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Query: UMLS:C0019693 (HIV)
 170,526 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To determine the folic acid absorption characteristics of patients with human immunodeficiency virus (HIV) infection, a prospective, controlled, result-blind single-dose oral absorption study was conducted. A total of 25 subjects were fasted and given 5 mg oral folic acid; blood samples were taken at time zero and after 30, 60, 90 and 180 min. Absorption of folic acid appears to be significantly impaired in HIV disease, irrespective of the stage of the disease and notwithstanding gastro-intestinal complaints, pathogen-negative diarrhoea or drug treatment. We here present functional data, complementary to previously reported structural and biochemical findings, to support the hypothesis that the virus can cause an enteropathy in the absence of opportunist infection. Folinic acid is absorbed by the same gut mechanism as folic acid, so caution may be needed when employing oral folinic acid rescue procedures in these patients, even when resting serum and red cell folate levels appear to be normal.
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PMID:Folic acid absorption in patients infected with the human immunodeficiency virus. 168 Jan 50

Early intervention guidelines in HIV infection require knowledge of CD4+ lymphocyte count; however, CD4+ determinations require special laboratory procedures and may not be readily available in all situations. Using data from 207 HIV-seropositive homosexual men without AIDS, we evaluated the association of difference clinical conditions or serologic tests with CD4+ count. Men with conditions including seborrheic dermatitis, hairy leukoplakia, oral candidiasis and chronic diarrhea, and men with beta2-microglobulin levels greater than or equal to 4.0 mg/l had significantly lower CD4+ counts. However, the probability that a subject with such parameters had less than 200 x 10(6)/l CD4+ cells was limited (25-63%). Although the probability that a subject with such parameters had less than 500 x 10(6)/l CD4+ cells was better (76-88%), the probability that a person without these parameters had greater than or equal to 500 x 10(6)/l CD4+ cells was only 45-50%. Clinical and serologic parameters may provide important prognostic information, but cannot be used to reliably determine the level of CD4+ cells.
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PMID:The association of clinical conditions and serologic tests with CD4+ lymphocyte counts in HIV-infected subjects without AIDS. 168 78

Nineteen colorectal biopsy specimens, stained by Hematein-Eosin-Safran (HES), were examined by light microscopy and showed a thick, blue and fuzzy brush border. Without any further microbiologic investigation, this histologic feature is considered strongly suggestive of colorectal spirochetosis. Our study concerned 19 male patients aged between 35 and 68 years, who had no risk factor for HIV infection, but who belonged to these three groups: (a) those suffering from chronic diarrhea; (b) those without intestinal symptoms; (c) those who had a colonic tumor removed. Rectal biopsy specimens were also taken from a control group of 35 patients seropositive for HIV-1. This thickening, which measured 3-7 microns, showed some variation within the same patient but did not depend on the site of the biopsy. It appeared as a blue fuzzy band on HES stain, was purple on Periodic-Acid-Schiff stain and basophilic after Giemsa stain. Silver stain by Warthin-Starry method confirmed the presence in three cases of numerous spirochetes attached to the epithelial surface. Two of the three patients had no symptom. In the control group, a thickening of the brush border, was observed in only one case, but no spirochete by silver stain was seen. The thickened blue, fuzzy brush border of the colonic mucosa is not a specific criterion. The pathologist must be aware of the possible presence of spirochetes that can only be confirmed by a silver stain. The pathogenicity of spirochetosis remains to be defined.
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PMID:[Colo-rectal spirochetosis: is it an anatomo-pathologic entity?]. 170 40

Tryptophan (Trp) is an indispensable amino acid required for biosynthesis of proteins, serotonin and niacin. Indoleamine 2,3-dioxygenase (IDO) is induced by infections, viruses, lipopolysaccharides, or interferons (IFNs) and this results in significant catabolism of Trp along the kynurenine (Kyn) pathway. Intracellular growth of Toxoplasma gondii and Chlamydia psittaci in human fibroblasts in vitro is inhibited by IFN-gamma and this inhibition is negated by extra Trp in the medium. Similarly, growth of a number of human cell lines in vitro is inhibited by IFN-gamma and addition of extra Trp restores growth. Thus, in some in vitro systems, antiproliferative effects of IFN-gamma are mediated by induced depletion of Trp. We find that cancer patients given Type I or Type II IFNs can induce IDO which results in decreased serum Trp levels (20-50% of pretreatment) and increased urinary metabolites of the Kyn pathway (5 to 500 fold of pretreatment). We speculate that in vivo antineoplastic effects of IFNs and clinical side effects are mediated, at least in part, by a general or localized depletion of Trp. In view of reported increases of IFNs in autoimmune diseases and our earlier findings of elevated urinary Trp metabolites in autoimmune diseases, it seems likely that systemic or local depletion of Trp occurs in autoimmune diseases and may relate to degeneration, wasting and other symptoms in such diseases. We find high levels of IDO in cells isolated from synovia of arthritic joints. IFNs are also elevated in human immunodeficiency virus (HIV) patients and increasing IFN levels are associated with a worsening prognosis. We propose that IDO is induced chronically by HIV infection, is further increased by opportunistic infections, and that this chronic loss of Trp initiates mechanisms responsible for the cachexia, dementia, diarrhea and possibly immunosuppression of AIDS patients. In these symptoms, AIDS resembles classical pellagra due to dietary deficiency of Trp and niacin. In preliminary studies, others report low levels of Trp and serotonin, and elevated levels of Kyn and quinolinic acid in AIDS patients. The implications of these data in cancer, autoimmune diseases and AIDS are discussed.
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PMID:Implications of interferon-induced tryptophan catabolism in cancer, auto-immune diseases and AIDS. 172 46

Gastrointestinal manifestations of AIDS are common. Opportunistic infections and tumors may affect any portion of the GI tract from oral cavity to anus. Esophageal involvement may result from Candida, CMV, HSV, HIV, and tumors. Biliary tract and pancreatic disease may cause abdominal pain. Diarrhea occurs in over 50% of AIDS patients and is multifactorial.
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PMID:Medical management of AIDS patients. Gastrointestinal manifestations. 172 41

In 1988, researchers recruited 18-35 year old women from pediatric and prenatal care clinics at the Centre Hospitalier de Kigali in Rwanda to observe HIV disease progression. They compared probability of survival of the 460 HIV-positive women with that of the 998 HIV-negative women. They used simple clinical and laboratory variables as predictors of mortality from AIDS. The researchers did not use the WHO clinical case definition of AIDS as the outcome measure since 40 and 30 women from each group, respectively, met the criteria for AIDS at entry. Only 66% (25) of the HIV=infected women who died met the criteria for AIDS during the study. After 2 years, mortality among HIV-infected women stood at 7% (39) which was more than 20 times higher than that among women not HIV infected (0.3%; p .001). Mortality was 21% for those who met the WHO criteria for AIDS. The wasting syndrome was the cause of the death in 51% of HIV-infected death cases. The baseline predictors of mortality in HIV-infected women in descending order of prevalence of predictor included an at most body mass index of 21 kg.sq. (48%; relative hazard [RH] 2.3), low income (46%; RH=2.6), mm/hour erythrocyte sedimentation rate (39%; rh = 4.9), chronic diarrhea (10%; RH = 2.6), a history of herpes zoster (9%; RH 5.3), and oral candidiasis (1%; RH 7.3). The erythrocyte sedimentation rate was a better predictor than lymphocyte counts (p .001) and p .11, respectively). Of the 40 HIV-infected women who met the criteria for AIDS, the health of 32 women improved so the physicians no longer considered them to have AIDS. Thus health workers should treat symptomatic HIV-positive cases. AIDS was responsible for 90% of all deaths among reproductive age women living in Kigali. Health workers in Africa can use the simpler erythrocyte sedimentation rate instead of the more costly CD4 counts as a predictor of progression to AIDS.
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PMID:Predictors of mortality among HIV-infected women in Kigali, Rwanda. 173 89

The article proposes that the clinical case definition for Acquired Immunodeficiency Syndrome in Africa is an unworkable concept, with the wrong definition, incorrect validation, improper use, and consequently is a poor surveillance tool. The definition was proposed by the World Health Organization in 1986 to satisfy the use in countries with limited diagnostic resources, and resources for serological testing. Critical review until now of this procedure was lacking. Currently serological testing is available and of high quality. It does not seem justifiable to continue using a provisional surveillance definition. Abandoning this classification procedure may also lead to the focus on problems other than opportunistic infections and AIDs. Clinical surveillance is important, but as well morbidity and mortality need monitoring. It is argued that the definition is an unworkable concept because patients with underlying immunosuppression disorders such as AIDs can not be easily distinguished from chronic disease patients; i.e., pulmonary tuberculosis, renal failure, uncontrolled diabetes, or diarrhea with weight loss. Clinical accuracy is insufficient. It is the wrong definition because pulmonary tuberculosis with a persistent cough cannot be distinguished for those HIV positive and those not. There is inconsistency in the WHO clinical definition and the Centers for Disease Control definitions of AIDs. The incidence of tuberculosis in countries with unmodified clinical case definitions may contribute to an inflated number of AIDs cases. The wrong standards were used to validate the WHO definition in evaluative studies. The reference sensitivity ranges indicate that the definition is insensitive to identifying seropositive patients. Also, the HIV status of patients does not equate with AIDs. Although designed for surveillance, the clinical case definition is used by doctors for individual patient management. Labeling a patient as having AIDs, when he is HIV negative, leads to negative consequences. Researchers compare African AIDs data with North American data with imprecise and noncomparable definitions. As a surveillance tool in countries with a fragmentary or without a vital registration system, it is an inaccurate tool. Alternatives to obtaining data about the spread and impact of HIV are cluster sampling, hospital surveillance of selected populations, anonymous testing of pregnant women or patients in sexually transmitted disease clinics. In Nairobi, a necropsy survey found that 16% had AIDs but 38% were HIV positive.
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PMID:What use is a clinical case definition for AIDS in Africa? 173 1

A 29-year-old man, a known heroin addict until 1984 in whom HIV antibodies had been first demonstrated in 1985, was hospitalized because of fever, nocturnal sweating, weight loss and treatment-resistant diarrhoea. An opportunistic infection of the gastrointestinal tract was excluded microbiologically and serologically. Coloscopy and biopsy revealed a highly malignant gastrointestinal B-cell lymphoma, which had caused a spontaneous rectosigmoid-ileum fistula. Lymphoma infiltrations were also found in the duodenum, jejunum, left lung and brain. Because the underlying disease was far progressed (CD4/CD8 ratio: 0.04) and the patient was in a poor general condition neither surgery nor chemotherapy was undertaken. He died of cerebral lymphoma involvement. Gastrointestinal lymphoma should be included in the differential diagnosis of chronic diarrhoea in HIV-positive patients.
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PMID:[A fistula between the rectosigmoid junction and the ileum as a complication of highly malignant AIDS-associated lymphoma]. 174 69

Case I: A middle-age homosexual male developed AIDS with Pneumocystis carinii pneumonia (PCP) and esophageal candidiasis in 1986 during his stay in an European country about five months prior to transfer to Tokyo Metropolitan Komagome Hospital, Tokyo, in 1987. He was also diagnosed as having cryptosporidiosis presenting with mild diarrhea a month following the diagnosis of PCP. Diarrhea was successfully treated with spiramycin. On transfer to Tokyo Metropolitan Komagome Hospital, he was febrile but had no diarrhea. Serum HIV and TPHA were positive and his blood lymphocyte subset T4a was markedly decreased. On the 13th day after transfer to the hospital, watery diarrhea appeared. Cryptosporidium oocysts were detected from the feces taken on the 17th hospital day. The patient died of Escherichia coli septicemia on the 38th hospital day. Autopsy finding yielded Cryptosporidium infection widely spread over the stomach, ileum, bile and pancreatic ducts. Case II: A 31-year-old previously healthy female presented with abrupt onset of mucous stool five times daily. Mucous passage continued on the subsequent days despite administration of loperamide, and the passage increased to 20 times daily with mucous to watery diarrhea associated with mild abdominal cramps and nausea on the 4th day after onset of illness. On the 6th day of illness, she visited Tokyo Metropolitan Komagome Hospital. She denied close contact with pet animals or contact with any person presenting diarrhea. She had no recent history of travelling anywhere outside Tokyo. On examination she was an apparently healthy woman except for a slightly distended abdomen with localized tenderness in the right upper quadrant.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Cryptosporidium diarrhea developing in two Japanese adults--one in AIDS and the other in a normal host. Research Group for Infectious Enteric Diseases, Japan]. 178 13

Autonomic nerves in jejunal mucosa of HIV-infected patients show severe structural damage on electron microscopic examination. The aim of this study was to quantify loss of autonomic axons from the lamina propria of HIV-infected patients in different clinical stages of disease. Jejunal biopsies were taken from 19 HIV-antibody-positive homosexual men and from 10 control patients. Autonomic fibres in the mucosa were stained with a neurone-specific polyclonal antibody, PGP 9.5. The density of axons was quantified by a point-counting technique using a Lennox eyepiece graticule under light microscopic examination. There was significant reduction in axonal density in the villi of HIV-infected patients [mean, 9.0; standard deviation (s.d.), 4.7] compared with controls (mean, 15.3; s.d., 5.2; P = 0.003), and in the pericryptal lamina propria of HIV-infected patients (mean, 17.8; s.d., 5.4) compared with controls (mean, 27.3; s.d., 6.2; P = 0.0002). Although autonomic denervation occurs throughout the jejunal mucosa of HIV-infected patients, there was no correlation between the clinical stage of HIV disease and the degree of denervation. The denervation was greatest in patients with the most severe diarrhoea, but this difference was not significant. This study provides the first quantitative morphological evidence for depletion of autonomic nerves in the jejunum of patients infected with HIV. Autonomic neuropathy may contribute to chronic diarrhoea in HIV disease.
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PMID:Autonomic denervation in jejunal mucosa of homosexual men infected with HIV. 178 51


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