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Biomedical subjects

W Rozenbaum

Publications and source records attributed to W Rozenbaum.

At least 109 records · Page 6Linked to original sources

Acute renal failure induced by foscarnet: 4 cases.

Foscarnet (FC) is a new antiviral agent which has been recently proposed for the treatment of severe cytomegalovirus (CMV) infections in immunocompromised patients. When used intravenously (i.v.), main adverse effects of FC are a fall in hemoglobin, and an increase in liver enzymes and serum calcium. Although increased serum creatinine have been noted in several patients, deterioration of renal function is often accounted for by the concomitant use of other nephrotoxic drugs, the severity of underlying disease or the presence of graft rejection. Consequently FC is often considered as a non or poorly nephrotoxic drug. We report 4 cases of acute renal failure (ARF) which can be exclusively attributed to FC. FC was used for CMV chorioretinitis in 3 AIDS patients and in one non-immunocompromised patient. ARF was diagnosed between the 6th and 15th day of treatment, with oligoanuria in two patients (one of whom required two hemodialysis periods). ARF was most likely secondary to acute toxic tubulopathy. Three patients did not receive any other nephrotoxic drug. The fourth patient received concomitantly sulfadiazine but renal function returned to baseline value after FC completion although sulfadiazine was continued. In conclusion, our 4 observations suggest that FC may be responsible for acute tubulopathy. We suggest that in these patients renal function should be carefully monitored and dehydration promptly corrected to limit the risk of nephrotoxicity.

Acquired Immunodeficiency Syndrome↗

Prognostic value of blood and bone marrow T-colony-forming cells (T-CFC) in patients with lymphadenopathy syndrome (LAS).

The in vitro proliferation capacity of peripheral blood committed T-cell precursors (T-CFC) from LAS patients was studied in order to define whether this parameter could be associated with transition to AIDS. In all patients a significantly (P less than 0.0001) decreased plating efficiency was detected. However, the lowest T-cell colony growth (less than 50 colonies/5 x 10(4) cells) was observed in the 23 patients who subsequently developed the full-blown disease within 150-570 days. Conversely, only one patient (n = 107) whose T-CFC generated greater than 50 colonies/5 x 10(4) cells developed AIDS after a mean follow-up of 867 days (range 120-1260 days). T-CFC from these patients displayed an impaired in vitro differentiation and self-renewal capacity which was independent of the clinical evolution of the disease. In 5 out of 12 AIDS patients, adherent cell-depletion of peripheral blood mononuclear cells (PBMC) enhanced the plating efficiency. Moreover, patients' but not normal adherent cells could inhibit normal T-cell colony growth in a dose-dependent manner. Media conditioned by patients' unstimulated adherent cells (LCM-A+p) also inhibited normal T-cell colony formation. In addition, LCM-A+p were capable of inhibiting interleukin 2-receptor (IL 2-R) expression and interleukin 2 (IL 2) production by normal mitogen-stimulated T-cells. These findings suggest that adherent cell-derived inhibitory activity(ies) could be responsible for the low T-cell colony formation observed in some AIDS patients.

AIDS-Related Complex↗

[Psychosocial consequences of HIV infection].

A questionnaire survey of 103 patients of the Paris Pitié-Salpêtrière Hospital measures the changes in family life, work relations and in sexual behaviour occurring after an HIV infection diagnosis. Most patients choose to keep their diagnosis secret, an attitude that places them into a double bind situation. This silence, chosen as a mean of self-protection, prevents patients from making themselves understood and from mobilising the material and psychological help they need.

Acquired Immunodeficiency Syndrome↗

Decreased expression of the C3b/C4b complement receptor (CR1) in AIDS and AIDS-related syndromes correlates with clinical subpopulations of patients with HIV infection.

Expression of the C3b/C4b receptor (CR1) was studied on erythrocytes of 153 individuals infected with HIV and 104 age-matched normal individuals by measuring the uptake of 125I-labelled monoclonal anti-CR1 antibody. The mean number of CR1 sites on erythrocytes of asymptomatic seropositive individuals (822 +/- 270; mean +/- s.d.) and of patients with persistent generalized lymphadenopathy (PGL; 775 +/- 320) did not differ significantly from that of normal subjects. The number was significantly lower in patients with AIDS-related complex (ARC; 543 +/- 233; P less than 5 x 10(-3)) and further decreased in patients with AIDS (442 +/- 271; P less than 1 x 10(-4)), whether they presented with Kaposi's sarcoma (KS) or opportunistic infections. An additional finding was that of decreased expression of antigenic and functional CR1 in neutrophils from patients with AIDS, as assessed by radioimmunoassay of CR1 in detergent-solubilized cells and the capacity of intact cells to form rosettes with C3b-coated erythrocytes. Low numbers of CR1 on cells from patients with AIDS were not due to occupation of the receptor by C3 fragments on immune complexes. The correlation that was observed between decreased numbers of CR1 on erythrocytes and clinical subpopulations of symptomatic HIV-infected patients suggests that CR1 expression on erythrocytes may represent a valuable marker of the severity and natural history of HIV-associated disease.

AIDS-Related Complex↗

[Neuropathological study of 31 cases of acquired immunodeficiency syndrome].

Post-mortem study of every patient who died from AIDS in Pitié-Salpêtrire Hospital from June 1984 to November 1985 was performed without regard to the presence of neurological signs and symptoms. Autopsy were performed in 31/48 cases. Patients had been hospitalized in the Departments of Parasitology-Infectious Disease (24 cases) Internal Medicine (4 cases) and Neurology (3 cases). In every case, formalin-fixed material from the brain and the spinal cord were embedded in paraffin (20 samples), stained with hematoxylin-eosin, PAS, Alcian blue, Giemsa, Grocott and Ziehl techniques and Bodian's silver impregnation along with Luxol fast blue, and, in celloïdin (8 samples), stained with hematoxylin-eosin and Loyez' impregnation. There were 30 men (27 caucasian, 1 egyptian, 1 haïtian, 1 senegalese) and one woman (congolese). Twenty eight (28) patients were homosexuals. AIDS was transfusion-associated in two cases. Neurologic complications revealed the disease in 2 cases. Eighteen (18) patients had neurological signs or symptoms before death. Age range at death was 22-58 (mean 38). Brain weight in AIDS (from 1150 gms to 1750 gms-mean 1428 gms) was not statistically different from the mean weight of 100 male patients in the same age range autopsied in the same laboratory during the identical period (mean 1427 gms, standard deviation: 23). Microscopic abnormalities were present in every brain examined. These included non-Hodgkin lymphoma (3 cases), opportunistic infections (21 cases: 13 toxoplasmosis, 4 cytomegalovirus encephalitis, 3 cryptococcal meningitis, 1 infection by mycobacterium avium-intracellulare), and subacute encephalitis (17 cases, 9 isolated, 8 associated with other disorders). The characteristic changes consisted of lympho-monocytic focal infiltrates (so-called microglial nodules) and mild lympho-monocytic perivascular cuffs in 10 cases. Typical giant cells were seen only in one case. Mild demyelinating changes were also seen in only one case. No spinal cord spongiosis, nor Progressive Multifocal Leukoencephalopathy was found. HIV localization was performed on frozen sections utilizing in situ hybridization techniques (2 cases) and immunohistologic techniques (5 cases). HIV, RNA and proteins, was detected in 2 cases with subacute encephalitis. Infected cells were labeled with macrophage markers, and rarely with T4 lymphocyte markers. Infected astrocytes (identified by anti-GFAP serum) or neurons (identified by anti-NSE serum) were never observed. No giant cells were seen in these two cases.

Acquired Immunodeficiency Syndrome↗

AIDS and lymphadenopathy syndrome (LAS) patients display similar abnormal in vitro proliferation and differentiation of T-colony forming cells (T-CFC).

T-cell colonies were generated from the peripheral blood and bone marrow of 61 patients with acquired immunodeficiency syndrome (AIDS), 54 patients with persistent lymphadenopathy syndrome (LAS), 14 clinically normal male homosexuals, and 17 healthy heterosexuals. Mononuclear cells were cultured in methylcellulose in the presence of IL2-containing conditioned medium. The number of T-cell forming cells (T-CFC) from healthy male homosexuals and AIDS and LAS patients was significantly (P less than 0.01) reduced compared to T-CFC from healthy heterosexuals. In AIDS patients, the low colony growth capacity of T-CFC was independent of the presence of either opportunistic infections or Kaposi sarcoma. Twelve LAS patients who subsequently developed AIDS showed the lowest capacity of peripheral blood and bone marrow T-CFC to proliferate. Pooled induced colonies from AIDS and LAS patients and normal homosexuals were composed of immature cells bearing the T3+, T4+, T6+, and T8+ surface phenotype, unlike colonies from normal heterosexuals, which displayed mature cells bearing the T3+, T4+, T6-, and T3+, T8+, T6- surface phenotype. Moreover, most T-CFC from primary colonies had lost their self-renewal capacity. In some AIDS and LAS patients but not healthy homosexuals peripheral blood and bone marrow T-CFC were capable of generating colonies with recombinant IL2 (rIL2) without any other mitogenic stimulation. The rIL2-induced colony growth was abrogated by a monoclonal antibody against the IL2 receptor. These results suggest that early impairment of T-CFC plays a predominant role in the pathogenesis of AIDS.

AIDS-Related Complex↗

AIDS subacute encephalitis. Identification of HIV-infected cells.

Human immunodeficiency virus (HIV) RNA and proteins were detected in the brains of several AIDS patients with subacute encephalitis, by in situ hybridization and immunohistology. The majority of infected cells were mononucleated and bore processes. Using single and double immunohistologic procedures, the authors identified these cells as macrophages. The majority of them had the phenotype of microglial cells (Leu-M3-, CD4-), others were labeled with markers of circulating macrophages (Leu-M3+, CD4+/-). The presence of HIV RNA and proteins in CD4- cells could be explained by depressed CD4 antigen expression, as a result of infection or macrophage tissue differentiation.

Acquired Immunodeficiency Syndrome↗

Abnormal in vitro proliferation and differentiation of T colony-forming cells in patients with lymphadenopathy syndrome.

Patients with acquired immunodeficiency syndrome (AIDS) present impaired colony growth and in vitro differentiation capacity of peripheral blood and bone marrow T colony-forming cells (T-CFC). We show that peripheral blood, bone marrow, and lymph node T-CFC from patients with persistent lymphadenopathy syndrome (LAS), a syndrome that can precede AIDS, displayed similar abnormalities. Indeed, peripheral blood T-CFC generated a low number of colonies in seven out of 12 patients, and almost no colonies were obtained from bone marrow cells of all patients. The simultaneous study of T-CFC from peripheral blood and lymph node mononuclear cells seems to provide a reliable indicator for the risk of developing AIDS. The six patients who developed AIDS displayed extremely low numbers of peripheral blood T-CFC (13 +/- 17 colonies per 5 X 10(4) cells), and in two of them, no colonies could be obtained from lymph node T-CFC. The remaining patients who had not developed AIDS displayed a higher number of peripheral blood T-CFC (141 +/- 113 per 5 X 10(4) cells) and lymph node T-CFC, which, in addition, preserved their clonogenic capacity. In some patients, peripheral blood and lymph node, but not bone marrow, T-CFC were capable of generating colonies in the absence of added growth factors or mitogens, whereas in others, colony formation was obtained with purified interleukin 2 (IL 2) alone. Both spontaneous and IL 2-induced colony formation was abrogated by a monoclonal antibody against the IL 2 receptor. Taken together, these findings suggest that at least some T-CFC expressed IL 2 receptors. Colonies generated either in the presence or in the absence of added growth factors were composed of T4+, T6+, and T8+ cells, indicating impaired in vitro T-CFC differentiation. These findings indicate that a dramatic quantitative and qualitative impairment of the proliferation and differentiation of peripheral blood and lymph node T-CFC precedes the clinical evolution from LAS to AIDS.

Acquired Immunodeficiency Syndrome↗

[Lymphomas and AIDS].

We report 21 cases of lymphomas associated with AIDS. Sixteen cases are Non Hodgkin's lymphomas of high grade malignancy. Immunoblastic B cell lymphomas are frequent: 11 cases/16, especially with extra nodal localisations. Three cases are Burkitt's lymphoma; 2 cases are large non cleaved cell lymphoma. Five cases of Hodgkin's disease are associated with AIDS related complex syndrome (ARC) showing the interest of lymph node biopsy in such patients. We analyzed 6 cases with lymphoid bone marrow infiltration and discuss the relationship between prelymphomatous states and low grade malignant lymphomas in AIDS or ARC patients.

Acquired Immunodeficiency Syndrome↗

[Maxillofacial manifestations of acquired immunodeficiency syndrome].

46 cases of acquired immunodeficiency syndrome permit the authors to detail the particular aspects of the oral and facial lesions in AIDS. In patients at risk, a lymphadenopathic syndrome is thought to represent a prodromic phase of the illness. The authors insist upon the differences between the classic Kaposi's sarcoma and that associated with the AIDS (mean age and initial sites of tumor). One third of these sarcomas is completed by a digestive candidiasis. The review of the literature reveals squamous cell carcinoma and Burkitt's lymphoma with the AIDS. We must be aware of early diagnosis and transmission factors in the individuals at risk with tumors and opportunistic infection.

Acquired Immunodeficiency Syndrome↗

Abnormal in vitro proliferation and differentiation of T colony forming cells in AIDS patients and clinically normal male homosexuals.

T cell colonies were generated from the peripheral blood and bone marrow of 11 patients with acquired immune deficiency syndrome (AIDS), 17 normal male and female heterosexuals and seven clinically normal male homosexuals. Mononuclear cells were cultured in methylcellulose both in the absence and presence of interleukin-2 (IL-2) containing conditioned medium. Clinically normal homosexuals showed a low number of T4+ (P less than 0.01) but not T8+ cells. The number of T cell colony forming cells (T-CFC) from both AIDS patients and homosexuals was significantly (P less than 0.01) reduced compared to T-CFC from normal heterosexuals. In seven and four out of 11 AIDS patients, T-CFC from peripheral blood and bone marrow, respectively, were able to generate colonies in the absence of added growth factors and/or mitogenic stimulation. Pooled spontaneous and induced colonies from AIDS patients as well as induced colonies from normal homosexuals were composed of immature cells bearing the T3+, T4+, T6+ T8+ surface phenotype, unlike colonies from normal heterosexuals which displayed mature cells bearing the T3+ T4+ T6- and T3+ T8+ T6- surface phenotype. Moreover, most T-CFC from primary spontaneous and induced colonies had lost their self-renewal capacity either in the absence or the presence of added growth factors. These results suggest that early impairment of T-CFC may play a predominant role in the pathogenesis of AIDS.

Acquired Immunodeficiency Syndrome↗