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

A 25 year old, human immunodeficiency virus (HIV) seropositive, severe haemophilic patient was treated for suspected Pneumocystis carinii infection with high dose intravenous cotrimoxazole and subsequently with prednisolone. When he improved he was discharged on oral treatment only to return two days later, extremely unwell, with headaches, fever, sweats, tachycardia and hypotension. A lumbar puncture showed modest neutrophil pleocytosis but despite empirical antibiotic treatment with intravenous benzylpenicillin and cefuroxime he continued to deteriorate. Culture of cerebrospinal fluid subsequently grew Enterococcus faecalis that was resistant to trimethoprim and sensitive to ampicillin, rifampicin, and vancomycin. After a change in treatment to intravenous ampicillin and rifampicin he dramatically improved. Enterococcal meningitis is rare in adults but important to recognise and treat appropriately in view of its high mortality and relative resistance to antibiotics. In our case the combination of HIV infection and previous treatment with antibiotics or steroids, or both, were probable predisposing factors.
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PMID:Enterococcal meningitis in an HIV positive haemophilic patient. 190 98

Eleven subjects who presented with a clinical illness characteristic of primary HIV-1 infection were treated with 1 g zidovudine daily for a median period of 56 days (range, 28-111 days). Primary HIV-1 infection was confirmed in each subject by seroconversion and virus isolation. The acute phase of the illness resolved a median of 4 days (range, 3-14 days) from commencement of zidovudine. Six subjects reported symptoms that may have been side-effects of zidovudine, the most common being nausea in four subjects and headache in two. Treatment was discontinued in one subject who had persistent headache and nausea. Haemoglobin, haematocrit and erythrocyte counts decreased and mean corpuscular volume increased significantly during the treatment. None of the subjects developed anaemia and none required dose modification or blood transfusion as a result of haematological side-effects. There were no significant differences in the granulocyte count or the lymphocyte count during any week of treatment when compared with baseline levels. There were no significant differences in T-cell subset numbers of the subjects during treatment compared with a group of historical controls. HIV-1 was isolated from several subjects during and after termination of zidovudine treatment. The results of this investigation indicate that zidovudine is a safe drug to administer to people with primary HIV-1 infection. There was no clear evidence, however, of any clinical benefit in terms of resolution of the acute illness and no indication that the treatment would prevent development of persistent infection.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Zidovudine in the management of primary HIV-1 infection. 190 59

To define the causes, clinical significance and characteristics of headaches in HIV-1-related disorders, we studied 49 consecutive HIV-1 infected patients who presented with headache. Work-up included CT scans, cerebrospinal fluid examinations (in the absence of a contraindication) and serologic studies. Overall, 40 of 49 patients (82 percent) had an identifiable serious cause of headache. Cryptococcal meningitis (39 percent) and CNS toxoplasmosis (16 percent) were the leading headache etiologies. Serious causes were more likely in patients diagnosed with AIDS prior to presentation but also occurred in most patients in early stages of infection. Based on this study, we suggest that patients with HIV-1 infection must be managed with a high index of suspicion when they present with new onset headaches.
Headache 1991 Sep
PMID:Headache in HIV-1-related disorders. 196 55

A 66-year-old French homosexual man and a 42-year-old Brazilian man with no known risk factors for HIV infection developed headaches, asthenia, and neurologic episodes of abrupt onset. CT showed multiple hypodense, nonenhancing lesions. Serology for HIV was positive. They died respectively 2 months and 1 month after onset of the illnesses. Autopsy in both cases showed multiple, well-demarcated, demyelinating foci in the white matter of the cerebral hemispheres, brainstem, and cerebellum with histologic features characteristic of recent plaques of multiple sclerosis. There were no multinucleated giant cells or microglial nodules. Immunostaining for HIV was negative. Although a random coincidence of MS and HIV infection cannot be ruled out, the close temporal relationship between the 2 disorders suggests a possible etiologic association.
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PMID:Fulminating multiple sclerosis-like leukoencephalopathy revealing human immunodeficiency virus infection. 206 57

We compared cranial CTs of 35 habitual cocaine abusers, 16 self-reported 1st-time users, and 54 headache patients using linear planimetric measures. All patients met the following criteria: age 20 to 40 years, no polydrug abuse (including alcohol), HIV seronegativity, normal albumin level, and no history of any other neurologic disease. The sex ratios and ages were not significantly different in the 3 groups. The planimetric measurements and calculated indices of cerebral atrophy were significantly different in the habitual cocaine abusers compared with the 2 other groups of patients. There were no differences between 1st-time cocaine users and controls. Among the habitual cocaine abusers there was a positive correlation between the approximate duration of cocaine abuse and the calculated atrophy indices. The findings suggest that cerebral atrophy develops in chronic cocaine abusers, and the severity correlates with the duration of abuse.
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PMID:Cerebral atrophy in habitual cocaine abusers: a planimetric CT study. 174 38

Hallmarks of central nervous system (CNS) disease in AIDS patients are headaches, fever, subtle cognitive changes, abnormal reflexes, and ataxia. Dementia and severe sensory and motor dysfunction characterize more severe disease. Autoimmune-like peripheral neuropathies, cerebrovascular disease, and brain tumors are also observed. Histological changes include inflammation, astrocytosis, microglial nodule formation, and diffuse de- or dysmyelination. Focal demyelination can also be seen. It is clear that AIDS-associated neurological diseases are correlated with greater levels of HIV-1 antigen or genome in tissues. In AIDS dementia, macrophages and microglial cells of the CNS are the predominant cell types infected and producing HIV-1. However, manifestations of the disease make it unlikely that direct infection by HIV-1 is responsible. It seems more likely that the effects are mediated through secretion of viral proteins or viral induction of cytokines that bind to glial cells and neurons. HIV-1 induction of such cytokines as interleukin 1 (IL 1) and tumor necrosis factor-alpha (TNF alpha) may lead to an autocrine feedback loop involving further productive virus replication and induction of other cytokines such as interleukin 6 (IL 6) and granulocyte-macrophage colony-stimulating factor (GMCSF). Interleukin 1 and TNF alpha in combination with IL 6 and GMCSF could account for many clinical and histopathological findings in AIDS nervous system diseases. As HIV-1 infected patients produce elevated levels of IL 1, TNF alpha, and IL 6, it will be important to make a formal connection between the presence of these factors in the CNS, which are all products of activated macrophages, astroglia, and microglia, their in vivo induction directly by virus or indirectly by virus-induced intermediates, and the clinical and pathological conditions seen in the nervous system in this disease.
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PMID:HIV-1, macrophages, glial cells, and cytokines in AIDS nervous system disease. 206 87

Zidovudine (ZDV) is the only approved antiviral for the treatment of human immunodeficiency virus infection (HIV) in the U.S. Although newer antivirals have reached Phase II testing, ZDV is now the accepted therapy against which all other agents will be compared. Zidovudine 1500 mg/d was previously prescribed only to adult HIV-infected patients who had developed AIDS or AIDS-related complex (ARC). However, results obtained from recently completed studies indicate that a lower daily dose (500 mg) appears to be equivalent. In addition, ZDV therapy appears to be beneficial to asymptomatic HIV-infected patients with CD4+ counts less than 500/mm3. The toxicity profile of ZDV, previously obtained from patients receiving 1500 mg/d, consisted of either acute (e.g., fever, rash, headache) or chronic (e.g., anemia, neutropenia, myopathy) adverse effects. ZDV pharmacokinetics are variable within and between the different subpopulations of HIV-infected patients who have been studied. Bioavailability ranges from 50 to 70 percent, and values for half-life, total body clearance, and volume of distribution are 1-2 h, 20-40 mL/min/kg, and 1-2 L/kg, respectively. Drug interactions occur primarily between ZDV and other agents that undergo hepatic glucuronidation (e.g., probenecid, sulfamethoxazole) resulting in decreased ZDV clearance. ZDV is currently measured by HPLC, radioimmunoassay and FPIA; however, the role of therapeutic monitoring is currently under investigation. Studies of ZDV therapy in neonates, pediatric patients, patients with resistant isolates of HIV, and HIV-infected patients receiving combined treatment with other reverse transcriptase inhibitors or immunomodulators are ongoing.
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PMID:Zidovudine update: 1990. 219 18

Because the acquired immunodeficiency syndrome (AIDS) virus is neurotropic, physicians will continue to see a rise in the number of neurologic complications of this syndrome. Much of this increase will be accompanied by headache, not only as a primary symptom of HIV infection or opportunistic disease but also as a result of diagnostic tests and therapeutic efforts. Complete understanding of the ramifications of headache in AIDS will be important in the 1990s as we continue to treat a younger population, usually affected by benign vascular and muscle contraction-type headache.
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PMID:Headache and acquired immunodeficiency syndrome. 225 21

We report cerebral vasculitis in 2 cocaine users who developed symptoms (transient blindness and persistent headache) while smoking "crack," followed by progressive widespread cerebral dysfunction with focal signs over the next few weeks. One patient had smoked crack exclusively, and the other also used cocaine intravenously. Sedimentation rates were elevated and HIV titers negative. Arteriography was normal in 1 patient and in the other showed multiple large-vessel occlusions without beading. Brain biopsy showed vasculitis involving small vessels in both patients. Multinucleated cells were present in the neuropil, but there were no granulomas or evidence of infection. One patient improved significantly with corticosteroid treatment, and made a good recovery. The other died despite corticosteroid and cyclophosphamide treatment.
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PMID:Biopsy-proven cerebral vasculitis associated with cocaine abuse. 235 10

In desperation, we have used retrovir in five hemophilic children (10-16 years old) over the past 22 months. All had presented with various clinical manifestations of acquired-immune-deficiency-syndrome (AIDS)-related complex or AIDS. Our decision to treat with retrovir was based on clinical manifestations and very low numbers of CD4 cells (less than 200). The most common clinical presentation was recurrent oral moniliasis. Other significant findings included recurrent herpes zoster, thrombocytopenia, growth failure, and biliary tract infection. Initially, all five children received the full adult dosage of retrovir (200 mg q 4 h x 6 doses/day). This dosage had to be reduced in four children because of toxicity. The most commonly observed toxic side effects were anemia and neutropenia. Alanine aminotransferase (ALT) levels rose to 4-10 times the upper limit of normal in four of five children. One was on concomitant ketokonazole prior to the rise in ALT level. Myalgia and headache were reported by two patients. Improvement in clinical and immunological status was observed in all children initially. After 12-18 months of retrovir therapy, infectious complications secondary to prolonged neutropenia were seen in these immunocompromized children. However, compared to historic controls, these children have had fairly stable disease. We feel that all hemophilic children with symptomatic human immunodeficiency virus infection should be offered this drug, even though the optimal dosage for children is not yet established.
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PMID:Retrovir therapy in hemophilic children with symptomatic human immunodeficiency virus infection: efficacy and toxicity. 237 12


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