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

Three drugs are currently available to treat HIV infection: zidovudine, didanosine, and zalcitabine. They resemble the natural nucleosides and inhibit retrotranscriptase, an enzyme which transforms HIV's genomic RNA into DNA. Indications for treatment are symptomatic HIV infection and, in asymptomatic patients, moderate immunodeficiency with a CD4-lymphocyte count below 350/mm3. In patients who have not yet received antiviral treatment, zidovudine remains the drug of choice, in spite of its toxicity for the bone marrow, which is particularly problematic in those with advanced immunodeficiency. Unfortunately, HIV develops resistance to zidovudine, and its efficacy wanes after a few months. When that happens, zidovudine may be replaced by didanosine, which is mainly toxic for the pancreas, or by zalcitabine, which causes peripheral neuropathy. A number of drugs are being developed. Among these, nonnucleoside retrotranscriptase inhibitors are well tolerated, but rapid development of resistance is problematic. Resistance seems less of a problem for inhibitors of the viral protease, but biodispensibility of these drugs is poor.
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PMID:[HIV infection--current possibilities in antiviral therapy]. 794 Apr 11

(1) We evaluated efficacy of several treatments for HTLV-I-associated myelopathy (HAM) on the basis of our study on 254 HAM patients and of literature review. Improvement of motor disability more than fair response was obtained as follows: 82% in prednisolone, 69% in interferon-alpha, 92% in fosfomycin, 82% in high-dose vitamin C, 72% in blood purification therapy, 70% in heparin, 59% in salazosulfapyridine, 56% in thyrotropin-releasing hormone, 55% in erythromycin, 50% in mizoribine. (2) In the absence of clear guideline, the efficacy of zidovudine in the AIDS dementia complex has been demonstrated. There are also efficacy of amytriptylinein controlling HIV headache, corticosteroid in mononeuritis multiple and inflammatory myositis, hydrocortisone in autonomic neuropathy and plasmapheresis in distal sensory neuropathy respectively. Otherwise, it is emphasized that ddI, ddC and d4T have peripheral neuropathy as major, dose related side effect.
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PMID:[Therapy for HAM/TSP and AIDS]. 799 4

In order to assess the central motor pathways of HIV-infected patients motor evoked potentials were recorded on the upper limbs after transcranial and cervical magnetic stimulations and compared with peripheral conduction velocities. Motor evoked potentials were measured on both sides of 28 patients, mostly at the AIDS stage. Our results showed that although peripheral neuropathy was often found, central motor pathways did not appear, at the level they were tested, to be directly or indirectly damaged by the virus. On the contrary, some hyperexcitability seemed to be present.
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PMID:[Central and peripheral nervous system motor conduction rate in HIV infection]. 824 55

To evaluate whether P300 testing might serve as a screening modality for the early detection of HIV-related neuropathology, we tested 26 HIV-infected men (23 without neurologic symptoms, 2 with peripheral neuropathy, 1 with AIDS-associated dementia) and 15 controls. Although they had no overt neurologic symptoms, the P300 latency was delayed or undetectable in 30% of patients without clinically evident neurologic disease. P300 latencies did not correlate with peripheral blood CD4 T-cell count, serum quinolinic acid or p24 antigen levels, or the numbers of activated peripheral blood monocytes. Three individuals with abnormal P300 latencies had been HIV-seropositive for < or = 1 year, suggesting that delayed evoked responses detect early neurologic dysfunction. P300 responses do not predict imminent dementia. In only one previously asymptomatic individual with abnormal P300 waveforms have overt neurologic symptoms developed during a 2-year followup. Extended longitudinal studies will be necessary to define the predictive value of P300 latencies in the development of AIDS-related dementia. However, the sensitivity, quantitative nature, and speed of administration of this test suggest that it may be useful for identification of early neurologic involvement in HIV infection.
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PMID:Auditory P300 abnormalities and leukocyte activation in HIV infection. 829 Mar 2

The physician caring for HIV-1-infected patients must have a good working knowledge of the broad spectrum of neurologic diseases that occur in association with this infection. As with any other neurologic disorder, the site of the neuraxis that is affected must be properly identified. In HIV-1-infected persons, more than one site may be involved simultaneously, such as the coexistence of myelopathy and peripheral neuropathy, often resulting in a confusing array of neurologic signs and symptoms. The frequent occurrence of two or more diseases affecting the neuraxis, such as progressive multifocal leukoencephalopathy and toxoplasmosis, further complicates the picture. With the AIDS patient, the physician cannot rely on the clinical adage that all attempts should be made to ascribe the patient's problems to one disease. Often, it is not the case. As with other illnesses, the approach to the HIV-1-infected person with neurologic disease needs to be thorough and fluid. After rendering a diagnosis and embarking on therapy, the physician needs to be open minded about the possibility of an incorrect or additional diagnosis not previously considered. Lastly, despite all the knowledge that has been accumulated in the first decade of the AIDS epidemic, new illnesses occurring with HIV-1 infection are recognized with regularity. The physician must always bear in mind that the illness with which he or she is confronted may be one that has not been previously described.
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PMID:The neurologic complications of human immunodeficiency virus infection. 838 Apr 78

We administered the antiviral agent 2',3'-dideoxycytidine (ddC) to HIV-infected patients with either ARC or AIDS as part of the AIDS Clinical Treatment Group protocol 012 and serially evaluated them with neuropathic symptom questionnaires, neurologic examinations, nerve conduction studies, and quantitative sensory testing (QST). All patients treated with high-dose ddC (0.06 and 0.03 mg/kg every 4 hours) developed a painful, predominantly sensory peripheral neuropathy, with a mean onset of 7.7 weeks, which reached severe intensity over several days. Abnormalities of vibration QST threshold preceded clinical symptoms. Treatment with 0.01 mg/kg every 4 hours produced a similar neuropathy, although of milder severity, later onset (mean, 9.3 weeks), and slower progression. In these patients, the onset of clinical symptoms and QST abnormalities were coincident. Only two of six patients treated with 0.005 mg/kg every 4 hours developed clinical or laboratory evidence of neuropathy; in both cases it was very mild and delayed in onset (26 weeks). All patients treated with high-dose ddC reported progression of symptoms (coasting) for 2 to 3 weeks following discontinuation of therapy. This study documents a painful sensory neuropathy resulting from treatment with ddC. With high-dose treatment, only the rapidity of onset and progression differentiated it from the distal, predominantly sensory neuropathy of AIDS.
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PMID:2',3'-dideoxycytidine (ddC) toxic neuropathy: a study of 52 patients. 838 49

Fifty four patients with peripheral nerve syndromes were seen during a 15 month period in a population of about 1500 HIV infected patients at all stages of the disease. Distal symmetrical peripheral neuropathies were seen in 38 of the 54 patients, (11.5% of AIDS patients) and could be distinguished into two forms. The most common (n = 25) was a painful peripheral neuropathy during AIDS, which is distinct clinically and pathologically, having axonal atrophy, and is associated with cytomegalovirus infection at other sites. The 13 non-painful neuropathies seen were more heterogeneous. Lumbosacral polyradiculopathy associated with cytomegalovirus and lymphomatous mononeuritis multiplex occurred in fewer than 1% of AIDS patients. Mononeuropathies were seen in 3% of AIDS patients. No patients with acute or chronic inflammatory demyelinating polyradiculoneuropathies were seen. The annual incidence of neuropathies during the AIDS related complex stage was less than 1%; none were seen in asymptomatic HIV seropositive patients.
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PMID:Nature and incidence of peripheral nerve syndromes in HIV infection. 838 98

One hundred and fifty-one patients intolerant to zidovudine (AZT) received didanosine (ddI) to a maximum dose of 12.5 mg/kg/day. Patient response was assessed using changes in CD4+ lymphocyte subset count, HIV p24 antigen, weight, and quality of life. Seventy patients developed major opportunistic infections whilst on therapy; this was the first AIDS diagnosis in 17. Only minor changes in CD4+ lymphocyte subset count were observed in AIDS patients, although a more significant rise occurred in those with earlier stages of disease. Of those positive for p24 antigen at the commencement of the study 67% showed a positive response, and this was most likely in those with CD4+ lymphocyte subset counts above 100 mm3. A positive weight response was seen in 16% of patients. Most patients showed improvement in individual parameters and global score of quality of life. Adverse reactions possibly attributable to didanosine were common. The most common side-effect was diarrhoea, which resulted in cessation of therapy in 19 individuals. Peripheral neuropathy occurred in 12 patients and pancreatitis in six. Thirteen patients developed a raised serum amylase without abdominal pain. Seven patients developed glucose tolerance curves characteristic of diabetes but these were mild, did not require treatment and returned to normal on ceasing didanosine.
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PMID:The use and toxicity of didanosine (ddI) in HIV antibody-positive individuals intolerant to zidovudine (AZT) 832 44

Seventeen HIV-1-infected individuals were given AZT (100 mg tid) and ddC (0.375 mg tid) for consecutive periods of four weeks each and for total periods ranging from 8 to 32 weeks (median 17). Thirteen patients were offered AZT/ddC after having received other anti-retroviral combinations containing AZT, whereas in four it was used as front therapy. Before and after AZT/ddC, the median CD4 cell count changed from 184 to 164/uL (p NS), and the median body weight from 60 to 61 kg (p NS). Increases in hematological parameters were observed in patients previously exposed to AZT. In eight patients the side effects of AZT (gastrointestinal intolerance, cephalalgia and fever) disappeared when switched to ddC, whereas in one a reversible peripheral neuropathy ensued. The dosages of AZT/ddC used in this trial were well tolerated.
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PMID:[Sequential dideoxycytidine and zidovudine in advanced HIV-1 infection. Phase II study]. 839 11

Neurologic illness related to HIV-1 infection can involve the entire neuraxis and result in a wide range of neurologic syndromes. This article reviews intracerebral mass lesions, meningitis, myelopathy, peripheral neuropathy, and occupational exposure to HIV-1.
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PMID:Neurologic critical care in patients with human immunodeficiency virus 1 infection. 842 16


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