Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0021051 (immunodeficiency)
 71,517 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To understand whether disease caused by the human immunodeficiency virus (HIV) affects zidovudine disposition, we compared the drug's pharmacokinetics in six healthy volunteers; six persons with the acquired immunodeficiency syndrome (AIDS) and no evidence of gastrointestinal (nausea, vomiting, diarrhea), renal (elevated blood urea nitrogen, serum creatinine), or hepatic (elevated liver function tests) disease; and three patients with AIDS and hepatic disease. After a single oral dose of zidovudine, serial blood samples were analyzed for drug concentration by radioimmunoassay. A one-compartment oral absorption model was fit to the concentration-time data. The absorption rate constant (4.05 vs 2.11 hr-1) and time to maximum concentration (0.61 vs 1.03 hr) were significantly different in healthy volunteers versus patients with AIDS without hepatic disease. Differences in half-life, oral clearance, and area under the curve were not statistically significant. In the three patients with AIDS plus hepatic disease, clearance was reduced an average of 63%, and area under the curve was increased by a factor of 2.3. These comparative pharmacokinetic data do not support profound differences between zidovudine's disposition in healthy volunteers and individuals with AIDS; however, the differences and trends that were observed may represent an effect of HIV disease. Although the presence of hepatic disease clearly indicates a need to modify individual dosages, these pharmacokinetic data may have more generalized implications for zidovudine dosing as the relationships between drug concentration and therapeutic or toxic effects are clarified.
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PMID:Comparative pharmacokinetics of zidovudine in healthy volunteers and in patients with AIDS with and without hepatic disease. 149 5

The clinical significance of the fastidious organism DF-3 isolated from stool cultures is unclear. We sought to improve our understanding of this organism and to further define its association with human disease. Stool cultures for DF-3 were obtained from three sources: an ongoing study of enteric pathogens in patients infected with the human immunodeficiency virus, a screening procedure in which all stool samples submitted for Clostridium difficile toxin assay were cultured for DF-3, and stool samples submitted specifically for DF-3 culture. Retrospective clinical data were obtained from chart reviews of patients with positive cultures. Antimicrobial susceptibility testing and cell wall fatty acid analysis were performed for each DF-3 isolated. Eight isolates of DF-3 were obtained over a period of 8 months. All patients either had severe underlying disease or were immunocompromised, including three patients coinfected with human immunodeficiency virus and two patients with inflammatory bowel disease. The spectrum of clinical disease ranged from chronic diarrhea with a well-defined response to therapy for DF-3 to an asymptomatic carrier state. Cell wall fatty acid analysis of these isolates demonstrated a consistent pattern with a large peak of 12-methyltetradecanoate. DF-3, a fastidious gram-negative coccobacillus, can be recovered from stool cultures of immunocompromised patients by using selective media. The presence of 12-methyltetradecanoate in cell wall fatty acid analysis assists in identification. The increased use of a selective medium-(cefoperazone-vancomycin-amphotericin B) in the evaluation of diarrhea in immunocompromised hosts, including persons with inflammatory bowel disease, may better define the association of DF-3 with human gastrointestinal disease.
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PMID:Clinical illnesses associated with isolation of dysgonic fermenter 3 from stool samples. 153 8

Immunodeficiency with hyper-IgM (HIM) is a rare disorder characterized by recurrent infections associated with low IgG and IgA, and normal to increased IgM serum levels. Both primary and secondary forms of HIM syndrome have been reported. Among primary HIM syndrome, evidence for genetic heterogeneity is provided by the occurrence of the disease as X-linked, autosomal recessive, or autosomal dominant trait. The most common clinical manifestations include upper and lower respiratory tract infections, otitis, diarrhoea, oral ulcers, lymphoid hyperplasia, and autoimmunity. Recurrent neutropaenia is a frequent finding. Immunological abnormalities consist of lack of IgG and IgA secretion, and failure to respond to vaccination. Lymph nodes show absence of germinal centres. Few patients with a concurrent T-cell defect, and clinical expression of combined immune deficiency, have been reported. The gene responsible for the X-linked HIM syndrome (HIGM1) has been tentatively assigned to Xq24-27. However, carrier detection and prenatal diagnosis are not yet possible. Pathogenetic hypotheses include failure of B-cell differentiation, and defective regulation of immunoglobulin isotype switching due to abnormal T-cell-mediated signals. Treatment is mainly based upon regular administration of intravenous immunoglobulins. Steroids may be useful in the treatment of neutropaenia and of severe autoimmune manifestations.
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PMID:Immunodeficiency with hyper-IgM (HIM). 155 97

Cryptosporidiosis was diagnosed in 4 cockatoos with psittacine beak and feather disease. Three of the birds had cryptosporidiosis confined to the epithelium covering the bursa of Fabricius. One bird had generalized parasitism of the small intestine, large intestine, and bursal epithelium. All of the birds had intermittent to protracted diarrhea before death. Presumably, acquired immunodeficiency from psittacine beak and feather disease promoted establishment of cryptosporidiosis and other secondary diseases including septicemia, peritonitis, chlamydiosis, and mycotic ventriculitis.
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PMID:Cryptosporidiosis in four cockatoos with psittacine beak and feather disease. 156 16

Individuals who are seropositive for the human immunodeficiency virus (HIV) frequently have disorders affecting the anorectum, yet little has been reported on this subject. We reviewed our initial experience with patients with HIV referred to the Division of Colon and Rectal Surgery. Forty patients (age range, 19-45 years; mean, 32.2 years) were seen between 1985 and 1989. The mean duration of symptoms was six months (range, one week to six years). In 25 patients (63 percent), more than one anorectal condition was identified. Condylomata were seen in 21 patients (52 percent), and in 11 these were associated with other pathologies. Fistulas and/or abscesses were identified in 15 patients (37 percent). Three had a "watering-can perineum," all without any identifiable predisposing factors. Nineteen patients had symptomatic hemorrhoids (seven), fissures (17), and/or perianal herpes infections (five), usually in combination with other lesions (89 percent). Three individuals developed neoplastic processes. Rectal disease was discovered in addition in nine patients. This included nonspecific proctitis in four, a rectal mass in four (polyps, two; rectal diverticulum, one; and Kaposi's sarcoma, one), and a nonspecific rectal ulcer in one. Four patients had other symptoms, including diarrhea, incontinence, soiling, frequency, and/or urgency, always in combination with other anal disorders. Seventy-one operative procedures were performed in 31 patients (78 percent). Only six (8 percent) of these were for diagnosis and biopsy alone. Mean follow-up was 15.5 months in the 23 patients followed for greater than one month. Only 6 of 23 (26 percent) had resolution of their problem. Nine (39 percent) developed new perianal conditions. Anorectal disorders are often seen in patients infected with HIV. They may be aggressive, cause significant morbidity, and be difficult to resolve.
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PMID:Perineal manifestations of HIV infection. 158 50

We report a case of colonic pneumocystosis in a human immunodeficiency virus (HIV)-positive homosexual male who presented with fever and diarrhea. Stool cultures for bacterial pathogens and examinations for ova and parasites were negative. The diagnosis was made by colonoscopic biopsy which revealed Pneumocystis carinii organisms in the lamina propria of the cecum, descending colon, and sigmoid colon. The patient subsequently developed pulmonary and ocular abnormalities consistent with P. carinii involvement of these organs. The diarrhea and other manifestations resolved with antipneumocystis therapy. Many sites of extrapulmonary pneumocystosis have been reported, but we believe this is the first report of colonic P. carinii found in the evaluation of persistent diarrhea in a patient with the acquired immunodeficiency syndrome.
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PMID:Pneumocystis colitis in a patient with the acquired immunodeficiency syndrome. 831 27

To date, the only microsporidian that has been associated with diarrhea and weight loss in acquired immunodeficiency syndrome patients is the newly identified Enterocytozoon bieneusi. A second species is now described that was associated with intestinal symptoms in a 32-year-old, human immunodeficiency virus- seropositive, Native American male homosexual. Stool studies and routine light microscopy of multiple small intestinal biopsies that showed atrophy with acute and chronic inflammation were without apparent pathogens. Light microscopy of semi-thin plastic sections, cytochemical stains of paraffin sections, and ultrastructural studies revealed extensive microsporidial infection of enterocytes and submucosal macrophages. No other pathogens were identified. Unlike E bieneusi, this microsporidian appeared to develop within septated parasitophorous vacuoles, and lacked polar disks and clear clefts. It most closely resembled, but was distinguishable from, members of the genus Encephalitozoon. Awareness of the microsporidia as potential opportunists in acquired immunodeficiency syndrome patients is increasing the incidence of identification of these organisms.
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PMID:A microsporidian previously undescribed in humans, infecting enterocytes and macrophages, and associated with diarrhea in an acquired immunodeficiency syndrome patient. 161 73

Intermittent or chronic diarrhea may be the initial symptom of hypogammaglobulinemia. In adult, that corresponds most frequently to common variable immunodeficiency. The pathogenesis of this syndrome is still undetermined. Diagnostic criteria are discussed as well as the therapeutic approach that can avoid multiple complications.
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PMID:[Primary hypogammaglobulinemia in adults]. 163 38

1. Small-intestine integrity in Caucasian and African patients infected with human immunodeficiency virus was determined by measuring the permeation across the mucosa of two sugars, lactulose and mannitol. 2. The sugars were assayed by h.p.l.c. and pulsed amperometric detection in 6 h urine samples. Stool microscopy for enteropathogens was performed in all patients. 3. The ratio of lactulose to mannitol recovered in urine was increased in Caucasian and African patients with advanced human immunodeficiency virus infection. Asymptomatic human-immunodeficiency-virus-infected subjects had a normal lactulose/mannitol ratio. African patients with diarrhoea showed a twofold reduction in mannitol excretion. Such a change in mannitol absorption was not detected in Caucasian patients and occurred regardless of the presence of enteropathogens. 4. Altered small-intestinal permeability is associated with symptomatic diarrhoea in human immunodeficiency virus infection in both Caucasian and African patients.
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PMID:Altered small-intestinal permeability associated with diarrhoea in human-immunodeficiency-virus-infected Caucasian and African subjects. 165 33

Cats infected with molecularly cloned FeLV-FAIDS develop an immunodeficiency syndrome characterized by persistent antigenemia, decline in circulating CD4+ T lymphocytes, and impaired T-cell-dependent immune responses and opportunistic infection. We evaluated the capacity of PMEA to inhibit the replication of FeLV-FAIDS in vitro and to inhibit the progression of FeLV-FAIDS infection in vivo. We found that PMEA inhibited replication of FeLV-FAIDS by greater than or equal to 50% at concentrations of greater than or equal to 0.5 microgram/ml (1.63 microM) in feline fibroblasts and prevented T lymphocyte killing at concentrations of 3 micrograms/ml. PMEA administered to cats at dosages of greater than or equal to 6.25 mg/kg/day from 0 to 49 days after FeLV-FAIDS infection prevented the development of persistent antigenemia and the induction of immunodeficiency disease. In contrast to placebo treated controls, cats successfully treated with PMEA contained viral infection, developed neutralizing antibody, and resisted a second virulent virus challenge without further therapy. Manifestations of PMEA toxicity produced by higher dosages (25 or 12.5 mg/kg/day) were anemia, leukopenia, and diarrhea. These results indicate PMEA to be a potent antiretroviral agent effective in aborting fatal progression of FeLV-FAIDS infection when therapy is initiated at the time of virus exposure.
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PMID:Early therapy of feline leukemia virus infection (FeLV-FAIDS) with 9-(2-phosphonylmethoxyethyl)adenine (PMEA). 166 30


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