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

Human immunodeficiency virus (HIV) infection has radically changed African orthopaedic practice within a decade. In Lusaka, a third of adults are infected, but most have no physical signs of the disease. Early experience showed that closed fractures healed normally, the risk of sepsis during osteosynthesis was increased and most open fractures became septic. Major orthopaedic surgery in HIV-positive patients has increased risks of sepsis which rise steeply in those with physical signs of HIV disease. Musculoskeletal infections such as tropical pyomyositis, adult haematogenous long-bone osteomyelitis, and late haematogenous infection of implants, appear as immune competence wanes. There is a dual epidemic of tuberculosis and HIV, and bone and joint tuberculosis is now common. Atypical features suggest that traditional diagnostic criteria for spinal tuberculosis may be inadequate. Rheumatoid diseases, especially reactive arthritis, are common and serious complications of HIV disease. The risk of transmission of HIV between patient and surgeon is small, especially if recommended precautions are universally applied.
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PMID:Orthopaedic surgery and HIV disease in Africa. 887 50

A 42-year-old, African-American man presented with a 2-month history of weight loss and fever for 2 weeks. Presumptive diagnoses of human immunodeficiency virus infection (HIV) and acquired immunodeficiency syndrome were made on the basis of a CD4 lymphocyte count of 23 lymphocytes/mL. Chest x-ray revealed right paratracheal adenopathy and a miliary pattern. The etiology of the patient's pulmonary infection was not known, but tuberculosis was an important consideration. Over 5 days, the pulmonary infection progressed and was complicated by acute respiratory distress syndrome (ARDS), septic shock, and death, despite vigorous antibiotic and supportive therapy. Serologic tests for HIV infection were reported as positive after the patient's demise. The etiology of the patient's pulmonary infection, ARDS, and sepsis was not known until autopsy study revealed enumerable yeast-like cells of Blastomyces dermatitidis in the extensively consolidated lungs and in disseminated foci of infection in most other major organs. Diffuse alveolar damage was closely associated with the pulmonary blastomycosis. Electron microscopic study of the yeast-like cells of B. dermatitidis in the autopsy lung obtained and fixed 5 days after the patient's death revealed excellent preservation of viable organisms.
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PMID:Disseminated blastomycosis and acquired immunodeficiency syndrome: a case report and ultrastructural study. 888 26

Thrombotic microangiopathy (TMA) is more common in HIV-infected individuals than in the normal population. In idiopathic TMA, plasmapheresis with or without prednisone decreases the mortality rate from almost 100 to 10%. Patients with HIV-associated TMA, who do not have AIDS, have a similar favorable outcome when treated with plasmapheresis. However, all 12 patients previously reported with AIDS-associated TMA have died. We report another patient with AIDS-associated TMA, who had a fulminant hospital course and died despite plasmapheresis. None of the reported AIDS-associated TMA patients had evidence of opportunistic infections, sepsis or disseminated malignancies at the time of their death. Since many infections and malignancies can be associated with TMA, it is possible that TMA can be an association of the terminal illness rather than an independent cause of death in AIDS patients. To examine this possibility, we reviewed the charts of all the patients who were hospitalized and died of AIDS at our medical centers from 1987 to 1994. Of the 214 patients reviewed, 15 patients (7%) had evidence of TMA at the time of their death. Seven of the 15 patients (47%) had no direct cause of death other than TMA. The remaining 8 patients had evidence of sepsis and other overwhelming infections. In conclusion, TMA is common in AIDS patients. While HIV-associated TMA has a good prognosis similar to that of idiopathic TMA, AIDS-associated TMA has a grave prognosis. The etiology of the higher mortality in AIDS-associated TMA as compared to HIV-associated TMA remains unclear.
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PMID:Disparate prognosis of thrombotic microangiopathy in HIV-infected patients with and without AIDS. 962 48

Human immunodeficiency virus (HIV) infection and infective endocarditis are serious complications of injection drug use. To determine whether HIV infection may increase the risk of endocarditis beyond that associated with drug injection, we performed a nested case-control study among injecting drug users taking part in an ongoing cohort. We identified 26 participants with infective endocarditis between cohort enrollment (in 1988-1989) and June 1992, through reviews of medical records and death certificates. We matched each endocarditis case with up to five controls (N = 120) on enrollment date, race/ethnicity, and follow-up time. Data were taken from baseline and from the one follow-up visit: the last visit before the endocarditis occurred for cases and the closest visit (+/- 3 months) for controls. We used conditional logistic regression to quantify the association between HIV serostatus at follow-up and subsequent endocarditis, after adjusting for a history of endocarditis or sepsis before enrollment, injection duration, current injection frequency, and a recent history of abscess at injection sites. Among current injectors at follow-up, the adjusted odds ratio (OR) of developing endocarditis for HIV-seropositive subjects with > or = 350 CD4 cells per microliter, compared with HIV-seronegative subjects, was 2.31 [95% confidence interval (CI) = 0.61-8.78]; the corresponding OR for HIV-seropositive subjects with < 350 CD4 cells per microliter was 8.31 (95% CI = 1.23-56.37). These data indicate that HIV-related immunodeficiency may independently increase the risk of infective endocarditis among injecting drug users.
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PMID:Human immunodeficiency virus infection and infective endocarditis among injecting drug users. 889 79

The pathophysiology of systemic inflammation and sepsis involves peripheral organs, causing gastrointestinal, renal, and cardiovascular alterations, as well as the central nervous system (CNS), affecting sleep, temperature regulation, behavior, and neuroendocrine function. The molecular basis of the CNS effects of systemic inflammation are not fully elucidated. Here we show that the CNS responds to systemic inflammation with pronounced IL-1beta gene expression and limited IL-1 receptor antagonist (IL-1ra), IL-10, and IL-13 gene expression. This pattern occurs throughout the CNS, including areas such as the subfornical organ, pineal gland, neurohypophysis, and hypothalamus. In contrast, in the anterior pituitary, we found limited IL-1beta gene expression but marked induction of the mRNA encoding for the secreted isoform of IL-1ra, secreted IL-1ra. We conclude that the central manifestations of peripheral inflammation are mediated by endogenous brain IL-1beta synthesized during systemic inflammation in the context of limited central cytokine counter regulation of IL-1. As IL-1beta is a potent stimulus for inducible nitric oxide synthase expression and activity, these findings explain our previous observation that systemic inflammation promotes inducible nitric oxide synthase gene expression in the brain and the spillover of NO metabolites into cerebrospinal fluid. The CNS transcription of the HIV-1 replication factor IL-1beta in the context of limited transcription of the IL-1 replication inhibitors IL-1ra, IL-10, and IL-13 might help explain the negative impact of systemic inflammation on the clinical course of AIDS. In addition, we propose that IL-1ra may be secreted by the anterior pituitary as a systemic anti-inflammatory hormone that is released in response to IL-1beta originated from multiple sources.
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PMID:Interleukin (IL) 1beta, IL-1 receptor antagonist, IL-10, and IL-13 gene expression in the central nervous system and anterior pituitary during systemic inflammation: pathophysiological implications. 899 Jan 90

To examine intensive care unit (ICU) admission rates and diagnoses of patients with HIV infection, and to determine the outcomes of different critical illnesses, we analyzed data derived from the 63 patients who were admitted to an ICU from among the 1,130 adults with HIV infection who did not have AIDS at the time of enrollment in a multicenter prospective study. Patients were admitted and treated according to the judgment of their physicians. During 4,298 patient-years of follow-up for the entire cohort, there were 1,320 hospital admissions, of which 68 (5%) included admission to an ICU. Twenty-five (40%) of the patients admitted to the ICU died during that admission. Twenty-four patients (38%) were admitted with a principal diagnosis of lung disease; 11 had Pneumocystis carinii pneumonia (PCP), one of whom was coinfected with Aspergillus fumigatus and Legionella pneumophilia, and six of them (55%) died. Four had bacterial pneumonia, two had pulmonary edema caused by renal failure, and one each had pulmonary tuberculosis, pulmonary Kaposi's sarcoma, pneumothorax, adult respiratory distress syndrome, severe pulmonary fibrosis, cytomegalovirus pneumonitis, and metastatic adenocarcinoma to the lungs. Eleven of these 14 patients (79%) died. Thirty-nine patients had 44 admissions for nonpulmonary diagnoses, including gastrointestinal disorders (14 admissions), cardiovascular disorders (nine), sepsis syndrome (six), neurologic disorders (four), monitoring and ICU nursing care during or after a procedure (four), metabolic disorders (three), trauma (two), drug overdose (one), and unknown reasons (one). Nine (23%) of these patients died. Twenty-eight patients underwent mechanical ventilation, and 16 (57%) died. Seven (25%) had PCP (five died), seven had other primary pulmonary diseases (six died), and 14 were placed on mechanical ventilation for nonpulmonary disorders (five died). Survival did not correlate with CD4 count determined within 6 mo of admission to the ICU. In conclusion, the range of indications for critical care in patients with HIV infection is diverse. PCP accounted for only 16% of the ICU admissions, and mechanical ventilation for PCP and other pulmonary disorders was associated with a high mortality rate. In contrast, mechanical ventilation for nonpulmonary disorders, and admission to the ICU for nonpulmonary diagnoses was associated with a more favorable outcome.
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PMID:Intensive care of patients with HIV infection: utilization, critical illnesses, and outcomes. Pulmonary Complications of HIV Infection Study Group. 900 Dec 91

HIV-infected patients may present with a variety of patterns of renal involvement. Acute renal failure is common and most often a result of sepsis, hypotension, and nephrotoxic agents. It is potentially avoidable, and support through the period of renal failure may lead to resolution of the renal dysfunction. HIV-associated nephropathy is a unique pattern of sclerosing glomerulopathy that ranges in prevalence from 1 to 10% of the HIV-infected population in different geographic locales. This complication of HIV infection will likely present a growing challenge to the medical community as HIV infection continues to spread worldwide. Deciphering the pathogenetic mechanisms of this most rapidly progressive form of focal segmental sclerosis is not only clinically relevant, but will hopefully provide valuable insights into the mediation of the more common idiopathic form of the disease. The potential for improved renal survival of patients with HIV-associated nephropathy has become more realistic with the development and use of antiretroviral agents, as well as studies on the role of immunosuppression and ACE inhibition in this population. An awareness of other glomerular lesion and tubulointerstitial lesions has broadened our understanding of populations with renal disease who have been infected by HIV. Moreover, as prolonged survival of HIV-infected individuals is being achieved with modern antiviral therapy, the percentage of patients surviving with nephropathy will likely grow in coming years. Awareness of the growth of this population and those requiring short- and long-term hemodialysis and peritoneal dialysis will allow appropriate planning for ESRD in the HIV-infected population.
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PMID:HIV infection and the kidney. 901 59

Leukocyte recruitment from the circulation into inflammatory tissues requires a series of soluble and cell-bound signals between the responding leukocyte and vascular endothelial barrier. Chemotactic factors are believed to be responsible for this selective adhesion and transmigration. A superfamily of small, soluble, structurally-related molecules called 'chemokines' have been identified and shown to selectively promote the rapid adhesion and chemotaxis of a variety of leukocyte subtypes both in vivo and in vitro. Chemokines are produced by almost every cell type in the body in response to a number of inflammatory signals, in particular those which activate leukocyte-endothelial cell interactions. These molecules also appear to play important roles in hematopoesis, cellular activation, and leukocyte effector functions. In addition, chemokines have been found in the tissues of a variety of disease states characterized by distinct leukocytic infiltrates, including rheumatoid arthritis, sepsis, atherosclerosis, asthma, psoriasis, ischemia/reperfusion injury, HIV replication, and a variety of pulmonary disease states. This review will primarily focus on the role of chemokines in cell adhesion and trafficking as well as their role as effector molecules.
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PMID:Chemokine-leukocyte interactions. The voodoo that they do so well. 902 58

Leucopenia and neutropenia in HIV appears to be much less common than in the context of haematological malignancies although severe neutropenia (< 0.75 x 10(9)/l) occurs in as many as 70% of patients with AIDS often related to concomitant drug therapy. In addition to low numbers of neutrophils there is also some evidence of defective neutrophil function in HIV/AIDS (chemotaxis, bacterial killing, phagocytosis and superoxide production). However the frequency and importance of these defects is as yet not known because simple and reproducible tests of neutrophil function are not yet available to the majority of clinicians. Despite the relative scarcity of severe neutropenia in early HIV, bacterial sepsis is a major clinical problem which usually manifests itself as either pneumonia, bacteraemia or both at a frequency of between 8-20 per 100 person years depending upon location, risk activity etc. Amongst drug users, the inhalation of recreational drugs particularly after Pneumocystis carinii pneumonia (PCP) has been shown to be a major risk factor for pneumonia. The incidence of bacterial sepsis in patients with AIDS is more difficult to determine since it is often overshadowed by other more dramatic opportunistic infections. However, throughout the course of AIDS, bacterial infections are a common problem particularly in the presence of one or both of concomitant drug therapy and indwelling intravenous lines utilized in late stage disease. Consequently, since bacterial infections are common and cause considerable morbidity and mortality they should be considered in the differential diagnosis of most presentations.
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PMID:Bacterial infections in HIV: the extent and nature of the problem. 904 75

Distinct cytokine profiles are clearly associated with and relate to the severity of several types of infections. Cytokine networks are apparent with selected human infectious diseases, such as mycobacterial infections (leprosy, tuberculosis), the parasitic infection leishmaniasis, human immunodeficiency virus (HIV) infection, and gram-negative sepsis. Cytokine profiles are determined to some extent by two functional subsets of T lymphocytes, Th1 and Th2. The Th1 cytokines (interferon gamma, interleukin-2 [IL-2], IL-12) enhance cell-mediated immunity, inhibit humoral immunity, and result in protective effect for pathogens that are removed primarily through cell-mediated immunity (Mycobacterium tuberculosis, Mycobacterium leprae, Leishmania). The Th2 cytokines (IL-4, IL-5, IL-10, IL-13) enhance humoral immunity and inhibit cell-mediated immunity, and result in protective effect for pathogens removed primarily through humoral mechanisms. Progression of HIV infection is associated with a switch from a Th1 to a Th2 profile. For sepsis, uncontrolled activation of proinflammatory cytokines (IL-1, tumor necrosis factor-alpha, interferon-gamma) may be a fundamental defect that promotes the detrimental aspects of inflammation, whereas Th2 cytokines may be beneficial in controlling inflammation. Knowledge of basic cytokine immunopharmacology, networks, and relationships with infectious processes will aid clinicians in determining treatment approaches that are likely to be effective.
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PMID:Cytokine networks with infection: mycobacterial infections, leishmaniasis, human immunodeficiency virus infection, and sepsis. 908 11


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