Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019693 (HIV)
 170,526 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

12 cases of peripheral facial nerve palsy in African patients attending the Centre National Hospitalier Universitaire de Bangui, Central African Republic, with HIV infections are described with clinical and serological findings. All sera were tested with ELISA and confirmed with Western blot for both HIV-1 and HIV-2 (ELAVIA 1, ELAVIA 2, LAV BLOT I, LAV BLOT II, Diagnostics Pasteur). All 12 were HIV-1 positive and HIV-2 negative. Clinically, 1 patient met the clinical definition of AIDS, 3 had AIDS-related complex, and 8 had been previously health. In 11 cases, facial nerve palsy was the 1st presenting syndrome of HIV infection. ONset was acute in all, and associated with flu-like symptoms in 7. The palsy resembled Bell's palsy in 9, but was associated with unilateral vesicular eruptions suggestive of Ramsay-Hunt syndrome, or varicella-zoster, in 2 cases. In 1 19-year old woman complete facial paralysis with peri-oral numbness and paresthesia of the cheek developed in 1 hour. All recovered in 2 weeks to 3 months. The T4 lymphocyte counts averaged 764 in the healthy patients and 373 in the ARC and AIDS patients, compared to 1949 in controls. T4/T8 ratios averaged 0.66 and 0.45 in these groups compared to 1.32 in controls. 4 other cases of facial palsy in persons testing negative for HIV are also described. Speculative explanations for the pathophysiology of these palsies were offered: local infection of the facial nerve or ganglion by HIV, inflammatory demyelinating neuropathy, or secondary infection, due to immunosuppression, by agents such as Herpes zoster.
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PMID:Peripheral facial nerve palsy related to HIV infection: relationship with the immunological status and the HIV staging in Central Africa. 168 26

Non-Hodgkin's lymphomas (NHL) presenting through oral symptoms are rare. Between 1976 and 1987, a total of 17 cases (7 male, 10 female) were diagnosed in our departments. The first symptom was an intraoral tumour mass in 9 cases, loosening of teeth in 2 cases and paraesthesia in another 2. Most tumours (13/17) were located in the lower jaw. In only 5 cases had the referring physician or dentist suspected malignancy. In 3 cases, the histological diagnosis was Burkitt's lymphoma. The grade of malignancy was classified as low in 4 cases, intermediate in 3 and high in 8. None of the patients was HIV-positive. Nine patients died of their disease within 1-132 months (mean 18.3 months).
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PMID:Non-Hodgkin's lymphomas presenting through oral symptoms. 211 52

A HIV-2 strain named HIV-2ben was isolated from peripheral blood lymphocytes of a patient who, since 1984, had developed neurological symptoms such as Raynaud's syndrome, followed by paresthesia of extremities and ataxia, and finally paraparesis of the legs and incontinence. This new isolate could be distinguished from HIV-2rod by antibody-binding epitopes, peptide maps of core p24 and p18 polypeptides and restriction endonuclease cleavage pattern.
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PMID:Isolation and characterization of HIV-2ben obtained from a patient with predominantly neurological defects. 211 42

Peripheral neuropathy following HIV infection is frequently seen among HIV-positive-, ARC- and AIDS patients who often complain of debilitating paresthesias. Indirect immunofluorescence technique showed antibodies directed either to myelin and/or axons and to endothelial cells of the blood vessels within the nerve tissue. Sural nerve biopsies from five patients showed demyelination, axonal degeneration and perivascular cellular infiltration. Two of the patients had nuclear inclusions and high anti-CMV titer. Plasma exchange was undertaken on five HIV infected patients which resulted in complete disappearance of symptoms in three, incomplete remission in one and no effect in one patient. The finding of autoantibodies against different nerve tissue components, cellular infiltration, positive effect of the plasma exchange and relapse suggests that autoimmunity may play a pathogenetic role in some of the HIV infected patients with peripheral neuropathy.
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PMID:[Plasmapheresis in the treatment of peripheral HIV neuropathy]. 255 Oct 89

The patient was a 49-year-old woman. Since her age of 42, she noticed a proximal weakness of both legs. She also experienced pedal paresthesia and urinary frequency. Physical examination disclosed a diffuse goiter and bilateral Babinski sign. Results of EMG and muscle pathology were compatible with the diagnosis of polymyositis. Treatment with prednisolone improved muscle weakness, urinary difficulties and struma. 7 years later, HTLV-I antibody happened to be strongly positive both in serum and CSF. Then most of her neurological problems were attributed to HAM. However, recent studies of re-biopsy muscle specimens disclosed scattered necrotic fibers, phagocytosis and endomysial or perivascular infiltration of inflammatory cells. These infiltrating cells were classed mostly as helper/inducer T cells. These observations suggested the coexistence of polymyositis in the present case as well. So far, the combination of HAM and polymyositis has not been reported. It seems important to decide if HTLV-I could induce chronic polymyositis as in the case of HIV infections.
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PMID:[HTLV-I associated myelopathy (HAM) complicated with chronic polymyositis]. 274 79

The most common type of peripheral neuropathy associated with human immunodeficiency virus (HIV) infection, predominantly sensory neuropathy, affects 10-30% of patients with acquired immunodeficiency syndrome (AIDS). From 40 individuals with peripheral neuropathy and HIV infection, we have identified 26 patients with this syndrome. All had constitutional symptoms when neuropathic symptoms developed; 20 had AIDS and six had AIDS-related complex. The most common complaint was pain on the soles. Paresthesias were frequent and usually involved the entire foot. Signs of peripheral neuropathy were present in all; the most frequent finding was absent or reduced ankle reflexes. Electrophysiologic studies revealed abnormal sensory and motor conduction, studies suggesting a dying-back axonopathy. Over time, the neuropathy progressed in all except one patient with ARC, who had spontaneous subjective improvement. Tricyclic antidepressants provided partial symptomatic relief. In three patients, the neuropathy did not change during azidothymidine treatment. Predominantly sensory neuropathy in HIV infection appears to be a distal axonal degeneration primarily involving sensory neurons. The mechanism is unknown, but the neuropathy is associated with the late manifestations of HIV infection.
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PMID:Predominantly sensory neuropathy in patients with AIDS and AIDS-related complex. 283 69

The purpose of this clinical study was to determine the effect of intralesional vinblastine administration on intraoral Kaposi's sarcoma (KS) in AIDS patients. One hundred and forty-four KS lesions in 50 HIV-positive homosexual males (mean CD4 count 64/mm3) were treated periodically with intralesional vinblastine injection (0.1 mg/cm2) until lesion resolution or no further reduction in lesional area. The most common lesion sites were: palate 56% (hard palate 42%, soft palate 14%); gingiva 22% (maxillary 15%, mandibular 7%); and maxillary tuberosity 6%. The mean lesion area was 4.6 cm2 (range = 0.1-35 cm2). Complete resolution occurred in 74%. The mean reduction in lesional area was 93% for all lesions. Lesions with only a partial response (26%) to vinblastine had a mean reduction in the lesional area of 69%. The mean number of treatments was 2.4 (range = 1-6). The recurrence rate was 26% with a mean disease-free period of 12.9 weeks. Recurrence rates were highest for nodular (40%) and purple macular lesions with focal nodularity (36%). The most frequent complications were transient pain (72%), superficial mucosal ulceration (22%) and transient paresthesia (12%). Intralesional vinblastine administration produced complete resolution in a substantial number of intraoral KS lesions and represents a well-tolerated treatment regimen for localised control of intraoral KS lesions. Owing to a 25% recurrence rate, re-evaluation is necessary for treatment of recurrent and new Kaposi's sarcoma lesions.
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PMID:Role of intralesional vinblastine administration in treatment of intraoral Kaposi's sarcoma in AIDS. 749 27

The objective of this study was to evaluate the reliability and validity of a brief index to measure symptoms in individuals infected with human immunodeficiency virus (HIV). From an ambulatory clinic that specializes in the care of HIV-infected individuals at a university hospital in northeast Ohio, 148 randomly selected outpatients (predominantly homosexual men) with a broad spectrum of HIV disease were enrolled in a prospective, cohort study. In standard interviews, patients rated the frequency of 36 symptoms related to HIV infection on an ordinal scale from zero (never) to three (daily); these interviews were repeated and outcomes determined every 3 months for one year. Clinical data were abstracted from the medical record with a standard chart review. Using specific criteria, 12 symptoms were selected for the HIV Symptom Index: fatigue, fevers, headache, imbalance, paresthesias, memory loss, cough, nausea, diarrhea, sadness, sleep disturbance, and skin problems. The HIV Symptom score (the sum of frequency ratings for the 12 symptoms) ranged from 0 to 31 with a mean of 9.4 (+/- SD 6.6). The test-retest reliability was high (intraclass correlation coefficient = 0.92) as was the internal consistency (Cronbach's alpha = 0.79). The validity of the index was established with three observations. (1) The HIV Symptom Index makes clinical sense and includes a representative spectrum of symptoms of infection. (2) Symptom Index scores were greater in patients with more advanced disease and in patients who were functionally impaired. (3) The Index was responsive to changes in health as the disease progressed.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:An index of symptoms for infection with human immunodeficiency virus: reliability and validity. 773 Aug 79

Tonic seizures are a poorly understood manifestation of demyelinating disease, first reported in 4 patients with multiple sclerosis. We describe a patient with tonic extension of the left limbs caused by a right-sided brainstem lesion as the first manifestation of demyelinating disease. A 19-year-old man was referred with a 4-month history of spontaneous attacks of mild paresthesias of the left arm and leg, followed by 15-45 s of rigid extension of the left limbs, occurring up to 25 times per day. Two months after onset, an MRI scan revealed areas of T2 abnormality in the lateral right cerebral peduncle and deep frontal white matter. The EEG was normal, including during hyperventilation which induced a typical episode. All attacks were successfully suppressed by carbamazepine, phenytoin, and valproate monotherapy. Serologic testing for toxoplasmosis, cytomegalovirus, Epstein-Barr virus, Lyme disease, and HIV was negative. Cerebrospinal fluid oligoclonal bands were absent but cerebrospinal fluid immunoglobulin G was mildly elevated (4.2 mg/dl). Over the next 30 months, serial MRIs revealed a normal spinal cord and persistence of the midbrain lesion, with resolution of some of the white matter lesions but reappearance of others. At 46 months, the midbrain lesion resolved on MRI, and the spasms no longer occurred spontaneously, nor could they be elicited by hyperventilation. While two previous reports have shown internal capsule lesions to underlie the tonic spasms in demyelinating disease, this is the first report in which a brainstem lesion has been causative.
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PMID:Tonic "seizures" in a patient with brainstem demyelination: MRI study of brain and spinal cord. 788 Mar 43

Neurological lesions are frequent complications of human immunodeficiency virus (HIV) infections. Organs involved include the brain, peripheral nerves and muscles. Since the widespread use of immunodepressive agents, spinal cord complications have also appeared although poorly documented in the literature. We observed six cases of spinal cord involvement which help indicate the modalities of practical management. In the first case, a 45-year old HIV1 + male presented dysesthesia evolving progressively over the T10 to L2 zones leading to the diagnosis of spinal cord toxoplasmosis. A gait disorder was the first sign in the second case, a 60-year old HIV1 + male. Neurological involvement progressed and the patient developed paraparesia, decreased muscular force with hypoesthesia and impaired proprioception of the lower limbs. Further complications led to coma and death and on autopsy, the patient was found to have cytomegalovirus myeloencephalitis. A 21 HIV1 + haemophiliac was our third case. Here paraplegia resulted from epidural compression due to Burkitt malignant lymphocytosis. The aggravation of paresthesia of the lower limbs, complicated by painful dysesthesia and proximal motor deficiency led to the suspected diagnosis of HIV-related myelitis in a particularly complicated case in a 52-year old seropositive male. In the fifth case, HIV infection led to major demelinization of the cervical and dorsal spinal cord due to toxoplasmosis and vacuolar myelopathy. In the sixth case, acute myelitis in an HIV2 positive male regressed spontaneously in 15 days. In clinical practice, spinal cord complications would appear to be frequent but less so than brain involvement. In the future, a better understanding of these complications should lead to specific identification of spinal cord signs in the neurological symptomatology of patients with HIV infection and allow adapted specific management.
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PMID:[Lesions of the spinal cord in HIV infection]. 789 90


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