Adrenocortical function in acquired immunodeficiency syndrome.

Clinical features of adrenal steroid deficiency occur in patients with the acquired immunodeficiency syndrome (AIDS). To determine the frequency of aberrations in peripheral steroid levels in patients with AIDS and AIDS-related complex (ARC) we measured morning recumbent plasma cortisol, deoxycorticosterone, 18-hydroxydeoxycorticosterone (18-OHDOC), corticosterone, aldosterone, and 18-hydroxycorticosterone concentrations before and after administration of 0.25 mg ACTH (Cosyntropin) in 74 randomly selected hospitalized patients with AIDS and 19 patients with ARC. Basal (0800 h) cortisol levels in the AIDS patients were significantly higher (P less than 0.01) than those in normal subjects, while other ACTH-dependent steroids of the 17-deoxypathway, deoxycorticosterone, corticosterone, and 18-OHDOC, were normal. These latter steroids increased subnormally in response to ACTH in patients with either AIDS (P less than 0.001) or ARC (P less than 0.005), but in ARC patients plasma 18-OHDOC levels were significantly higher than in those with AIDS (P less than 0.001). Supraphysiological doses of ACTH were then administered for 3 consecutive days to 14 patients with AIDS and 9 with ARC, which confirmed and amplified the subnormal responses of these steroids in AIDS. The mean plasma cortisol response was reduced on the third day only in AIDS patients, whereas in the ARC patients the steroid responses were normal. Angiotensin III infusion and postural stimulation increased plasma aldosterone and 18-hydroxycorticosterone levels in AIDS and ARC patients. Defective stimulation of 18-OHDOC alone or in combination with defective stimulation of other 17-deoxysteroids can be a harbinger of subsequent impaired adrenal capacity in AIDS.

Changes in the hypothalamic-pituitary-gonadal axis in human immunodeficiency virus-infected homosexual men.

Serum total testosterone, total 17 beta-estradiol, LH, FSH, and PRL concentrations were measured by RIA in 59 homosexual men infected with the human immunodeficiency virus (32 clinically healthy antibody-positive men (HH+), 20 men with acquired immune deficiency syndrome (AIDS), and 7 men with AIDS-related complex (ARC). The results were compared with those of 26 antibody-negative homosexual men (HH-) who served as controls. The mean serum total testosterone concentration was significantly lower in the men with AIDS [414 +/- 230 (+/- SD) ng/dL (14.5 +/- 8.0)] than in the HH- men [550 +/- 172 ng/dL (19.0 +/- 6.0 nmol/L); P less than 0.05]. The mean serum LH level was significantly higher in the men with AIDS (26 +/- 14 vs. 14 +/- 4 IU/L in HH- men; P less than 0.01) and slightly but significantly higher in the men with ARC (19 +/- 8 IU/L; 0.10 greater than P greater than 0.05). Serum FSH also was significantly higher in the men with AIDS (P less than 0.05). Serum PRL was significantly higher in the men with ARC (10 +/- 2 micrograms/L; P less than 0.05) and AIDS (16 +/- 10 micrograms/L; P less than 0.001) than in the HH- men (8 +/- 3 micrograms/L). Serum sex hormone-binding globulin levels were similar in HH- men and men with AIDS as were serum T responses to hCG administration for 2 days. These results suggest that alterations of the hypothalamic-pituitary-gonadal axis indicative of primary hypogonadism accompany human immunodeficiency virus infection in homosexual men.

Sensory testing in human immunodeficiency virus type 1-infected men. HIV Neurobehavioral Research Center Group.

Patients with acquired immunodeficiency syndrome frequently suffer peripheral neuropathy. We investigated its prevalence and relationship to clinical stage of human immunodeficiency virus (HIV) infection using quantitative sensory testing and nerve conduction testing. Vibratory threshold was determined in the right great toe and index finger of 179 men seropositive for HIV (28 with acquired immunodeficiency syndrome [AIDS] or AIDS-related complex [ARC], 151 asymptomatic) and 32 HIV-seronegative controls. None had clinical peripheral neuropathy. Abnormal threshold was control mean plus 2.5 SDs. In the toe, 10 (36%) of 28 subjects with AIDS or ARC had abnormal vibratory thresholds, compared with seven (5%) of 151 asymptomatic seropositive subjects and none of 32 controls. A subgroup of 168 seropositive subjects underwent nerve conduction testing. Abnormality rates were similar, but abnormalities of nerve conduction coincided with quantitative sensory testing abnormalities in only half the cases. Mean (+/-SD) vibratory threshold was significantly greater in subjects with AIDS or ARC (3.00 +/- 0.51 vibratory units) than in asymptomatic subjects (1.56 +/- 0.27 vibratory units) and controls (1.63 +/- 0.54 vibratory units). Finger abnormality rates did not differ, although subjects with AIDS or ARC had greater mean vibratory threshold. Subclinical peripheral neuropathy is thus related to stage of HIV infection and is present by quantitative sensory testing in 36% of patients with AIDS or ARC.

Ten-year follow-up of HIV-infected homosexual men with lymphadenopathy syndrome: evidence for continuing risk of developing AIDS.

Seventy-five homosexual men with lymphadenopathy syndrome (LAS), subsequently shown to be seropositive for the human immunodeficiency virus (HIV), were enrolled in a prospective study in Atlanta in 1982 and 1983. Subjects have been followed up at 3- to 6-month intervals with clinical and immunologic evaluations, including analysis of T-cell subsets. As of February 28, 1991, AIDS had developed in 36 (48%) of the 75 men. The AIDS cases continued to occur through the 10th year after onset of LAS; the 10-year cumulative incidence of AIDS was 56.6% (Kaplan-Meier survival analysis). Six-year incidence rates following the first observation of a T-helper cell count greater than or equal to 500/mm3, 400-499/mm3, 300-399/mm3, 200-299/mm3, and less than 200/mm3 were 29, 35, 50, 58, and 88%, respectively. Among individual symptoms and signs, only thrush conferred a poorer prognosis (odds ratio = 5.80; 95% confidence interval, 2.93, 11.39, p less than 0.001, Mantel-Byar analysis). The risk of AIDS persists 10 years after the onset of LAS. The AIDS incidence is related directly to T-helper cell depletion; with the exception of thrush, the presence or absence of symptoms and signs appears to be of lesser prognostic significance.

An open-label, dose-ranging trial of AL 721 in patients with persistent generalized lymphadenopathy and AIDS-related complex.

AL 721, a lipid mixture with reported in vitro activity against human immunodeficiency virus (HIV) via cell membrane or virion cholesterol depletion, was evaluated in a multicenter, open-label, dose-ranging trial. Forty men with persistent generalized lymphadenopathy or AIDS-related complex were treated with doses of 20, 30, 40, or 50 g orally twice daily for 8 weeks, and monitored for toxicity, disease progression, and with immunologic, virologic, and serum lipid profiles. The compound was found to be well tolerated over the broad range of doses examined; adverse reactions were confined to the gastrointestinal tract, of mild to moderate severity, and self-limited in duration. Modest weight gains observed on treatment were reversed within 4 weeks following cessation of therapy. While disease progression was not observed in this short-term study, we could find no indication of an immunorestorative or antiviral effect of AL 721, as determined by T-lymphocyte subset quantitation or HIV culture. All three patients who were HIV p24 antigenemic at entry retained positive antigen levels throughout treatment. As a consequence of therapy, however, significant increases in serum lipids were observed, including elevations in both triglyceride and total cholesterol levels. In conclusion, our experience on the largest group of HIV-infected patients treated with the highest doses of AL 721 provides no support for the use of this compound as an antiretroviral agent.

Autonomic function and human immunodeficiency virus infection.

We compared autonomic function in 26 patients infected by the human immunodeficiency virus (HIV) (18 AIDS and 8 ARC) to 22 controls. A significant decline in autonomic function was present across groups. Autonomic dysfunction correlated strongly with signs of HIV-associated nervous system disease. We observed significant differences across groups in tests of heart rate variation (expiratory-inspiratory ratio, maximum minus minimum heart rate difference, and mean square successive difference), the mean arterial blood pressure fall to tilting, and the blood pressure response to isometric exercise. A trend of declining autonomic function from controls to AIDS was present in the 30:15 ratio, the Valsalva ration, the systolic blood pressure fall to standing and tilt, and the cold pressor test. We did not observe any correlation between autonomic dysfunction and individual neurologic signs, prior therapeutic agents, and concurrent HIV-associated inflammatory or neoplastic processes. This study provides support for the presence of autonomic dysfunction in association with HIV infection. Autonomic dysfunction occurs more frequently and with greater severity in patients with AIDS; however, it may be present in the early stages of HIV infection and appears to progress during the illness.

Signs of cognitive change in HIV disease: an event-related brain potential study.

We recorded event-related brain potentials (ERPs) from 2 groups of human immunodeficiency virus (HIV)-positive men with no physical illness or neurologic involvement: 9 asymptomatic (AS+) and 9 classified as having either acquired immunodeficiency syndrome (AIDS; 7) or AIDS-related complex (ARC; 2). In separate choice reaction time tasks, the subjects pressed buttons to randomly presented auditory or visual stimuli at probabilities of either 20/80 or 50/50. There were no group differences on any of the neuropsychological tests commonly used in screening batteries for HIV patients. In contrast, reduced P300 amplitudes and increased P300 latencies occurred in ARC/AIDS patients in response to both auditory and visual stimuli, while in AS+ patients such alterations occurred only in the visual modality. Significant delays in P2 latency were found only in the auditory modality and then only in ARC/AIDS patients. ARC/AIDS patients alone showed delayed response times, and only in the auditory modality. The P300 results demonstrate alterations in stimulus evaluation and processing speed in the earliest stages of HIV disease, even before cognitive deficits can be detected by more traditional measures.

Myopathies associated with human immunodeficiency virus and zidovudine: can their effects be distinguished?

Myopathy may occur as a complication of human immunodeficiency virus type 1 (HIV) infection or from its treatment, zidovudine (ZDV). We reviewed our experience with HIV-infected subjects referred for neuromuscular evaluation and compared features of myopathy in ZDV-treated (+ZDV) and untreated (-ZDV) patients. Fifty patients had myopathy, 25 diagnosed by pathologic criteria and 25 by clinical and other laboratory support. Twenty patients with myopathy had weight loss sufficient for the diagnosis of HIV wasting syndrome. Thirty-one subjects were +ZDV and 19 were -ZDV. Patients in each group presented with proximal weakness, although myalgia was more common in +ZDV patients. Both groups had elevated serum CK to a similar degree (medians: +ZDV, 485; -ZDV, 471). Muscle biopsies revealed myofiber degeneration, variable inflammatory infiltrates, inclusion bodies, and mitochondrial abnormalities in both groups. We followed response to ZDV withdrawal in 15 patients. Four had increased strength, three noted less myalgia, and eight had no clinical improvement. Twelve of 13 patients improved with prednisone. Although it is difficult to distinguish the myopathies of HIV and ZDV by clinical or pathologic criteria, in the majority of our patients, myopathy is due to HIV rather than ZDV.

Progression to AIDS in patients with lymphadenopathy or AIDS-related complex: reappraisal of risk and predictive factors.

PURPOSE: In 1985, we reported that acquired immunodeficiency syndrome (AIDS) developed in 14 of 81 (17%) men with generalized lymphadenopathy followed prospectively for an average of 13 months. The presence of oral thrush or constitutional symptoms, or both, or severely impaired T4+ cell responses to specific antigen (interferon-gamma production) accurately identified patients at immediate risk for AIDS. The purpose of the current report is to describe the progress of these 81 patients during the three and a half years since enrollment and to include new data on initial serum levels of beta 2 microglobulin and human immunodeficiency virus (HIV) p24 antigen. PATIENTS AND METHODS: The mean age of the 81 patients was 35.4 years; 79 were homosexuals and two were drug abusers. Immunologic testing was performed once at the time of enrollment in all patients. Seventy-seven of the 81 patients were seropositive for HIV antibody. Frozen samples of serum, also obtained at initial study, were assayed in 1988 for beta 2 microglobulin and HIV p24 antigen. The clinical status of patients was determined six, 14, and 36 months after enrollment was closed (June 1984) by either interview and examination or telephone contact with private physicians. RESULTS: After three and a half years of follow-up, 42 patients have developed AIDS, including (1) 77% who had had thrush or symptoms, or both, (2) 80% to 88% of those who originally demonstrated marked immunologic abnormalities (skin test anergy, less than 200 T4+ cells/mm3, T4/T8 cell ratio of less than 0.5, severely impaired interferon-gamma production [less than 25 U/mL], or elevated serum beta 2 microglobulin level [greater than 3.0 mg/L], and (3) 95% of patients with HIV p24 antigenemia. However, AIDS also developed in 51% of patients who had had more apparently benign initial manifestations (lymphadenopathy alone, herpes zoster), in 41% to 54% despite normal initial results for either T4+ cell number, interferon-gamma secretion, beta 2 microglobulin, or skin testing, and in 44% of those whose sera did not contain HIV antigen. CONCLUSION: These updated results demonstrate the remarkably poor prognosis of patients with generalized lymphadenopathy or AIDS-related complex irrespective of initial clinical, immunologic, and serologic findings, and suggest that essentially all such persons may be candidates for antiviral therapy.

A randomized, double-blind, phase I/II trial of tumor necrosis factor and interferon-gamma for treatment of AIDS-related complex (Protocol 025 from the AIDS Clinical Trials Group).

To determine safety and efficacy of tumor necrosis factor (TNF) and interferon-gamma (IFN gamma) in the treatment of patients with acquired immunodeficiency syndrome (AIDS)-related complex, a randomized, double-blind study was conducted. Twenty-five patients with AIDS-related complex and CD4 lymphocytes less than or equal to 500 x 10(6)/L attended an AIDS Clinical Trials Unit of a tertiary referral center. Patients were administered tumor necrosis factor (TNF) (10 micrograms/m2) or IFN gamma (10 micrograms/m2), or both intramuscularly three times weekly for 16 weeks. Side effects from all three preparations included fever, constitutional symptoms, and local reactions. No significant hematologic, hepatic, renal, or coagulation abnormalities were observed. CD4 lymphocyte counts, beta 2-microglobulin, p24 antigen levels, and anti-p24 antibody did not change significantly during therapy. Similarly, no significant change was noted in rates of HIV isolation from peripheral blood mononuclear cells or plasma. TNF and IFN gamma were tolerable after premedication with acetaminophen; however, no significant change in markers of human immunodeficiency virus infection was demonstrated. These cytokines alone do not appear to be of benefit, nor do they appear to hasten the progression of HIV infection.

Blood vessels in human immunodeficiency virus-related lymphoadenopathy: high endothelial venules and lymphocyte migration.

The vasculature of 25 lymph nodes of patients with human immunodeficiency virus-related lymphadenopathy was investigated morphometrically. The number of small vessels, the morphological features of high endothelial venules and the migratory index of the lymphocytes passing through the high endothelial venules, as well as the stage-dependent change of each parameter, were analysed. Twenty reactive lymph nodes served as controls. The total number of vessels in the HIV-infected lymph nodes was relatively stable. However, the small vessels with flat endothelium increased in number, while the number of high endothelial venules decreased as the disorder progressed, and the decrease in the lymphocyte migration seemed to precede the change in the morphology of high endothelial venules. The presumptive role of these alterations in the pathogenesis of the investigated disorder is emphasized.

Pediatric acquired immunodeficiency syndrome-related complex: clinical and immunologic features.

The long term clinical outcome for infants and children with the pediatric acquired immunodeficiency syndrome-related complex is unknown. This report describes our experience with 14 patients with acquired immunodeficiency syndrome-related complex who have been followed for 11 to 71 months since the onset of their symptoms. The most frequent clinical features at presentation were persistent generalized lymphadenopathy (14 of 14), hepatosplenomegaly (11 of 14) and a history of recurrent otitis media (7 of 14). Except for hypergammaglobulinemia (14 of 14) and reversed T4/T8 ratios (9 of 14), immunologic analyses, including in vitro responses to mitogens and antibody responses following immunization, revealed no consistent abnormalities. Over the course of follow-up, none of the patients have developed serious or opportunistic infections and 12 of 14 have shown catch up or age-appropriate growth. The T4/T8 ratios have remained stable in 8 of 11 and improved in 2 of 11 patients. Gradual regression of hepatosplenomegaly and lymphadenopathy has been noted patients. Although follow-up studies over a longer period are needed to confirm our observations to date, acquired immunodeficiency syndrome-related complex may represent a prolonged plateau in the course of human immunodeficiency virus infection in many infected children. Detailed immunologic evaluation of these patients may help to identify a subset of children that could benefit from periodic gamma-globulin or chronic antibiotic therapy.

HIV and the brain: evidence of early involvement and progressive damage.

AIDS is often accompanied by progressive encephalopathy and 'subcortical' dementia, but there is uncertainty regarding how early the brain involvement may begin in the course of HIV infection. This study used a cognitive auditory 'oddball' paradigm to elicit sensory and cognitive event related potential (ERP) components from healthy controls and from patients at different stages of HIV infection. Sensory component latencies did not differ between groups, but cognitive components showed progressive delays corresponding to increasingly severe clinical stages of HIV infection. The earliest changes were found among asymptomatic HIV + patients, suggesting that this test is a sensitive indicator of early subclinical CNS damage. In contrast, neither frequency analysis nor nonlinear dynamical analysis of the EEG showed differences between healthy controls and patients.

Deficits in perimetric performance in patients with symptomatic human immunodeficiency virus infection or acquired immunodeficiency syndrome.

PURPOSE: We measured the perimetric performance in patients with either acquired immunodeficiency syndrome (AIDS) or human immunodeficiency virus (HIV) disease but without AIDS. METHODS: Light-difference sensitivity in the central field was measured in 74 eyes of 37 patients. The Humphrey Field Analyzer 640, program 30-2 was used. Additionally, 143 eyes of 143 normal control subjects were studied. RESULTS: Mean deviation was significantly reduced in patients with HIV disease compared with control subjects (mean +/- S.E.M., -4.30 +/- 0.52 vs -0.77 +/- 0.15, respectively; P < .0001). Analysis of subgroups demonstrated that patients with lymphadenopathy syndrome or AIDS-related complex (N = 40 eyes; -3.52 +/- 0.41; P < .0001) as well as patients with AIDS (N = 34 eyes; -5.23 +/- 0.97; P < .0001) had a reduced mean deviation. Those comparisons remained significant (P < .0001) when data were analyzed independently for the right eyes and for the left eyes. Corrected pattern standard deviation (3.15 +/- 0.30 vs 1.39 +/- 0.09; P < .0001) was higher in patients with HIV disease compared with control subjects. Again, analysis of subgroups disclosed a significant increase in patients with lymphadenopathy syndrome or AIDS-related complex (2.55 +/- 0.36; P < .0001) as well as in patients with AIDS (3.85 +/- 0.51; P < .0001). Both comparisons remained significant when data were analyzed independently for the right and left eyes. CONCLUSIONS: This study demonstrates visual dysfunction despite normal visual acuity in patients with HIV disease. Our results are consistent with the hypothesis of damage at the neuroretinal level.

Effects of smoking and clinical status on lung function in human immunodeficiency virus (HIV)-seropositive subjects.

Lung function was measured at 3-month intervals for up to 1 yr in a group of Caucasian HIV-seropositive subjects. The objective was to document any deterioration in lung function and seek correlations between such deterioration and smoking history and Centers for Disease Control (CDC) status. Ninety-nine subjects were studied at enrollment; 43 were followed-up (mean duration 9 +/- 3 months). Ninety-five of the 99 enrolled subjects remained free of HIV-related respiratory disease and were included in the analysis. At enrollment, carbon monoxide diffusing capacity (TLCO) was significantly lower than predicted in non-smokers, smokers and ex-smokers (88, 77 and 88%, respectively, P < 0.001). The TLCO measurements in the smoking group were significantly lower than those of the life-long non-smoking subjects (P < 0.01). Residual volume (RV) was significantly higher than predicted in smokers (111%, P = 0.02). During follow-up, all three groups demonstrated significant declines in TLCO (7%, P = 0.01; 9%, P = 0.005; 13%, P < 0.001, respectively), and increases in RV (9%, P = 0.03; 13.5%, P = 0.02, 22%, P = 0.02, respectively). At enrollment, significantly lower than predicted values of TLCO were observed in groups stratified by CDC criteria: in asymptomatic HIV-seropositive subjects (CDC 11) 89%, P = 0.01; persistent generalized lymphadenopathy (PGL) 84%; AIDS-related complex (ARC) 81%; and in non-pulmonary AIDS (IV C1) 69%, P = 0.0001, respectively. Residual volume was significantly higher than predicted in CDC II (114%, P = 0.05). During follow-up, TLCO fell in groups PGL and ARC by 7 and 9%, respectively, while RV increased in groups CDC II, PGL and ARC by 17, 15 and 8%, respectively. Only the TLCO decline in PGL showed any linkage to clinical deterioration. This study demonstrates deficits at enrollment, and a continuing decline of TLCO and increase in RV in HIV-seropositive subjects without overt lung disease.

Supervised exercise training improves cardiopulmonary fitness in HIV-infected persons.

We attempted to measure cardiopulmonary effects, CD4 counts, and perceived sense of well-being in 25 individuals moderately to severely immunocompromised from HIV infection (mean entry CD4 count = 144.microliters-1) before and after a 24-wk program of exercise training. Only six subjects completed the 24-wk program. All six showed evidence of a training effect. Statistically significant improvements were seen in maximal oxygen consumption (VO2max), oxygen pulse, and minute ventilation. Submaximal exercise performance improved significantly by 12 wk in the 10 individuals available for testing: decreases were seen in heart rate, rate pressure product, and rate of perceived exertion. White blood cell counts and T-lymphocyte subsets were stable at 12 and 24 wk in the subjects available for testing. High depression/anxiety scores on a mental health inventory (General Health Questionnaire) correlated with low CD4 counts. Scores did not correlate with compliance with the exercise program. There was a trend (P < 0.10) for scores to improve over time among those individuals who attended > or = 80% of scheduled exercise sessions. We conclude that exercise training is feasible and beneficial for some HIV-infected individuals.

Dietary intake in patients with acquired immunodeficiency syndrome (AIDS), patients with AIDS-related complex, and serologically positive human immunodeficiency virus patients: correlations with nutritional status.

One of the major clinical manifestations of the acquired immunodeficiency syndrome (AIDS) and AIDS-related complex (ARC) is the development of cachexia. This most likely results from a multifactorial interplay of poor diet, malabsorption, and altered metabolism. To assess the potential role of nutrient intake in the development or persistence of malnutrition, a detailed analysis was performed of a 72-hr diet record in clinically stable patients with AIDS (N = 18), ARC (N = 12) and in human immunodeficiency virus (HIV) seropositive controls without significant manifestations of disease (N = 13). Total calorie intake was 39.1 +/- 13.2 kcal/kg/day in AIDS patients vs 34.6 +/- 7.8 kcal/kg/day in ARC patients or 31.9 +/- 17.7 kcal/kg/day in HIV seropositive cases (all p = NS). Likewise, mean protein intakes were similar among the groups and exceeded recommended daily dietary allowance (RDA) guidelines. The mean body weight changes from the inception of illness were -11 +/- 1% in AIDS, -6 +/- 7% in ARC, vs +3 +/- 2% in HIV-seropositive-only cases (p less than 0.05 vs AIDS and ARC). Dietary vitamin and mineral analysis revealed that 88% of AIDS, 88% of HIV seropositive, and 89% of ARC patients were ingesting less than 50% RDA for at least one nutrient. The mean number of deficiencies per patient was 1.8 +/- 1.3 in AIDS, 3.8 +/- 3.5 in ARC, and 2.9 +/- 2.5 in HIV-seropositive-only cases (p less than 0.05 AIDS vs ARC). There were no significant correlations between specific anthropometric measurements and dietary intakes of protein or fat.(ABSTRACT TRUNCATED AT 250 WORDS)

The clinical spectrum of the HIV infection. A working hypothesis.

Many clinicians have realised that AIDS is only the most dreadful aspect of HIV infection. Together with the "asymptomatic carrier" condition, other syndromes have been described, including LAS, ARC and Lesser-AIDS. We have developed a working hypothesis to explain the natural history of HIV infection, basing our assumptions on the international literature and our own experience. We have found many analogies and some slight differences between the clinical courses of HIV infection and other chronic infections, especially syphilis. It is possible that, on clinical grounds, the natural histories of both diseases are so similar as to allow us to describe one of them within the scheme of the other. Only careful and prolonged clinical observation will solve the problem of the natural history of HIV infection and solve the problems which are still present in its comprehension.

Electrophysiological study (VEP, BAEP) in HIV-1 seropositive patients with and without AIDS.

One hundred-twenty nine HIV-1 seropositive patients (39 females, 90 males) were studied by means of pattern visual evoked potential (VEP) and brainstem auditory evoked potential (BAEP) recording. Utilizing the criteria of the Centers for Disease Control the patients were clinically defined and then subdivided into four groups: group A included patients of category II (n:11); group B patients of category III (n:29); group C patients of category IVa and IVc2 (n:55) and group D patients belonging to the other subgroups of category IV (n:34). EP were altered in 26.35% of the entire group with a marked prevalence of BAEP alterations (21.7%) rather than of VEP (4.65%). A considerable amount of BAEP abnormalities (24.13%) were found in patients with persistent generalized lymphadenopathy (group B). A significant increase of BAEP mean interpeak latencies were observed in group B, C, D patients when compared with those of the control group. On the whole, EP were altered in 20.65% of the neurologically asymptomatic patients. EP alterations may precede any clinical manifestation and can be found during the earlier phases of HIV-1 infection.