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

A patient admitted to your unit this morning presents a dauntingly complex clinical picture. Maria DeJesus, 34 years old, has HIV infection, which progressed to AIDS last year with an episode of Pneumocystis carinii pneumonia. She's also experienced recurrent vaginal and esophageal candidiasis and cryptococcal meningitis, and her more recent history includes peripheral neuropathy, causing pain and numbness, as well as cognitive and motor function problems. Her admission was prompted by diarrhea that has persisted despite outpatient treatment. To provide the best care for patients like Ms. DeJesus, you need to understand HIV infection and the diseases associated with it. Yet that's a challenging task, given that the possible manifestations of advanced infection are so many and varied. Though your approach to care is holistic, you may find it helpful to consider the numerous facets of the patient's illness individually. In the following pages, we'll examine how HIV enters the body, infects immune cells, and eventually cripples the immune system. We'll look at some of the more common opportunistic infections preying on people with HIV. And we'll explore the less well-charted territory of complications attributed to HIV infection of the central and peripheral nervous systems.
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PMID:Understanding the devastation of AIDS. 924 79

The bis triazole agent fluconazole is used widely in the treatment of superficial and deep mycoses. A single oral dose of fluconazole 150 mg gives a mean long term clinical cure rate of 84 +/- 5% and is considered a valuable alternative to other topical antifungal drugs for vaginal candidiasis. A clinical cure rate of 90.4% for oropharyngeal candidiasis was obtained with 100mg daily for a minimum of 14 days; however, as for the other azoles the rate of relapse was large (40%) in immunocompromised patients. A daily dose of 100mg for at last 3 weeks gave satisfying outcomes for oesophageal candidiasis. Most patients (71 to 86%) with signs and symptoms of urinary tract candidiasis show beneficial clinical results when given oral fluconazole 50mg for several weeks. Fluconazole 50 to 150 mg given for weeks or months results in over 90% clinical cure or improvement for cutaneous mycosis including tinea, pityriasis, cryptococcosis and candidiasis. Prolonged (6 to 12 months) fluconazole 150 mg once a week is needed to treat onychomycosis successfully. Higher oral doses (200 to 400 mg daily) for long periods are generally used to treat deep mycoses such as meningitis, ophthalmitis, pneumonia, hepatosplenic mycosis and endocarditis. Fluconazole is effective for treating the fungal peritonitis which can complicate continuous ambulatory peritoneal dialysis (CAPD). A regimen of 50 mg intraperitoneally or 100 mg orally was used in these patients with impaired renal function. The dosage schedules used to treat disseminated fungal infections due to systemic mycoses with different or multiple foci of infections vary widely, with doses of 50 to 400 mg given orally or intravenously for between 1 week and several months. The most recent clinical reports have investigated the use of prophylaxis with fluconazole 100 to 400 mg daily, in immunocompromised patients. Fluconazole is found in body fluids such as vaginal secretions, breast milk, saliva, sputum and cerebrospinal fluid at concentrations comparable with those determined in blood after single or multiple doses. There is an excellent linear plasma concentration-dose relationship, but the mycological and clinical responses do not appear to be well correlated with the dose. A total maximum daily dose of 1600 mg is recommended to avoid neurological toxicity. Data from pharmacokinetic studies conducted in patients, mainly those with AIDS, and using a 1-compartment model give very constant parameters similar to those obtained in healthy individuals. Bioavailability, measured in HIV-positive patients and those with AIDS, exceeded 93% for tablets, suspension and suppositories. The time to reach peak plasma concentrations (tmax) was 2.4 to 3.7 hours. The peak plasma drug concentration (Cmax) obtained after a 100 mg oral dose was 2 mg/L. Areas under the concentration-time curve (AUC) obtained in different studies all correlate well with the dose (r = 0.926). The AUC determined after 200 and 25 mg suppositories were similarly well correlated. Hypochlorhydria does not affect the absorption of fluconazole, neither does food intake, race (Japanese or Caucasian) or gastrointestinal resection. Binding to plasma protein is low (11.14%) and is increased to 23% in cancer patients. Fluconazole is rapidly distributed to the tissue, where it accumulates. Tissues fall into 1 of 4 groups of increasing drug concentration: blood, bone and brain have the lowest concentrations, and spleen has the highest. The volume of distribution (Vd) remains stable at 46.3 +/- 7.9L and is considered to be an 'invariant' parameter across species. Fluconazole is poorly metabolised and is mainly eliminated unchanged in the urine. The percentage of the dose recovered in the urine in 48 hours is close to 60%. Concentrations in the urine are high and the half-life (t1/2) is long (37.2 +/- 5.5h) in patients, mainly those with AIDS, which is not significantly different from the t1/2 (31.4 +/- 4.7 hours) in healthy individuals. (ABSTRACT TRUN
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PMID:Clinical pharmacokinetics of fluconazole in superficial and systemic mycoses. 925 Apr 23

To investigate the interaction of fluconazole and zidovudine in HIV-positive non-smoking male patients with AIDS categorized as CDC group IV we studied two groups, each consisting of 10 male, non-smoking, HIV-positive patients with CDC group IV disease, with the patients in the first group additionally suffering from candida esophagitis. In the first group, the pharmacokinetics of 500 mg oral zidovudine were determined both before and after 7 days of treatment with fluconazole 400 mg/d. In the second group, the pharmacokinetics of 200 mg oral fluconazole were determined before and after 14 days of treatment with zidovudine 4 x 250 mg/d. In order to determine the microsomal enzyme activity, the 6-beta-hydroxycortisol/17-hydroxycorticosteroid ratio and antipyrine pharmacokinetic parameters were determined. 6-beta-hydroxycortisol was quantitated by RIA. The 17-hydroxycorticosteroids were determined by a colorimetric method. Zidovudine (ZDV) and zidovudine glucuronide (GZDV), and the fluconazole and antipyrine plasma and urine concentrations were measured by HPLC. Administration of fluconazole resulted in a significant increase in the half-life of zidovudine and antipyrine (0.97 +/- 0.17 h prior to vs. 1.11 +/- 0. 14 h after fluconazole administration and 11.9 +/- 1.9 h prior to vs. 13.7 +/- 3.0 h after fluconazole, respectively) while the 6-beta-hydroxycortisol excretion decreased significantly (472.3 +/- 80.6 microg/24 h before and 340.6 +/- 82.1 microg/24 h after administration of fluconazole). No changes were found in the GZDV plasma kinetics and the ZDV and GZDV urinary excretion. Treatment with ZDV did not have any impact on the half-life of fluconazole. Administration of zidovudine did, however, result in a significant reduction in antipyrine half-life (11.7 +/- 2.0 h before vs. 9.9 +/- 2.3h after ZDV) and a significant increase in 6-beta-hydroxycortisol excretion (438,7 +/- 138.2 microg/24 h before and 684.6 +/- 157.3 microg/24 h after ZDV). Since the antipyrine clearance is altered after administration of ZDV, it is assumed that zidovudine induces cytochrome P450 enzymes. This effect, however, does not alter the pharmacokinetics of fluconazole. High doses of fluconazole can inhibit the plasma elimination of both antipyrine and zidovudine, but the extent of this inhibitory effect is so small that no clinically relevant accumulation is to be expected.
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PMID:Pharmacokinetic interaction of fluconazole and zidovudine in HIV-positive patients. 930 Sep 34

The authors describe a clinical case of AIDS presented by three opportunistic infections (esophageal candidiasis, tuberculosis and atypical mycobacteriosis) and a dermatological manifestation--acanthosis nigricans--not described in medical literature as accompanying those entities. The exclusion of most common etiologies of acanthosis nigricans and its regression following treatment for those infections suggests that with AIDS it behaves like a paraneoplastic syndrome. Screening for HIV antibodies should be the rule whenever this dermatological manifestation is present.
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PMID:[Will acanthosis nigricans be a new cutaneous manifestation of human immunodeficiency virus infection?]. 934 Oct 43

To assess time trends in incidence of AIDS illnesses in Australia, a retrospective cohort of people diagnosed with AIDS from January 1, 1983 to December 31, 1994 in three HIV medicine units in Sydney, Melbourne, and Perth was established. Data on initial and subsequent AIDS illnesses were available for 2580 AIDS cases, or 45% of Australian AIDS notifications over the study period. Males represented 97.2% of the cohort, and HIV exposure category was homosexual contact for 89.9%. Subcohorts were formed by interval of AIDS diagnosis: 1983 through 1987, 1988 through 1990, and 1991 through 1994, with estimation of cumulative risk for each AIDS illness by the Kaplan-Meier method. The cumulative risk declined for Pneumocystis carinii pneumonia (PCP) (p < 0.0001) and for Kaposi's sarcoma (KS) (p < 0.0001); PCP cumulative risk estimates 2 years following AIDS diagnosis were 70% for people diagnosed with AIDS in 1983 through 1987 and 48% in 1991 through 1994, and KS cumulative risk estimates 2 years following AIDS diagnosis were 44% in 1983 through 1987 and 32% in 1991 through 1994. In contrast, cumulative risk increased from 34% to 40% for cytomegalovirus (CMV) disease (p = 0.005), from 47% to 50% for Mycobacterium avium complex (MAC) (p < 0.0001), and from 26% to 33% for esophageal candidiasis (p < 0.0001). Corresponding to this changing spectrum of AIDS illness has been an increase in severity of immunodeficiency at AIDS, with median CD4 cell count declining from 54 cells/mm3 in 1983 through 1987 to 34/mm3 in 1991 through 1994 (p = 0.002).
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PMID:Trends in incidence of AIDS illnesses in Australia from 1983 to 1994: the Australian AIDS cohort. 937 23

Little is known about how widely HIV-related drugs are used outside controlled clinical trials. We therefore assessed factors associated with use of antiretroviral (ARV) therapy and primary prophylactic regimens to prevent HIV-associated opportunistic infections. Baseline data from a prospective study from May to August 1994, on 3122 consecutive HIV infected patients with a CD4 count <500 cells/microl, followed in 37 centers from 16 European countries, were analyzed. Two thousand and twenty patients (65%) were receiving at least 1 ARV drug at the time of the study. ARV therapy was more frequently used among patients from southern and central Europe as compared with patients from northern Europe, especially among patients with CD4 counts >200 cells/microl (73%, 57%, and 42%, respectively, p < 0.0001). Of patients on ARV therapy, 34% received open-label combination therapy. This proportion was higher in central Europe compared with other regions (27%, 50%, and 31% for southern, central, and northern Europe, respectively, p < 0.0001). Primary prophylaxis against Pneumocystis carinii pneumonia (PCP) was used by 85% of patients with a CD4 count <200 cells/microl, without marked regional differences. In patients without esophageal candidiasis or other invasive fungal infections, antifungal drugs were far less frequently used in patients from southern and central Europe compared with patients from northern Europe (10%, 10%, and 25%, respectively, p < 0.0001). Only 5% of patients with a CD4 count <100 cells/microl received rifabutine as primary prophylaxis against nontuberculous mycobacterioses. ARV and antifungal therapies are used differently in different parts of Europe, whereas primary PCP prophylaxis is uniformly administered to most at-risk patients. U.S. recommendations on the use of antimycobacterial prophylaxis have not been implemented in Europe.
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PMID:Regional differences in use of antiretroviral agents and primary prophylaxis in 3122 European HIV-infected patients. EuroSIDA Study Group. 939 May 66

Candida oesophagitis is a common concomitant disease in neutropenic cancer patients after chemotherapie as well as in HIV-patients. In order to characterize the features of oesophagitis in each population, we reviewed the medical history and pathology records of 23 patients (18 cancer-patients, 5 HIV-patients) with culture and autopsy-proven Candida oesophagitis. Histopathological patterns of morphology, invasion, angioinvasion and inflammation were evaluated. Virtually all patients, 17/18 cancer- and 5/5 HIV-patients, had a history of previous mucosal candidosis or candidemia. There was a significant difference histopathologically in depth of invasion of the Candida-organisms between cancer and HIV-patients. Only in HIV-patients organisms were observed within the muscularis propria and the adventitia (2/5 vs 0/18; p = 0.04). The frequency of angioinvasion (12/18 vs 3/5) was similar in both groups. Neutropenia (< 500/microliter) was present in 12 (68%) of 18 cancer patients vs 0/5 HIV-patients (p = 0.01). Correspondingly there was a significant higher PMN/MN ratio in the oesophageal inflammatory infiltrate in HIV-patients, reflecting chemotherapy-induced neutropenia in cancer patients (p = 0.02). Oesophageal candidosis in HIV-patients may be highly invasive despite the presence of neutrophils. These findings suggest an impaired inflammatory response of HIV-patients to invasive candidosis, leading to impaired mucosal host defence.
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PMID:[Patterns of Candida esophagitis in cancer and AIDS patients: histopathological study of 23 patients]. 941 19

The prevalence of human immunodeficiency virus (HIV) infection among Central Americans is increasing. The purpose of this study was to describe the epidemiology of HIV infection among local Central American immigrants in the United States. Medical records of HIV-infected Central Americans treated at Harris County Hospital District (HCHD) facilities, the major source of indigent care in Houston, Texas, were retrospectively reviewed. Between January 1, 1990 and February 28, 1995, 18,156 Central Americans were seen at HCHD facilities, of whom 56 (13 females and 43 males) were identified as HIV-infected (0.3% versus 1.3% of all locally treated patients; P < 0.001, by test of binomial proportions). Most were from Honduras (n = 25) or El Salvador (n = 23). The mean age was 28.7 years, the mean CD4+ lymphocyte count at presentation was 173 cells/mm3, and 36 (64%) had acquired immunodeficiency syndrome (AIDS) at presentation. The 13 women (23% versus 22% for all locally treated HIV patients) were disproportionately Honduran (10 of 25 Hondurans versus 3 of 31 other Central Americans; P = 0.011). The HIV risk factors included heterosexuality in 46%, homosexuality in 29%. and a history of injection drug use in 7% (versus 10%, 57%, and 34%, respectively, for all locally treated HIV patients). The 76 diagnosed opportunistic infections (OIs) included a disproportionately greater number of patients with tuberculosis (n = 14, 33% versus 6% of all locally treated AIDS patients), toxoplasmosis (n = 10, 24% versus 7%), and cryptococcal meningitis (n = 9, 21% versus 7%), and a lower number of patients with pneumocystosis (n = 12, 29% versus 43%) and candida esophagitis (n = 2, 5% versus 16%). Central American immigrants infected with HIV present with relatively advanced disease, and the most frequent OIs are diseases for which effective prophylaxis exists. Targeted HIV screening and early intervention in this group are warranted.
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PMID:Epidemiology of human immunodeficiency virus infection in Central Americans treated in Harris County, Texas Hospital District facilities. 943 May 26

Azole-resistant oropharyngeal and oesophageal candidiasis is a recent phenomenon observed in patients with AIDS usually previously treated with fluconazole. Some variation has been observed in antifungal susceptibility testing among separate colonies of Candida albicans from the same patient. This raises the question of whether there are multiple clones present or simply phenotypic variation in expression of azole resistance. To address this question we took 18 isolates grown from multiple swabs taken before and after experimental azole therapy from a single HIV-positive individual with fluconazole-resistant oral candidiasis and compared morphotype, karyotype, PCR-based DNA typing and azole susceptibility. Ten of the isolates were from a single 2-day period. Amongst these 10 there were seven morphotypes, five karyotypes and four polymerase chain reaction (PCR) types. Three further morphotypes, one karyotype and two PCR types were found amongst the eight isolates obtained during the subsequent 4 months. Limited variation in susceptibility to two azoles--fluconazole and D0870--was also seen. This work emphasizes both the large genotype and phenotypic variability of C. albicans isolates in the mouth of AIDS patients with fluconazole resistance, and the difficulties in interpretation of present typing methods.
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PMID:Variation in morphotype, karyotype and DNA type of fluconazole resistant Candida albicans from an AIDS patient. 951 70

Mucocutaneous candidiasis, such as oropharyngeal candidiasis, esophageal candidiasis, and vulvovaginal candidiasis, are common problems in patients with HIV infection. These conditions adversely affect patient quality of life and morbidity status. New oral triazole agents provide improved treatment options for patients with these and other opportunistic fungal infections; however, the development of resistance in some Candida species poses new challenges. This article provides an overview of the diagnosis of mucocutaneous candidiasis, current treatment modalities, concomitant drug interactions, common adverse drug reactions, and the emergence of fungal resistance, and it suggests nursing interventions to maximize patient benefits from antifungal therapy.
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PMID:Triazole therapy for mucocutaneous candidiasis in HIV-infected patients. 974 79


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