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

Fifty-four infants with the malabsorption syndrome and cow's milk intolerence seen during 1962-1971 were investigated. All had diarrhoea and failed to thrive. Most had vomiting and about 20% had atopic eczema and recurrent respiratory infections. Laboratory investigations revealed malabsorption, raised serum IgA, and precipitins to cow's milk. Biopsies showed that the jejunal mucosa was damaged, and in about half the cases was flat. The patient did well on human milk but reacted clinically to cow's milk challenge, either in a few hours or gradually during 3-4 weeks. Some patients showed first a quick, but later a slow, reaction. Clinical symptoms of cow's milk intolerance disappeared at the age of about one year. At that time 81% had normal faecal fat, but only 29% had a normal proximal jejunal mucosa. Many of the patients developed intolerances to other food proteins, such as soya and wheat, if these were given during the sensitive period. Forty-two patients have been followed up for 2 years on a normal gluten-containing diet. Of these, 37 have a normal or nearly normal jejunal mucosa and 5 (12%) have subtotal villous atrophy indicative of coeliac disease. It is concluded that the malabsorption syndrome with cow's milk intolerance is a clear-cut clinical entity. However, the symptomatology, results of laboratory tests, and jejunal biopsy findings closely resemble those of other entities where damage to the intestinal mucosa causes a malabsorption snydrome. Follow-up studies showed that the disease is transient, but about 10% of the patients have coeliac disease, regarded in such cases as the primary disorder.
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PMID:Malabsorption syndrome with cow's milk intolerance. Clinical findings and course in 54 cases. 124 23

Intestinal permeability to probe molecules has been shown to correlate closely with the presence or absence of villous atrophy in a jejunal biopsy. The purpose of this study was to establish if there exist groups of patients with functional derangement of intestinal permeability but normal histopathology of the small bowel mucosa. In 135 patients a cellobiose/mannitol permeability test was performed at the same time as jejunal biopsy. Diagnosis included coeliac disease, Crohn's disease, irritable bowel syndrome, idiopathic diarrhoea, self diagnosed food allergy, atopic eczema and postinfectious malabsorption. The value of the cellobiose/mannitol test in identifying patients with abnormal jejunal biopsy histopathology was confirmed. The permeability test was abnormal in all 28 patients with partial or subtotal villous atrophy, and also in all 10 in whom there was a high intraepithelial lymphocyte count despite normal villi and crypts. Functional abnormality of the small intestine has not previously been reported in patients with this jejunal biopsy abnormality. Abnormalities of permeability were also found in patients with idiopathic diarrhoea, folate deficiency, postinfectious or traveller's diarrhoea, small bowel Crohn's disease, and atopic eczema. These results show that sugar permeability tests have more potential in clinical investigation than merely serving as screening tests before jejunal biopsy. There are groups of patients without morphological changes in the small bowel in whom intestinal permeability is abnormal.
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PMID:Cellobiose/mannitol sugar permeability test complements biopsy histopathology in clinical investigation of the jejunum. 643 13

Macromolecular absorption of food and microbial antigens being enhanced in the intestine under pathological conditions may well be the cause of such diseases as food allergy, coeliac disease, Crohn's disease, atopic eczema, etc. The polyethyleneglycol-4000 (PEG-4000) and food antigens absorption was found to be similar in the animal intestine. The PEG-4000 gastrointestinal permeability is considerably increased in the rats with anaphylaxis, experimental biliary malabsorption and experimental colitis. Fatty acids of the omega-3 and omega-6 series as well as histidine were found to change the permeability for the PEG-4000.
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PMID:[Disordered permeability of the gastrointestinal tract barrier for macromolecules and the possibilities for its experimental dietetic correction]. 840 45

The study deals with the physical growth of 38 infants with atopic dermatitis and 11 controls. The SD scores of hight and wight in severe group was significantly lower than those of mild and modelate groups. And serum IGF-1 levels showed lower than those of mild and modelate groups. On the otherhand, the SD scores of weight and serum IGF-1 levels showed no significant difference between the patient with and without avoidance of allergenic foods, though a lot of patients belonged to severe group avoided their allergenic foods. These results suggested that pathogeneses of the impaired physical growth of severe atopic infants due to malnutrition because of their malabsorption. In conclusion, avoidance of allergenic foods may needs to prevent from the growth failure in severe atopic infants.
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PMID:[Growth impairment in infants with atopic dermatitis]. 885 15

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

Food intolerance is a reproducible adverse reaction to a specific food ingredient that is not psychologically based. Food allergy is a form of food intolerance in which there is evidence that the response is caused by an immunological reaction to food. Other mechanisms of food intolerance include enzyme defects (e.g. lactase deficiency), pharmacological effects (e.g. histamine), toxic properties (e.g. haemagglutinating lectins) and irritants (e.g. spices). Food allergy in children is a highly contentious subject and there is often a striking lack of published evidence from which to base clinical decisions. The true prevalence of food allergy in children is unknown, although there is evidence of an increasing incidence of allergic reactions to some foods, especially peanuts. Our understanding of why some children are unable to tolerate certain foods (e.g. cow's milk, egg), or how they grow out of this intolerance, is very poor. Symptoms of food allergy in children are diverse and include vomiting, poor weight gain, abdominal pain, malabsorption, cough, wheeze, rhinitis, atopic eczema, urticaria and angioedema. Despite the lack of objective data to support the notion that food intolerance contributes to behaviour in children, this is a belief firmly held by many parents and some professionals. The gold standard for diagnosing food intolerance is the double-blind placebo-controlled food challenge (DBPCFC). There is often a poor correlation between the results of food provocation tests and those of skin prick tests of radioallergosorbent tests for specific food antibodies. For proven food allergy, elimination diets are the mainstay of management. In children these must be closely supervised to avoid nutritional deficiency and compromise of growth. Some children who have had severe (anaphylactic) reactions after food need to have a supply of self-injectable adrenaline made available to their parents and teachers and must also practice strict avoidance of the offending food.
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PMID:Food allergy and food intolerance in childhood. 1113 67