Transmyocardial laser revascularization combined with intramyocardial endothelial progenitor cell transplantation in patients with intractable ischemic heart disease ineligible for conventional revascularization: preliminary results in a highly selected small patient cohort.

OBJECTIVE: Transmyocardial laser revascularization for angina relief and intramyocardial autologous endothelial progenitor cell injection for neoangiogenesis may offer a new treatment strategy for patients with intractable ischemic heart disease. METHODS: Transmyocardial laser revascularization and intramyocardial injection of bone marrow-derived CD133+ cells was performed in six highly symptomatic patients. Transmyocardial laser channels were created and isolated CD133+ cells were injected intramyocardially. All patients were followed up for a minimum of 6 months postoperatively. RESULTS: One patient died shortly after the operation due to refractory heart failure. In the five survivors, CCS class improved as well as left ventricular ejection fraction. Left ventricular end-diastolic volume and myocardial perfusion varied between the patients. All patients described a considerable improvement in quality of life postoperatively. Repeated 24-hour Holter monitoring revealed no significant arrhythmias. CONCLUSIONS: In this small patient cohort, intramyocardial CD 133+ cell injection combined with transmyocardial laser revascularization led to an improvement in clinical symptomatology in all patients and in left ventricular function in 4 out of 5 patients, with an unclear effect on myocardial perfusion. Caution is advised when employing this therapy in patients with severely depressed left ventricular function.

Chronic inborn erythrocytosis leads to cardiac dysfunction and premature death in mice overexpressing erythropoietin.

The most common cause of an increase of the hematocrit is secondary to elevated erythropoietin levels. Erythrocytosis is assumed to cause higher blood viscosity that could put the cardiovascular system at hemodynamic and rheological risks. Secondary erythrocytosis results from tissue hypoxia, and one can hardly define what cardiovascular consequences are caused by chronic erythrocytosis or hypoxia. Herein, a novel transgenic (tg) mouse line is characterized that is erythrocytotic because of chronic overexpression of the human erythropoietin gene. These mice grow up well, reaching a hematocrit of about 0.80 in adulthood. Blood volume of adult tg mice was markedly increased by 75%. Unexpectedly, blood pressure was not elevated and cardiac output was not decreased. Still, the adult tg mice showed features of cardiac dysfunction with increased heart weight. In vivo, high-frequency echocardiography revealed marked ventricular dilatation that was confirmed by histologic examination. Furthermore, by transmission electron microscopy, a prominent intracellular edema of the cardiomyocytes was seen. Exercise performance of the tg mice was dramatically reduced, unmasking the severity of their compromised cardiovascular function. In addition, life expectancy of the tg mice was significantly reduced to 7.4 months. Our findings suggest that severe erythrocytosis per se results in cardiac dysfunction and markedly reduced life span.

Measurement of peripheral tissue thickness by ultrasound during the perioperative period.

We have studied changes in peripheral tissue thickness with a novel hand-held ultrasound device during the perioperative course of 60 healthy surgical patients in three different intraoperative body positions. The nil-by-mouth period led to a significant decrease in forehead tissue thickness. Standardized infusion therapy with Ringer's solution at a rate of 8 ml kg-1 h-1 resulted in a gradual increase in tissue thickness, which was significantly different from preoperative baseline values after 90 min. Packed cell volume decreased significantly after the start of infusion and remained low over the rest of the observation time. Different body positions did not influence changes in tissue thickness. We conclude that changes in perioperative tissue thickness in healthy patients can be detected easily by ultrasound, independent of body position. This method may prove useful for the non-invasive assessment of fluid balance state.

Is CD30 (Ki-1) immunostaining in cutaneous eruptions useful as a marker of Th1 to Th2 cytokine switching and/or as a marker of advanced HIV-1 disease?

CD30 is a member of the tumour necrosis factor/nerve growth factor receptor superfamily, which is expressed on CD4+ and CD8+ T-cell clones which produce T helper (Th) 2-type cytokines. It has been proposed that disease progression in HIV-1 is associated with Th1 to Th2 cytokine switching. In 70 cutaneous biopsies from HIV-1 positive patients in different stages of disease, we performed a battery of immunohistochemical stains. These included antibodies to CD3, UCHL-1, OPD-4, L-26, KP-1 and CD30 (Ki-1). In addition, we used a similar battery of stains on cutaneous biopsies of HIV-1 negative patients with inflammatory dermatoses which are established as Th1 or Th2 dominant, e.g. polar leprosy. CD30+ cells were rarely present in early stages of HIV-1 disease, but commonly present in later stages of disease. However, there were cases of late HIV-1 disease which did not contain CD30+ cells. Increased numbers of CD30+ cells were more commonly seen in later stages of HIV-1 disease. However, the expression of CD30 appeared to be better in predicting other established Th2 cutaneous infiltrates in HIV-1 negative patients than in predicting a Th2 cutaneous cytokine pattern in advanced HIV-1 disease.

Lymphoid markers, activation markers, and adhesion molecules in cutaneous biopsy specimens from HIV+ patients with disease progression. The Military Medical Consortium for the Advancement of Retroviral Research.

BACKGROUND: One important factor in understanding the pathogenesis of human immune deficiency virus (HIV) disease is documenting the patterns of immune dysregulation present in HIV-positive patients. The cells which home to skin are mainly certain subsets of T cells and, as opposed to the peripheral blood, where circulating factors may inhibit terminal phenotypic differentiation, the cutaneous environment potentiates differentiation during cutaneous eruptions. OBJECTIVE: The authors' aim was to characterize the inflammatory dermatoses in biopsy specimens from HIV-positive patients with immunohistochemical stains for lymphoid markers, activation markers, and adhesion molecules and to determine if there was any correlation with the type of dermatosis and the HIV-disease stage. METHODS: Lymphoid and activation markers as well as adhesion molecules were studied on cutaneous biopsy specimens from 96 inflammatory dermatoses in HIV-positive patients. The dermatoses included psoriasiform dermatoses with and without a lichenoid component, perivascular lymphoid dermatoses, perivascular and periadnexal inflammatory dermatoses, spongiotic dermatoses, granulomatous dermatoses, and neutrophilic dermatoses with and without vasculitis. RESULTS: Although there was a decrease in CD4/CD8 ratios in the cutaneous inflammatory dermatoses with progression of the disease, the ratios of CD4/CD8 cells were far higher than those in the peripheral blood. There were also increasing numbers of CD23+ cells and increased E-Selectin expression on endothelial cells from the early stages of disease, with no consistent pattern of ICAM-1 expression on epithelial cells with disease progression. CONCLUSIONS: The expression of lymphoid markers, activation markers, and adhesion molecules in the skin with progression of HIV disease, is consistent with a T helper (Th)1 to Th0/Th2 cytokine pattern of immune dysregulation. This cytokine pattern may be modified by the cytopathic effects of HIV on lymphoid and dendritic populations and by effects of other concurrent infections. Significant numbers of CD4+ T cells in skin infiltrates, with low peripheral CD4 T-cell counts, suggest that the cutaneous T-cell populations may be distinctive.

Cutaneous reactions at the site of post-infection gp160 vaccination therapy in HIV-1+ patients. Military Medical Consortium for the Advancement of Military Medicine.

BACKGROUND: Post-infection vaccination with human immunodeficiency virus type 1 (HIV-1) specific antigens has been hypothesized as a mechanism for generating a more effective immune response to the HIV-1 virus. Cutaneous reactions at the site of immunization may provide information on the pattern of immune activation induced by the vaccine. OBJECTIVE: To evaluate exaggerated local cutaneous reactions in eight HIV-1+ patients enrolled in a phase I and II gp160 vaccine study. METHODS: Cutaneous biopsy specimens were obtained and evaluated using routine histologic, immunofluorescence, and immunohistochemical techniques. RESULTS: A mononuclear cell infiltrate with tissue eosinophilia, in some cases forming flame figures, was present on histologic sections. There was no evidence of immune complex deposition. Activated T-helper cells formed a major portion of the mononuclear cell infiltrate. CONCLUSIONS: A delayed-type hypersensitivity reaction, mediated by T cells with a T-helper 2 cytokine pattern, was favored by clinical and histologic features. The most likely antigen stimulating this reaction is residual lepidopteran used in the preparation of the vaccine; however, baculovirus antigens may also play a role. In addition, the adjuvant, aluminum phosphate, as well as the underlying patterns of immune dysregulation present in HIV-1+ patients, may potentiate these reactions.

Once weekly azithromycin therapy for prevention of Mycobacterium avium complex infection in patients with AIDS: a randomized, double-blind, placebo-controlled multicenter trial.

We conducted a randomized, double-blind, placebo-controlled multicenter trial of azithromycin (1,200 mg once weekly) for the prevention of Mycobacterium avium complex (MAC) infection in patients with AIDS and a CD4 cell count of < 100/mm3. In an intent-to-treat analysis through the end of therapy plus 30 days, nine (10.6%) of 85 azithromycin recipients and 22 (24.7%) of 89 placebo recipients developed MAC infection (hazard ratio, 0.34; P = .004). There was no difference in the ranges of minimal inhibitory concentrations of either clarithromycin or azithromycin for the five breakthrough (first) MAC isolates from the azithromycin group and the 18 breakthrough MAC isolates from the placebo group. Of the 76 patients who died during the study, four (10.5%) of 38 azithromycin recipients and 12 (31.6%) of 38 placebo recipients had a MAC infection followed by death (P = .025). For deaths due to all causes, there was no difference in time to death or number of deaths between the two groups. Episodes of non-MAC bacterial infection per 100 patient years occurred in 43 azithromycin recipients and 88 placebo recipients (relative risk, 0.49; 95% confidence interval, 0.33-0.73). The most common toxic effect noted during the study was gastrointestinal, reported by 78.9% of azithromycin recipients and 27.5% of placebo recipients. Azithromycin given once weekly is safe and effective in preventing disseminated MAC infection, death due to MAC infection, and respiratory tract infections in patients with AIDS and CD4 cell counts of < 100/mm3.

Size and duration of zidovudine benefit in 1003 HIV-infected patients: U.S. Army, Navy, and Air Force natural history data. Military Medical Consortium for Applied Retroviral Research.

OBJECTIVES: The study's objectives were to determine the size and duration of benefits of early versus delayed versus late treatment with zidovudine (ZDV) on disease progression and mortality in HIV-infected patients, and whether patients rapidly progressing before ZDV treatment had a different outcome from those not rapidly progressing before ZDV. DESIGN: The design was an inception cohort of 1003 HIV-infected patients. One hundred and seventy-four of the 1003 patients were treated before CD4 counts fell to <400 x 10(9)/L, ("early treatment"); 183 of 1003 patients were treated after CD4 counts fell to <400 x 10(9)/L but before clinical disease developed ("delayed treatment"); and 646 of the 1003 patients had either been treated after clinical disease developed or had not been treated at all by the end of follow-up ("late treatment"). Outcomes were progression to clinical HIV disease and mortality. RESULTS: The relative risk (RR) of progression for early versus delayed treatment was 0.58 (p < .03), and durability of ZDV benefits on progression was estimated at no more than 2.0 years; however, this estimate had wide confidence intervals. The RR of progression for delayed versus late treatment was 0.54 p < .0001, and durability of ZDV benefits was estimated at 1.74 years; this estimate had narrow confidence intervals. Survival was better for the early versus delayed treatment (RR = 0.55), but this difference was not statistically significant. In the subgroup of patients with more rapid CD4 decline prior to ZDV therapy, significant benefits on progression were observed for early versus delayed ZDV therapy (RR = 0.42, p = .02) and delayed versus late ZDV therapy (RR = 0.51; p = .0004). Duration of benefit was estimated to be 4.5 years (early versus delayed) and 1.7 years (delayed versus late). For patients with less rapid pre-ZDV decline in CD4 levels, a significant progression benefit was observed for delayed versus late therapy (RR = 0.50; p = .02). Duration of benefit in this subgroup was estimated to be 1.8 years. No significant benefit was found for early versus delayed treatment (RR = 1.12) in the less rapid pre-ZDV CD4 cell decline subgroup. CONCLUSIONS: Early treatment compared with delayed treatment was associated with a sizable reduction in HIV progression, but the duration of benefits was estimated to last only about 2 years. Delayed treatment compared with late treatment with ZDV was associated with substantial reduction of progression, but this reduction was also clearly limited in duration. Benefits on progression and mortality for the early treatment group were heavily dependent on the pre-ZDV CD4 slope. In the subgroup of patients with the most rapid pre-ZDV CD4 cell declines, the duration of benefit was much longer, possibly as long as 4 years.

Histopathologic features seen in cutaneous photoeruptions in HIV-positive patients. Military Medical Consortium for the Advancement of Retroviral Research (MMCARR).

BACKGROUND: There have been scattered reports of HIV+ patients with increased reactions to light as well as anecdotal reports of HIV+ patients with increased morbidity secondary to radiation therapy. METHODS: As a part of a military study of HIV+ patients, we followed 987 patients for cutaneous disease for 4 years. All patients were questioned on a periodic basis about increased sensitivity to light. These patients received a physical examination at each protocol visit, and they were given the opportunity to receive all their dermatologic care within the HIV clinic. Fourteen of the patients with photo-induced eruptions were evaluated clinically at the time of the eruption, and 11 of these were biopsied. RESULTS: Thirty-three of the patients reported photo-induced reactions unrelated to oral medications. Although sensitivity to light often began in the early stages of HIV disease, reactions became more severe and more chronic with disease progression. Histologic features varied from few to numerous apoptotic/necrotic keratinocytes within the mid to upper levels of the epidermis associated with a perivascular inflammatory infiltrate, to apoptotic/necrotic keratinocytes throughout an acanthotic epidermis with a lichenoid/interface infiltrate. CONCLUSIONS: Although the pathogenesis of these light reactions is not known, these reactions may be related to depletion of endogenous scavengers which results in increased oxidative stress and is modulated by the pattern of immune dysregulation and metabolic dysregulation induced by HIV disease.

Increased cutaneous toxicity to ionizing radiation in HIV-positive patients. Military Medical Consortium for the Advancement of Retroviral Research (MMCARR).

BACKGROUND: There are reports of increased reactions in HIV-1+ patients to ultraviolet light sometimes in association with medication. In addition, there are also reports of increased morbidity associated with radiation therapy in HIV-1+ patients. METHODS: Three HIV-1+ patients developed cutaneous toxic reactions to radiation therapy; two with Kaposi's sarcoma (KS) and one with non-Hodgkin's lymphoma. CONCLUSIONS: Although the mechanisms which resulted in these reactions are not clear, they may be related to depletion of endogenous scavengers and may be accentuated by the pattern of immune dysregulation present in HIV-1 disease.

Impaired induction of the apoptosis-protective protein Bcl-xL in activated PBMC from asymptomatic HIV-infected individuals.

Progression to AIDS in asymptomatic HIV-infected individuals is characterized by a gradual but progressive loss of CD4+ T cells. While the mechanisms underlying this decline are currently unknown, recent evidence suggests that these cells are abnormally sensitive to apoptosis in response to activation signals. Recent work has implicated downregulation of Bcl-2 with the increased spontaneous apoptosis in lymphocytes from HIV-infected patients. We have evaluated the roles of the apoptosis-protective proteins Bcl-2 and Bcl-x in stimulated PBMC from asymptomatic HIV-infected and HIV-uninfected individuals. We found that Bcl-2 was constitutively expressed in PBMC from both HIV-infected and uninfected samples. However, Bcl-x induction was delayed and responses were decreased in stimulated HIV-infected samples. Additionally, single-cell intracellular staining of Bcl-x revealed a significant inverse correlation between PWM-induced Bcl-x expression and apoptosis (r = -0.695, P = 0.05). This was confirmed at the single-cell level in direct experiments when stimulated cells were sorted based on Bcl-x induction and then measured for apoptosis. Furthermore, low Bcl-x expression was not due to reduced lymphocyte activation following PWM stimulation. Our data indicate that the induction of Bcl-x is markedly impaired in asymptomatic HIV-infected patients and that stimuli which induce inadequate expression of Bcl-x are associated with increased levels of apoptosis in these cells.

Increased drug reactions in HIV-1-positive patients: a possible explanation based on patterns of immune dysregulation seen in HIV-1 disease. The Military Medical Consortium for the Advancement of Retroviral Research (MMCARR).

Drug reactions are common in HIV-1 disease, with the incidence having been reported to increase with increasing stage and with CD4+ T-cell counts below 200/microliters. However, there have been numerous reports of patients in which rechallenge, dosing changes or continued therapy have resulted in no recurrence or else clearing of the eruption. We followed 974 HIV-1-positive patients for 46 months as a part of a military study of HIV-1 disease. Within this group there were a total of 283 drug eruptions, with cutaneous manifestations in 201 patients in which clinical characteristics were noted and 86 patients in which cutaneous biopsies were performed. Serological evidence of reactivation or acute Epstein-Barr virus (EBV) or cytomegalovirus (CMV) infections were also noted, as well as peripheral eosinophilia. The incidence of drug eruptions significantly increased with increasing Walter Reed stage and decreasing CD4 counts and CD4/CD8 ratio, as well as with increasing age and in patients with increased numbers of other dermatological diagnoses. In addition, white patients had significantly more drug eruptions than did black. Serological or culture evidence of acute or reactivated EBV or CMV was significantly increased in patients with drug eruptions. The majority of the eruptions were maculopapular or morbilliform with a predominantly perivascular mononuclear cell infiltrate. HIV-1 positive patients have an increased incidence of drug reactions, the incidence having been reported to increase in patients with less than 200 CD4+ T cells/microliter. However, at very low T4 counts, especially those less than 25/microliter, and at a CD4/CD8 ratio of less than 0.10, the probability of reactions to trimethoprim-sulphamethoxazole (TMP-SMZ) is decreased in late-stage HIV-1 patients. Maculopapular or morbilliform eruptions are the most common clinical presentations, often accompanied by one or more of the following: fever, arthralgias, eosinophilia, and serum transaminase elevation. Histologically the majority of these eruptions show a perivascular mononuclear cell infiltrate, sometimes with focal interface changes and apoptotic, necrotic cells within the epidermis. Acute hypersensitivity reactions and toxic epidermal necrolysis (TEN) or Stevens-Johnson's syndrome (SJS) with diffuse epidermal apoptosis and necrosis have also been less commonly described. In a study of cutaneous manifestations in an HIV-1 positive military population, drug reactions were evaluated in terms of clinical features, histopathology, demographic features and laboratory findings.

Evolution of human immunodeficiency virus type 1 env sequence variation in patients with diverse rates of disease progression and T-cell function.

We examined the relationship between env sequence variation and disease progression in 10 human immunodeficiency virus type 1 (HIV-1)-seropositive subjects selected from a longitudinal cohort receiving zidovudine therapy. Five subjects were chosen for stable clinical status and CD4 counts (slow progressors), and five were selected for rapid clinical deterioration and CD4 count decline (rapid progressors). The slow progressors had significantly lower plasma viral RNA loads and greater lymphoproliferative responses to mitogens than the rapid progressors. DNA sequences representing the C1 through C3 regions of env were amplified from two peripheral blood mononuclear cell DNA samples from each subject separated by an average of 2.5 years. Molecular clones of these amplicons were then sequenced, and DNA sequence and deduced amino acid sequence distances were compared. Inter-time point sequence comparison showed a higher rate of sequence evolution for the rapid progressors in three of five matched pairs of rapid progressors and slow progressors and for the slow progressors in the remaining two subject pairs. However, intra-time point sequence comparisons showed that four of five slow progressors developed a more diverse quasispecies over time and one showed no change. In contrast, four of five rapid progressors showed no change in quasispecies diversity over time and one showed a significant decrease in diversity. The overall C1 through C3 region quasispecies diversity in the slow progressors at baseline was lower than that for the rapid progressors, but this difference was not significant at the follow-up time points. These diversity relationships were obscured if sequence analyses were limited to the 300-bp C2 to V3 region. Thus, HIV-1 quasispecies diversity increased over time in subjects with more functional immune systems.

Mucosal immune responses in four distinct compartments of women infected with human immunodeficiency virus type 1: a comparison by site and correlation with clinical information.

Because mucosal immune responses may be important in protection against human immunodeficiency virus type 1 (HIV-1), HIV-1-specific immune responses at mucosal sites in natural infection were compared. Total antibody concentrations and HIV-1-specific binding antibody responses in four distinct mucosal sites and serum were assessed in 41 HIV-infected and 19 HIV-seronegative women. HIV-1 gp160-specific IgG responses were detected in >99% of mucosal samples in infected subjects, with the highest titers in genital secretions. HIV-1-specific IgA was detected in the majority of endocervical secretions (94%) and nasal washes (95%) but less often in vaginal washes (51%) and parotid saliva (38%). There was no significant correlation between mucosal immune response and most clinical factors. Based on methodologic considerations, frequencies of detection, and HIV-1-specific responses, nasal washes and genital secretions may each provide important measures of HIV-1-specific mucosal immune responses in infected women.

Pityriasis lichenoides et varioliformis acuta in HIV-1+ patients: a marker of early stage disease. The Military Medical Consortium for the Advancement of Retroviral Research (MMCARR).

BACKGROUND: The high incidence of cutaneous disease in HIV-1+ patients may be a marker of the chronic state of immune activation. In addition, specific cutaneous diseases may be related to the pattern and degree of immune dysregulation present in the patients at the time of the eruption. We have observed that HIV-1+ patients with pityriasis lichenoides et varioliformis acuta (PLEVA) were in the early to midstage of HIV-1 disease. MATERIALS AND METHODS: To determine if there was a correlation between the phenotype of the lymphoid infiltrate and surface markers of the epidermis and the known changes in early or late-stage HIV-1 disease, we studied five HIV-1+ patients with PLEVA. Cutaneous biopsy specimens were obtained and immunohistochemical stains were used to determine the expression of ELAM-1, ICAM-1, and HLA-DR and the phenotype of the lymphoid infiltrate. RESULTS: The HIV-1+ patients showed increased expression of HLA-DR on keratinocytes as well as on the mononuclear and dendritic cell populations in the epidermis and dermis. The majority of T cells were activated CD8+ cells. CONCLUSIONS: Immunophenotyping of the inflammatory infiltrate in these patients is consistent with a pattern of immune dysregulation seen only in earlier stages of HIV-1 disease. Thus, PLEVA may be useful as a marker of early to midstages of HIV-1 disease.

Hyaluronidase enhances the therapeutic effect of vinblastine in intralesional treatment of Kaposi's sarcoma. Military Medical Consortium for the Advancement of Retroviral Research (MMCARR).

BACKGROUND: Although intralesional vinblastine has been used with some success in the treatment of cutaneous lesions of Kaposi's sarcoma (KS), lesions commonly recur. When large lesions are treated, frequently there is considerable discomfort and, in some cases, secondary ulceration. Hyaluronidase has been used to increase dispersion of drugs administered by local injection. OBJECTIVE: Our purpose was to determine whether intralesional hyaluronidase administered before intralesional vinblastine increases the dispersion of vinblastine and decreases toxicity. METHODS: We treated six patients who had multiple cutaneous plaque lesions and tumors of KS with intralesional vinblastine, intralesional vinblastine preceded by intralesional hyaluronidase, or intralesional hyaluronidase alone. RESULTS: Both intralesional vinblastine and intralesional vinblastine preceded by intralesional hyaluronidase caused clinical regression of lesions of KS; however, the combination of hyaluronidase and vinblastine was more effective in treating tumor nodules. In addition, lesions treated with hyaluronidase and vinblastine recurred less often than those treated with vinblastine alone and showed no evidence of residual KS in two patients undergoing biopsy between 4 and 6 months after therapy. CONCLUSION: Intralesional hyaluronidase enhances vinblastine in the treatment of cutaneous lesions of KS without adding to the systemic toxicity.

Measurement of CD69 induction in the assessment of immune function in asymptomatic HIV-infected individuals.

Peripheral blood mononuclear cells from many asymptomatic HIV-infected patients exhibit defects in cytokine production and impaired proliferative responses in vitro but the mechanisms underlying this subclinical immune deficiency are controversial. To determine whether abnormalities in the earliest events following receptor engagement may help to explain the in vitro immune dysfunction, we measured the inducibility of the early activation marker CD69 in T cells from asymptomatic HIV-infected individuals in response to stimulation with anti-CD2 or anti-CD3 mAb. In a whole blood assay, we found that induction of CD69 was markedly impaired in CD4+ T cells from later-stage HIV-infected patients (CD4 counts 200-400/mm3) compared to uninfected controls. Among early stage patients (CD4 > 400/mm3), a subset (29%) had impaired CD69 induction. CD69 responses were equally depressed after stimulation through the CD3 or CD2 receptor pathways. Survey of a panel of immunophenotypic markers and propensity for apoptosis demonstrated a significant association between depressed induction of CD69 and decreased percentages of CD4+CD26+ and CD4+CD95+ cells but no association with the level of apoptosis. These data indicate that defects in T lymphocyte activation through CD3 and CD2 can be measured within hours of receptor stimulation in asymptomatic HIV-infected individuals and might be useful to monitor as an indicator of immune function in these patients.

Preservation of allergic contact dermatitis to poison ivy (urushiol) in late HIV disease. The implications and relevance to immunotherapy with contact allergens.

BACKGROUND: Delayed hypersensitivity reactions (DTH) are lost with progression of HIV disease. This loss of DTH commonly occurs before the onset of opportunistic infections and is an independent predictor of disease progression. OBJECTIVE: We wanted to determine whether patients in late HIV disease with a history of allergic contact dermatitis (ACD) to poison ivy continue to react to poison ivy. METHODS: Twelve HIV+ patients with a past history of ACD to poison ivy were tested with an extract prepared from poison ivy leaves. All but 1 patient had CD4+ T cell counts < 200/microliters, and 5 patients had had an opportunistic infection. RESULTS: All 12 patients showed positive reactions ranging from mild erythema and infiltration to marked erythema with bulla formation. CONCLUSIONS: ACD is considered a variant of DTH, and as DTH results in a T helper 1 cytokine pattern. However, the antigen-specific effector cells in ACD may be more diverse than in DTH. This diversity could explain the continued reaction to some contact allergens in late disease and may be important in the use of contact allergens for immunotherapy.