[Hepatosplenic tuberculous abscess in acquired immunodeficiency syndrome. Apropos of 2 cases].
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Biomedical subjects
Publications and source records attributed to D Vittecoq.
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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.
Seventeen Caucasian patients with acquired immunodeficiency syndrome (AIDS) contracted after long stays in Africa are reported. Central Africa was concerned in all cases. Men are particularly exposed to AIDS whatever their occupation. This study suggests that the risk of contracting AIDS in Africa is high; the transmission of the virus was related to sexual contact, particularly with prostitutes, in Africa in most of the cases. It suggests also that Caucasians who travel in Africa spread the virus throughout the world by means of their heterosexual relations.
Adherent cells display an important accessory role on normal T-cell colony formation. Since the in-vitro proliferation of T colony-forming cells (T-CFC) from AIDS patients is extremely impaired we studied the effect of patients' adherent cells on T-CFC growth. Patients' peripheral blood mononuclear cells (PBMC) were fractionated on the basis of rosette formation with sheep red blood cells and complement-mediated cytotoxicity with OKT3 monoclonal antibody (E-T3-). Both mature (E+) T cells and E-OKT3- cell fractions failed to generate T-cell colonies although colony growth could be obtained from unfractionated PBMC. In five out of 12 AIDS patients, adherent cell-depletion of 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 inhibit normal T-cell colony formation. In addition, LCM-A+p were capable of inhibiting interleukin 2-receptor (IL2-R) expression and interleukin 2 (IL2) production by normal mitogen-stimulated T cells. These LCM-A+p did not contain detectable reverse transcriptase activity nor could they infect the CEM T-cell line which is permissive to human immunodeficiency virus (HIV). Conversely, this adherent cell-derived inhibitory activity could be abrogated by heating or treatment with proteolytic enzymes. These findings indicate that the low T-cell colony formation in some AIDS patients could be due to adherent cell-derived inhibitory activity(ies).
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The frequency, mode of occurrence, diagnostic criteria and main features of systemic and visceral candidiasis have been evaluated in a retrospective study of all cases managed in St Louis Hospital, Paris, during the [June 1, 1985-May 31, 1986] period. During this one year period 23 patients suffered from systemic or visceral candidiasis and Candida spp. accounted for 9.6% of all positive blood cultures, fourth in number after Enterobacteriaceae, Staphylococcus and Pseudomonas. Abnormal underlying condition was present in all patients, mainly haematologic malignancies, serious abdominal surgery and AIDS. In patients with haematologic malignancies C. tropicalis was the main species involved in contrast with surgical patients in whom the dominant responsible species was C. albicans. No Candida oesophagus was common. Therapeutic regimens included amphotericin B in all patients with systemic disease. We conclude that in an institution mainly oriented toward management of cancer and surgical patients, systemic and visceral candidiasis are common and represent a serious problem.
Systematic autopsy studies of 100 patients with AIDS confirmed a high incidence of adrenal lesions. Eighty eight cases were analysed, 79 men and 9 women; 57 had opportunist infection alone, 6 had Kaposi sarcomas and 30 had an association of both pathologies. The adrenal glands were normal in 19 cases and abnormal in 64 cases. One case has non-specific spongiocytic depletion and 4 were uninterpretable because of necrosis. The main adrenocortical changes were inflammatory (N = 37) or necrotic (N = 22). The commonest sites were in the adrenal medulla in the cortex or at the cortico-medullary junction. There was a high incidence of cytomegalic inclusion bodies (44 cases). In 7 cases specific lesions were observed; cryptococcus (1), toxoplasmosis (1), tuberculosis (2), Kaposi (3). Adrenal insufficiency was diagnosed before death in only 3 cases.
LAV/HTL VIII virus found in 1983, renamed HIV in 1986, is doing with many clinical manifestations among which AIDS is only ultimate one, and the more serious aspect of infection by the virus. At each stage of the disease, oro-facial manifestations can be encountered, often the first one. That emphasises for oral medicine the need of perfect knowledge of these clinical aspects concerning 111 patients, we will describe these clinical aspects and hygienical and preventive precautions we choose.
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.
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The penetration of aztreonam into the cerebrospinal fluid was determined in 16 patients with bacterial meningitis undergoing treatment with other antibiotics. Three aztreonam doses of 30 mg/kg were infused intravenously over 30 to 45 min at 8-h intervals, first between days 2 and 4 and again between days 11 and 20 after onset of the disease. Concentrations of aztreonam in serum and cerebrospinal fluid samples obtained at 60, 90, 120, and 240 min after the third aztreonam dose were measured by high-pressure liquid chromatography. The concentrations of aztreonam in cerebrospinal fluid ranged from 3.5 to 62 micrograms/ml, depending on the sampling time and the time elapsed since the onset of the disease. These concentrations were equal to or higher than the MICs for most of the gram-negative bacilli (including Pseudomonas aeruginosa).
Liver biopsies were systematically performed in 20 patients with evidence of an acquired immunodeficiency syndrome (18 with opportunistic infections, 9 with Kaposi's sarcoma). Hepatitis, related to hepatitis-B virus in 3 cases and to cytomegalovirus in 3 cases, was present in 6 of them. All patients had at least one of the three following lesions: non-specific portal inflammatory infiltration (6 cases), granulomatous lesions (12 cases), vascular abnormalities (12 cases). Among hepatic granulomatous lesions: 3 were due to acid-fast bacilli and 1 to Cryptococcus. Sinusoidal abnormality included proliferation of Küpffer cells (9 cases), sinusoidal dilatation (2 cases), peliosis (4 cases) and Kaposi's sarcoma (1 case). A relationship between these abnormalities cannot be excluded.