed food compound. A general elimination diet (lactose-free protein hydrolysate formula) is not necessary in the majority of cases but may be life-saving in individual infants. In West European countries postenteritis problems have become less in quality and quantity during the last few years.
Monatsschr Kinderheilkd 1989 Sep
PMID:[Secondary carbohydrate and protein intolerances following gastroenteritis]. 268 14

Epidemiological data indicate that exogenous noxes are important in the etiology of nonspecific inflammatory bowel disease. In several studies the influence of nutritional factors in the pathogenesis of Crohn's disease was investigated. The conflicting results, the inappropriate methods of investigation, the limited number of patients, and differences between patients and controls in many of these studies require a careful interpretation. Evidence for an etiological significance of nutrition in the development of Crohn's disease is still missing. Therefore, a specific diet for these patients does not exist. The physician should recommend a balanced diet which considers the needs in energy supply, corrects preexisting deficiencies, and is adapted to subjective intolerances and to disease related complications such as malabsorption or partial intestinal obstruction.
Z Gastroenterol 1989 Sep
PMID:[Nutrition and Crohn disease--an etiologic factor?]. 268 38

A 40-year-old man who was resected ascending colon and terminal ileum (10 cm) in Aug. 1978, with the diagnosis of Crohn's disease, was admitted to our hospital with general fatigue, paresthesia and tremor in May. 1984. A peripheral blood examination on admission revealed Hb 10.1 g/dl, RBC 234 X 10(4)/mm3, MCV 131.4 fl, MCH 43.2 pg. A bone marrow specimen showed marked erythroid hyperplasia (W/E 1.44) with megaloblastic change. While serum folate level was normal, serum vitamin B12 value was low and Schilling test showed vitamin B12 malabsorption. Roentgenologic and endoscopic examinations revealed diffuse cobblestone appearances in small intestine (from anastomosis part to duodenal bulb). These examinations suggested vitamin B12 malabsorption with diffuse Crohn's disease caused megaloblastic anemia. The patient had been treated with vitamin B12 1,000 micrograms/day injection and, in Sep. 1984, he recovered from megaloblastic anemia (Hb 13.4 g/dl, RBC 440 X 10(4)/mm3, MCV 90.7 fl, MCH 30.4 pg).
 ...
PMID:[Megaloblastic anemia associated with diffuse intestinal Crohn's disease]. 271 98


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