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)

Microsporidia are emerging as opportunistic pathogens in patients with AIDS. Enterocytozoon bieneusi and Encephalitozoon (Septata) intestinalis have been implicated in enteric infections in AIDS patients with chronic diarrhea, a wasting syndrome, and malabsorption. We used the polymerase chain reaction (PCR) and primers that amplify the conserved regions of the small-subunit rRNA (SSU-rRNA) gene of E. bieneusi and E. intestinalis in tissue specimens from HIV-infected patients with and without diarrhea to examine the association between microsporidia and diarrhea in patients with AIDS. Tissue specimens were obtained from 68 patients with AIDS and diarrhea (mean CD4 lymphocyte count, 21/mm3) and 43 AIDS patients without diarrhea (mean CD4 lymphocyte count, 60/mm3). By means of PCR with use of the SSU-rRNA primers specific for E. bieneusi and E. intestinalis, we found that 44% of patients with diarrhea were infected with microsporidia, whereas only 2.3% of the patients without diarrhea were infected with microsporidia (P < .001). There was a clear association between the presence of microsporidia and diarrhea. In addition, the SSU-rRNA primers proved to be sensitive and specific when used in this clinical setting.
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PMID:Prevalence of microsporidiosis due to Enterocytozoon bieneusi and Encephalitozoon (Septata) intestinalis among patients with AIDS-related diarrhea: determination by polymerase chain reaction to the microsporidian small-subunit rRNA gene. 892 93

We measured plasma levels of all the antioxidant-micronutrients in subjects with HIV infection and controls. Plasma levels of all the carotenoids, including lutein, cryptoxanthin, lycopene, alpha-carotene and beta-carotene as well as vitamins A, C and E and cholesterol were assayed in 35 subjects with HIV infection and 38 controls. We found a significant depletion of all the carotenoids (P < 0.001) and vitamin C (P < 0.01) and cholesterol (P < 0.001) but not vitamins A or E in HIV-infected subjects. Further analysis of the HIV-infected subjects revealed that plasma levels of 4 of the groups of carotenoids and cholesterol were correlated with CD4 count but that beta-carotene and vitamins A, C and E were not. These results are reviewed in the light of the published literature and we conclude that these abnormalities of antioxidant-micronutrients are likely to reflect a metabolic phenomenon associated with HIV infection. However, an additional contribution to these deficiencies from malabsorption later in HIV disease cannot be ruled out.
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PMID:Antioxidant-micronutrients and HIV infection. 911 64

The polyglandular autoimmune syndromes (PGA) are well known and are distinguished into type I, type II and type III. PGAI, also called APECED (autoimmune polyendocrinopathy, candidiasis and ectodermal dystrophy), is an autosomal recessive disorder, appearing in childhood and typically characterized by hypoparathyroidism (unusual in PGAII and PGAIII) and adrenal insufficiency. In APECED, autoimmune destruction of the pancreatic beta cells with development of insulin-dependent type 1 diabetes is possible, but less frequent than in the other PGAs, especially PGAII. The pathogenesis of this unique autoimmune disease is unknown. No HLA association seems to exist and genetic studies have assigned the autosomal APECED locus to chromosome 21. The case of a 28-years-old female suggesting the diagnosis of APECED, is presented, characterized by psycho-somatic abnormal development, teeth alterations, post-puberal gonadal failure with dystrophic hypoplasia of external genitalia, previous vaginal candidiasis, a slowly developing juvenile brittle diabetes. Intestinal malabsorption induced by Giardia lamblia occurred (probably resulting, like candidiasis, from immunological anergy). A strong familiarity linked to female sex was noticed (the mother, a sister, the little nice and some maternal female cousins being affected) while the father and a brother were healthy. Diabetes seems to be characterized by early onset and severe complications. In this patient no organo-specific antibodies were detected and the only immunologic disorder was a small decrease of CD3 and CD4/CD8 ratio, both CD4 and CD8 being at the lower normal range. This patient (and her female maternal relatives) needs a long-term follow-up in order to evaluate the function of endocrine glands and to initiate early treatment for hormonal deficits, as well as to detect the non-endocrine components of disease.
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PMID:[A rare case of juvenile diabetes mellitus associated with APECED (autoimmune poly-endocrinopathy, candidiasis and ectodermal dystrophy) with strong X-linked familial inheritance]. 930 48

Malnutrition is common in human immunodeficiency virus (HIV) infection and plays an important role in morbidity and mortality. Malnutrition can affect hospitalizations, disease complications, quality of life, and survival, and has adverse clinical consequences that may be independent of CD4 lymphocyte count. There have been recent advances in knowledge concerning the pathogenesis of malnutrition and the nature of weight loss in HIV patients. The onset of body cell mass depletion may occur early in the infection and predate significant immune deficiency, implying that the virus itself may be involved. Hypogonadism, a common finding in HIV patients, is associated with body composition changes and is involved in body cell mass depletion. In addition, intestinal dysfunction and malabsorption contribute to weight loss in HIV patients. Several studies have evaluated the use of appetite stimulants, enteral and parenteral nutritional support, anabolic agents, and other agents in the management of weight loss and malnutrition in HIV patients. Results of a randomized trial comparing total parenteral nutrition (TPN) and an oral semi-elemental diet (SED) in AIDS patients with malabsorption indicate that the TPN group consumed more calories and gained more weight than the SED group, but the gain was due to increased body fat. The effect of nutritional support on malnutrition and weight loss in HIV patients and potential secondary benefits to quality of life, physical and mental performance, immune function, and disease progression require further study.
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PMID:Management of nutritional alterations and issues concerning quality of life. 938 9

Intestinal parasite infections are very frequent in HIV patients with severe immunodeficiency (CD4 < 100/mm3) causing chronic diarrhea and malabsorption in the majority of cases. The most frequent microorganisms are microsporidia and Cryptosporidium parvum while Cyclospora cayetanensis and Isospora belli are more prevalent in subtropical and tropical areas and rare in industrialized areas. The diagnosis can be obtained by stool examination (differences in size and form of cysts), although microsporidia is frequently demonstrated by intestinal biopsy and/or duodenal aspirate. The treatment with cotrimoxazole for C. cayetanensis and I. belli is very effective and does not present any problems in the acute phase, however, due to a high percentage of relapses the treatment must be maintained while the patient is in a severe immunodeficiency state. E. intestinalis usually responds satisfactorily to albendazole while E. bieneusi is resistant to some drugs except in some cases (albendazole, atovaquone ad fumagillin). C parvum is also resistant to most medicaments but shows an adequate or partial clinical: response to paramomicine (< 50%). When there is no response, it is advised to administer octreotide since in half the cases the response is positive either total or partial. Nowadays with the use of protease inhibitors in the antiretroviral treatment a decrease in the incidence of these infections has been observed (microsporidia and C. parvum) even in the stools samples taken from the patients who had them before. As primary prophylaxis for C. parvum, it is better to avoid been exposed to the microorganism taking into account the 1997 preventive measures recommended by the USPHS/IDSA Prevention of Opportunistic Infections Working Group. The coinfection Leishmania-HIV is frequent in the mediterranean area. The most common specie is L. infantum. The incidence is most frequent in immunosuppressed patients (CD4 < 200 mm3) and in parenteral drug addicts. The symptomatology is similar to the one from immunocompetent patients, although in some cases it appears to be subclinical. A chronic development with relapses is frequent. The most effective diagnostic method for the finding of the parasites is thru bone marrow puncture and the culture in Novy-McNeal-Nicolle (NNN) medium. Serological tests have a low sensibility and the PCR is useful in asymptomatic cases, for therapeutical control and in relapses. The treatment is similar to that of immunocompetent patients, using primarily antimonials or amphotericine B (standard or lipid or liposomal forms). Relapses are very frequent, therefore, it is important to perform a secondary prophylaxis. However, no treatment has been completely effective. Mortality rate is high (approximately 25%) during the first month after diagnosis. This fact may be related to the severe immunodeficiency state and/or to the toxicity of the drugs used. The main priority for the future is to find a first line treatment with higher efficacy, decrease in relapses and a lower toxicity.
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PMID:[Intestinal parasitic infections and leishmaniasis in patients with HIV infection]. 985 20

Human immunodeficiency virus (HIV) is often combined with unexplainable diarrhoea and weight loss. This study was designed to see if changes in the intestinal mucosal structure could explain the malabsorption found in HIV-infected patients with diarrhoea. Twenty acquired immunodeficiency system (AIDS) patients, 19 men and 1 woman, CD4 < 0.01, with severe weight loss and with non-infectious chronic diarrhoea, were evaluated using a new intestinal function test (D-xylose breath test). Fifteen of the subjects were examined with an upper intestinal endoscopy with biopsy specimens taken from the duodenal mucosa. The function test showed that the D-xylose uptake was markedly decreased to the same extent as for patients with coeliac disease (breath index AIDS patients 9.4 (4.3-14.4), coeliac patients 15.6 (7.6-23.6), reference level 2.5 (2.4-2.9), urine excretion AIDS patients 20% (13-26), coeliac patients 22% (14-24), reference level 37% (32-42)). The severe malabsorption could not be explained by the slight mucosal changes occasionally seen by light microscopy with small mucosal inflammation and almost normal villi. However, electron microscopy showed enterocytes with signs of hypofunction and degeneration correlating better to the intestinal malabsorption found in patients with advanced HIV infection and chronic diarrhoea.
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PMID:Changes in small intestinal structure and function in HIV-infected patients with chronic diarrhoea. 1006 44

We describe a rare case of cytotoxic gastrointestinal T-cell lymphoma with protein-losing enteropathy. Initial examination revealed the coexistence of T-cell lymphoma and tuberculosis in the mesenteric lymph node and liver. Despite anti-tuberculosis and anti-cancer treatment, the patient experienced chronic diarrhea and malabsorption and died approximately 3 years after onset. Autopsy specimens revealed medium-sized lymphoma cells, with a phenotype of CD3+, CD4-, CD7+, CD8+, CD30-, CD56-, CD103 (HML-1)-, TIA-1+, and granzyme B+, proliferating primarily and consistently in the mucosa of the entire bowel tract from esophagus to rectum. Interestingly, Epstein-Barr virus (EBV)-encoded small nuclear RNAs were detected in the tumors by in situ hybridization. Southern blot analysis revealed monoclonal proliferation in the EBV-infected T cells. Although the present case can possibly be categorized as an intestinal T-cell lymphoma according to the Revised European-American Lymphoma Classification, the case showed a unique clinical course and distribution of lymphoma cells. We present here an interesting case of gastrointestinal cytotoxic T-cell lymphoma and examine the possible association with infectious agents.
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PMID:Cytotoxic T-cell lymphoma diffusely involving the entire gastrointestinal tract associated with Epstein-Barr virus and tubercle bacilli infection. 1090 59

Diarrhea and malabsorption due to intestinal dysfunction are common symptoms in HIV infection. The pathophysiologic mechanisms of these alterations are often not known, and the role of HIV per se is still controversially discussed. We measured the epithelial transport and barrier function by means of a miniaturized Ussing chamber system in the duodenum of HIV-infected patients in different disease stages, determined by the CD4 cell count in the serum as well as symptoms in patients with and without diarrhea. We could show that diarrhea induced by HIV per se is caused by a leak flux mechanism due to impaired epithelial barrier function. Antisecretory therapy does not seem to be useful in these patients, because we did not find increased active ion secretion. Along the course of the HIV infection, the epithelial transport and barrier function varies with HIV disease stage (expressed by CD4 cell status). In addition, an in vitro model was studied to characterize the effect of HIV-infected human immune cells on the epithelial barrier function using the human colonic epithelial cell line HT-29/B6. HIV infection of human immune cells induced an increase in cytokine release--for example, TNF-alpha, IL-1 beta, IFN-alpha, and IFN-gamma--downregulating the epithelial barrier function of the human colonic epithelial cell line HT-29/B6. Taken together we postulate a specific stage-dependent cytokine pattern released from HIV-infected immune cells in the mucosa, which, corresponding to the HIV disease stage, is responsible for the variation in epithelial function.
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PMID:Mechanisms of epithelial barrier impairment in HIV infection. 1119 91

We studied the cellular immune response against malabsorption syndrome (MAS) in two broiler chicken lines, A and B. We determined the number of pan T-lymphocytes (CD3), helper T-lymphocytes (CD4), cytotoxic T-lymphocytes (CD8) and macrophages/monocytes in the small intestine in the first 2 weeks after oral inoculation of two MAS homogenates, MAS80 and MAS97-1. The immune cells were detected on cryostat tissue by immunohistochemistry and counted by villus area. In trial 1, we compared the two broiler lines for weight gain depression, intestinal lesion and number of CD3, CD4, CD8 cells and macrophages/monocytes after MAS80 inoculation. Although there was no significant difference in weight gain depression between the two broiler lines, line B had significantly higher numbers of CD8+ T-cells per villus area than had line A. To confirm part of the results of trial 1, trial 2 was done in which we compared different homogenates in broiler line B. Broiler line B was orally inoculated with either MAS97-1, intestinal homogenate obtained from healthy chickens (healthy homogenate), or phosphate buffered saline (PBS). In this trial, the MAS97-1 homogenate also induced weight gain depression and intestinal lesions, whereas the "healthy homogenate" and PBS did not induce weight gain depression or intestinal lesions. The broilers inoculated with MAS97-1 homogenate had significantly more CD8+ T-cells per villus area than had broilers inoculated with "healthy homogenate" or PBS. Increased CD8+ T-cells per villus area in the affected small intestines of broilers suggests an increase of cytotoxic T-cell activity.
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PMID:Cellular immune response in the small intestine of two broiler chicken lines orally inoculated with malabsorption syndrome homogenates. 1186 67

Because of the wide variations in the clinical presentation of celiac disease and because treatment exists that is effective in most cases, screening of the general population for celiac disease has been considered. There is still no evidence that patients who have symptom-free celiac disease are at increased risk of small intestinal lymphoma or other complications. Prevention of osteoporosis seems to be the strongest indicator for widespread screening today [22]. The major cause of failure to respond to a gluten-free diet is continuing ingestion of gluten, but other underlying diseases must be considered. Many different drugs (eg, anti-tumor necrosis factor [TNF]-alpha) have been used in patients who have RCD [23]. Steroid treatment has been reported to be effective even in patients who have underlying early EATL. Histologic recovery in patients who have celiac disease usually takes several months but can take up to 1 year, even if the patient remains on a strict gluten-free diet. Some patients report celiac-related symptoms for months after a single gluten intake. The definitions for RCD in literature vary. The authors consider the definition give by Daum and colleagues [24] suitable. They defined true RCD as villous atrophy with crypt hyperplasia and increased IELs persisting for more than 12 months in spite of a strict gluten-free diet. If a patient is not responding well to a gluten-free diet, three considerations are necessary: (1) the initial diagnosis of celiac disease must be reassessed;(2) the patient should be sent to a dietician to check for errors in diet or compliance problems, because problems with the gluten-free diet are the most important cause for persisting symptoms; (3) other reasons for persisting symptoms (eg, pancreatic insufficiency, irritable bowel syndrome, bacterial overgrowth, lymphocytic colitis, collagenous colitis, ulcerative jejunitis, protein-losing enteropathy,T-cell lymphoma, fructose intolerance, cavitating lymphadenopathy, and tropical sprue) should be considered. Other causes for villous atrophy are Crohn's disease, collagenous sprue, and autoimmune enteropathy. Abdulkarim and colleagues [25] examined 55 patients who had a diagnosis of nonresponsive celiac disease. He found that 6 did not have celiac disease, and25 still had some gluten ingestion.Tursi and colleagues [26] reported 15 patients who had celiac disease with persisting symptoms. Because histology improved in all patients after several months, RCD was excluded. Of the 15 patients, 10 had small intestinal bacterial overgrowth, 2 showed lactose malabsorption causing the described symptoms, 1 had mistakenly taken an antibiotic containing gluten, and 1 patient each had Giardia lamblia and Ascaris lumbricoides. Thus, other entities must be considered in patients who have celiac disease and ongoing symptoms. In a follow-up clinical trial, 158 patients who had celiac disease underwent follow-up small intestine biopsies within 2 years after starting a gluten-free diet. Eleven patients (7.0%) with persisting (partial) villous atrophy were considered to have RCD; 5 of them developed EATL [27].RCD type I is characterized by normal expression of T-cell antigens and polyclonal TCR gene rearrangement.RCD type II is characterized by an abnormal IEL phenotype with the expression of intracytoplasmic CD3e, surface CD103, and the lack of classic surface T-cell markers such as CD8, CD4, and TCR-alpha/beta. This clonal IEL population can be considered crypt IEL [24]. RCD II has a poor prognosis, which is a problem for therapy. Clonal TCR gene rearrangements and loss of T-cell antigens such as CD8 and TCR-beta in IELs may indicate the development of an EATL in patients who have RCD. The markers for an overt EATL are a positive stool blood test, increased lactate dehydrogenase, or beta2-microglobulin [24]. If an overt lymphoma is suspected, upper and lower endoscopy, an ear, nose, and throat work-up, CT scan, capsule endoscopy, and possibly double-balloon enteroscopy should be performed. Most reports of the difficulties in treating patients who have true RCE are casereports. Turner and colleagues [28] reported on an induction of remission by useof the anti-TNF-alpha antibody infliximab and maintenance with prednisoloneand azathioprine. Olaussen and colleagues [29] and Mandal and colleagues [30]tried a nonimmunogenic elemental diet. Gillet and colleagues [31] reported successful treatment of a patient who hadRCD using anti-TNF-alpha antibodies (infliximab) for induction and azathioprinefor maintenance. Maurino and colleagues [32] studied seven consecutive patients diagnosed ashaving refractory sprue and no response to oral or parenteral steroids. Aftertreatment with azathioprine (2 mg/kg/d) and oral prednisone (1 mg/kg/d), fivepatients had a complete clinical remission. Two patients who did not respond totreatment at any time died. Goerres and colleagues [33] described 18 patients who had RCD, 10 of whomhad type I RCD, and 8 of whom had type II RCD. Treatment consisted ofazathioprine combined with prednisone for 1 year. Consistent with reports byother investigators, the response rates in the two groups differed. Eight of the10 patients who had type I RCD had a histologic response. Seven of the eightpatients who had type II RCD died, and six of the eight developed a lymphoma. At present there is no effective treatment for type II RCD.Fig. 3 presents a proposed algorithm for monitoring patients who have ce-liac disease.
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PMID:Monitoring nonresponsive patients who have celiac disease. 1687 29


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