Search PubMed⌕ Search

Biomedical subjects

D Milo

Publications and source records attributed to D Milo.

At least 19 recordsLinked to original sources
PubMed1997

[Azithromycin combined with pyrimethamine in the treatment of neurotoxoplasmosis, in an AIDS patient].

We report one case of successful treatment of cerebral toxoplasmosis in acquired immunodeficiency syndrome (AIDS) with azithromycin combined with pyrimethamine. Toxoplasmic encephalitis had been diagnosed on the basis of multiple lesions exhibiting ring like contrast enhancement on double contrast Computed Tomographic (CT) scan of the brain. Thereby our patient had been treated with pyrimethamine 25 mg/die, after an attack dose of 100 mg in the first day, and clindamycin 2400 mg/die, because of sulfa-drug allergy, but clindamycin had to be discontinued because of rash development. At this point azithromycin, at a dose of 1000 mg/die for 21 days and 1500 mg a week for the following 50 days of follow-up, was added to pyrimethamine. Follow-up CT scan after 20 days of treatment (10 with clindamycin+pyrimethamine and 10 with azithromycin+pyrimethamine) revealed partial resolution of the brain lesions and subsequently (after 50 and 80 days of treatment) complete resolution.

AIDS-Related Opportunistic Infections↗
PubMed1995

Use of furazolidone for the treatment of microsporidiosis due to Enterocytozoon bieneusi in patients with AIDS.

The efficacy of furazolidone for treatment of intestinal microsporidiosis due to Enterocytozoon bieneusi was studied in three patients with AIDS. All patients had chronic diarrhoea and weight loss. Mean CD4 cell count was 34.6/mm3. A course of furazolidone (100 mg orally four times a day) was given for 20 days. The drug was well tolerated and neither side effects nor alterations in the laboratory parameters were noted. Diarrhoea ceased within a mean of 12 days of starting treatment and clearance of microsporidian shedding in stool was observed. In one of the patients, however, symptomatic microsporidiosis recurred. Therefore furazolidone seems to have a transient but significant effect on intestinal infection due to Enterocytozoon bieneusi.

Acquired Immunodeficiency Syndrome↗
PubMed1994

Combined antineoplastic and antiretroviral therapy for patients with Hodgkin's disease and human immunodeficiency virus infection. A prospective study of 17 patients. The Italian Cooperative Group on AIDS and Tumors (GICAT).

BACKGROUND: The optimal therapeutic approach for patients with Hodgkin's disease (HD) and human immunodeficiency virus (HIV) infection is unknown. In an attempt to improve the results obtained with standard chemotherapy and to decrease the occurrence of opportunistic infections (OI) during chemotherapy and follow-up observed in a previous experience, the authors designed a prospective combined antineoplastic and antiretroviral approach. METHODS: Between March 1989 and March 1992, 17 consecutive previously untreated patients (median age, 30 years) with HD and HIV infection were enrolled. They had Stage III and IV or Stage I and II disease with adverse prognostic factors. The median CD4+ cell count was 184/microliters. Patients were stratified in two groups and treated accordingly. Group A was made up of patients with an Eastern Cooperative Oncology Group (ECOG) performance status (PS) of less than 3 and without OI. These patients received epirubicin 70 mg/m2 intravenously on day 1, bleomycin 10 mg/m2 IV on day 1, and vinblastine 6 mg/m2 IV on day 1 (regimen EBV). Group B was made up of patients with PS of 3 or greater or previous OI who had received a 50% reduced dose of epirubicin and vinblastine and a full dose of bleomycin. Courses were repeated every 21 days for six cycles. Zidovudine was given at the dose of 500 mg/day from the beginning of chemotherapy in Group B and after the third cycle in Group A. RESULTS: Overall, 14 of 17 (82%) patients had an objective response and 9 of 17 (53%) achieved a complete remission (CR) of disease for a median duration of 20 months. Toxicity was moderate with Grade 3-4 leukopenia in eight patients and Grade 3 thrombocytopenia in one patient. Thirteen of 17 patients received zidovudine as planned with a median duration of 9 months. Only one patient had OI during or after chemotherapy (median follow-up, 11 months). No worsening of HIV markers during the combined therapy was seen, with the median CD4+ cell count before and after therapy being 184/microliters and 203/microliters, respectively. The median survival time was 11 months, with an actuarial survival rate of 48% at 36 months. The median survival time for the nine patients with CR has not been reached at the time of this analysis. CONCLUSIONS: These results revealed the feasibility and the activity of the combination of EBV regimen and zidovudine. Objective response rate seems similar to those previously observed in patients receiving standard chemotherapy, but only one patient had OI, and this compares favorably with the 16 OI observed in 28 patients treated with standard chemotherapy (6% versus 57%) in the authors' previous experience. Thus, it seems that the addition of antiretroviral therapy to the EBV regimen decreased the occurrence of OI during chemotherapy or follow-up.

Adult↗
PubMed1993

White lichenoid lesions of the buccal mucosa in patients with HIV infection.

We report on eight patients who developed white lichenoid lesions of the buccal mucosa during the course of human immunodeficiency virus infection. In five patients the lesions appeared after the administration of zidovudine, in two after the intake of both zidovudine and ketoconazole, and in one after ketoconazole. In the majority of cases, lesions presented as bilateral reticular keratosis or atrophic changes of the buccal mucosa. Three patients manifested lichenoid atrophic changes of the dorsum of the tongue. The histopathologic features were hyperkeratosis, epithelial atrophy, basal cell liquefaction, and the presence in the lamina propria of either a patchy or diffuse lymphocytic infiltrate. All specimens tested negative for Epstein-Barr virus and human papillomavirus. Our study suggests that lichenoid lesions of the buccal mucosa, similar to what has been described as lichenoid drug reactions or idiopathic lichen planus, can be observed during human immunodeficiency virus infection and that administration of zidovudine and ketoconazole should be considered as a possible cause.

Adult↗
PubMed1992

Hairy leukoplakia with involvement of the buccal mucosa.

Oral hairy leukoplakia occurs mainly on the tongue of human immunodeficiency virus (HIV)-infected persons. An HIV-infected patient with hairy leukoplakia involving the tongue and buccal mucosa was studied by light and electron microscopic methods, in situ hybridization, and polymerase chain reaction. Our findings indicate that hairy leukoplakia may involve the buccal mucosa and should be considered in the differential diagnosis of white oral lesions in HIV-positive patients. Epstein-Barr virus particles were found in the epithelial cells of both buccal and tongue mucosa.

Adult↗
PubMed1992

[Isosporiasis and sarcocystosis. The current findings].

A review on infections by Isospora belli and Sarcocystis spp. both in healthy and in AIDS patients is done on the basis of literature and personal data. In this view a special focus is made on isospora belli infection in AIDS because of its high recurrence after successful attack therapy. Consequently the most recent protocols for maintenance and attack therapy in these patients are reported. At the end, concerning ultrastructural pathology, the features of some Isospora belli developing stages are described by means of electron microscopy on duodenal biopsy specimens from a patient.

AIDS-Related Opportunistic Infections↗
PubMed1991

In vitro infection with HIV enables human CD4+ T cell clones to induce noncognate contact-dependent polyclonal B cell activation.

Eleven (nine CD4+ and two CD8+) protein purified derivative-specific and eight tetanus toxoid-specific T cell clones (TCC), established from the peripheral blood of healthy persons, were cocultured in vitro with irradiated mononuclear cells from patients infected by HIV in the presence of PHA and polybrene. Two weeks post-HIV exposure, all 17 CD4+, but neither of the two CD8+, TCC exhibited integration of HIV in their genoma, as detected by polymerase chain reaction analysis, and released HIV into their supernatants, as detected by measuring both reverse transcriptase activity and p24 Ag. When co-cultured with either autologous or allogeneic B cells, all CD4+ HIV-infected TCC induced the synthesis of extraordinarily high amounts of IgM, IgG, and IgA. In contrast, their noninfected counterparts could provide helper function for Ig synthesis by autologous B cells only in the presence of the specific Ag (or anti-CD3 antibody), and induced allogeneic B cells to synthesize Ig only upon stimulation with anti-CD3 antibody. The supernatants of HIV-infected TCC failed to stimulate Ig synthesis in B cells. More importantly, when HIV-infected clonal T blasts and B cells were cultured in different chambers separated by a millipore membrane, permeable to molecules but not to cells, Ig synthesis did not occur. The Ig synthesis induced by HIV-infected TCC was also markedly inhibited by the addition in culture of either anti-CD4 or anti-LFA-1 antibody. In contrast, HIV-infected TCC maintained their ability to provide helper function for Ig synthesis in the absence of any stimulus, even after fixation with p-formaldehyde. These data demonstrate that in vitro infection with HIV enables human T cells to stimulate Ig synthesis by B cells by an Ag-nonspecific, MHC-unrestricted, contact-dependent mechanism. This may explain, at least in part, the hypergammaglobulinemia and other phenomena related to polyclonal B cell activation frequently seen in HIV-infected persons.

B-Lymphocytes↗
PubMed1990

Morphology and membrane antigens of nonlymphoid accessory cells in oral hairy leukoplakia.

We have investigated the features and distribution of accessory cells (ACs) and the relationship of these cells to each other and to lymphocytes in the epithelium and lamina propria of oral hairy leukoplakia (HL), with the objective of better defining the differentiation and mutual interactions of immune-response cells within HL as a preliminary step to understanding the onset and significance of this lesion during human immunodeficiency virus (HIV) infection. Twenty-four HIV-infected patients with HL, two asymptomatic HIV-positive subjects, and three HIV-negative subjects were studied by immunohistochemistry; five HIV-positive patients with HL and three asymptomatic HIV-positive subjects were studied by electron microscopy. In both the epithelium and the lamina propria of HL, we found cells with the immunohistochemical and ultrastructural features of variably differentiated ACs; differences were found between the epithelium and lamina propria. In the lamina propria, ACs were characterized by dendritic shape, multiple contacts with lymphocytes, expression of CD1a antigen, and ultrastructural features of fully differentiated ACs. Conversely, in the epithelium ACs showed bluntly dendritic shape, low expression of CD1a, absent expression of HLA-DR, constant expression of CD11c and CD14 antigens, only occasional contacts with lymphocytes, and ultrastructural features of variably, but always incompletely, differentiated cells of monocyte-dendritic lineage. Seventy-nanometer wide intracisternal particles, closely resembling A particles described in retroviral infections, were found in the intraepithelial ACs in two patients with HL. The defective differentiation of ACs in the epithelium of HL--possibly influenced by the perturbation of the epithelial microenvironment induced by Epstein-Barr virus, and following the direct HIV infection of these cells--and the exceptional finding of close contacts with lymphocytes suggest that the lesional epithelium of HL may constitute a pathway for the entry of foreign antigens which circumvent monitoring by ACs and can induce immune tolerance. The impairment of the local immune response in HL may contribute to the development of full blown, systemic immunodeficiency.

Acquired Immunodeficiency Syndrome↗
PubMed1990

[Pseudo-Whipple disease caused by atypical mycobacteriosis in AIDS: a clinical and electron microscopic study of 2 cases].

The Authors focus on two cases, studied by electron and light microscopy, of Whipple-like disease caused by atypical mycobacteria in AIDS. Differential characteristics between the cases and classical Whipple's disease are analyzed with regard to the diagnostic and therapeutical peculiarities of Mycobacterium avium-intracellulare infection which accounts for over 80% of atypical mycobacterial infections in AIDS. In this regard the Authors stress the role of histological findings of pale blue striated histiocytes as a marker of Mycobacterium avium-intracellulare infection.

Acquired Immunodeficiency Syndrome↗
PubMed1990

Neurological involvement in group iv HIV-positive patients. Neurophysiological and clinical data.

Spinal and cortical SEP responses were recorded during tibial and median nerve stimulation in 58 HIV+ subjects (8 IV/C1, 24 IV/C2 & IV/A, 11 III and 15 II), all asymptomatic from a neurological point of view. The electrophysiological features were compared with clinical assessment and serum HIV markers for purposes of prognosis and therapy. In group IV we observed a slowing of conduction along the afferent pathway in the spinal tracts and afferent ways to the cortex. The major part of the delay occurred in the mid and lower medullary tract. These results agree with neuropathological finding from post-mortem examination in AIDS pts.

Acquired Immunodeficiency Syndrome↗
PubMed1989

Campylobacter laridis bacteraemia in an AIDS patient.

The likely first case of Campylobacter laridis bacteraemia in AIDS is reported. Microbiological, epidemiological and clinical characteristics of C. laridis human infection are also described.

Acquired Immunodeficiency Syndrome↗
PubMed1988

Oral hairy leukoplakia among HIV-positive intravenous drug abusers: a clinicopathologic and ultrastructural study.

During a prospective investigation of oral lesions of 120 consecutive patients positive for human immunodeficiency virus, belonging to the intravenous drug abuser risk group and other risk categories, we observed hairy leukoplakia (HL) in 23 cases (19%). The median age of the patients was 27 years (range, 20 to 50 years). Twenty patients were men and three were women. All but two of the twenty three patients used intravenous drugs for a median period of 6 years (range, 5 to 18 years) and were involved in several episodes of needle sharing. Eight men were also bisexual, one man was homosexual, and one man was hemophiliac and bisexual. Eleven patients had asymptomatic infection, five had lymphadenopathy syndrome, six had AIDS-related complex, and one had acquired immunodeficiency syndrome. In all patients, HL lesions were localized on the lateral borders of the tongue. In twelve patients, the lesion was unilateral, and in eleven patients, it was bilateral. Microscopically, hyperparakeratosis and the presence of koilocytes were observed in all cases. Surface candidiasis could be detected with staining with periodic acid-Schiff in two thirds of the cases. In four cases, electron microscopy showed the presence of intracellular and extracellular hyphae of Candida albicans in the parakeratin layer associated with coccobacilli in the spaces between surface epithelial cells. The spinous layer included koilocytes, which had a clear cytoplasmic matrix, sparse organelles and tonofilaments, and dispersed chromatin. These cells were found to be infected by a herpes-type virus in all cases examined. There was no ultrastructural evidence of human papillomavirus in the nuclei of the epithelial cells.(ABSTRACT TRUNCATED AT 250 WORDS)

AIDS-Related Complex↗
PubMed1987

Diminished production of interleukin 2 and gamma-interferon by cloned "T" cells from patients with the acquired immunodeficiency syndrome (AIDS).

A total of 76 T-cell clones established from peripheral blood (PB) of 2 patients with the acquired immune deficiency syndrome (AIDS) and of 141 T-cell clones established from PB of 3 normal donors were compared for their ability to produce interleukin 2 (IL-2) and gamma-interferon (gamma-IFN). Twenty-seven clones from AIDS patients and 85 clones from controls expressed the CD4 phenotype, whereas 49 clones from AIDS patients and 56 clones from controls expressed the CD8 phenotype. There were no significant differences in the proportions of IL-2-producing CD4 T-cell clones established from PB of patients with AIDS and controls, but the mean concentration of IL-2 produced by CD4 clones from AIDS patients was significantly lower than that produced by CD4 clones from controls. Both the proportion of gamma-IFN-producing CD4 clones and the mean concentration of gamma-IFN produced by CD4 clones were significantly lower in AIDS patients than in controls. In contrast, there were no differences between AIDS patients and normal individuals in the proportion of IL-2- or gamma-IFN-producing CD8 clones, or in the mean concentration of IL-2 and gamma-IFN produced by CD8 clones. These data suggest that the reduced ability of PB T-cells from patients with AIDS to produce IL-2 and gamma-IFN is not simply due to altered proportions or numbers of T-cell subpopulations, but also reflects intrinsic abnormalities of individual CD4 T lymphocytes.

Acquired Immunodeficiency Syndrome↗
PubMed1987

Reduced production of interleukin 2 and interferon-gamma and enhanced helper activity for IgG synthesis by cloned CD4+ T cells from patients with AIDS.

Purified T lymphocytes (E rosetting cells) isolated from peripheral blood (PB) of four patients with acquired immune deficiency syndrome (AIDS) were cloned under culture conditions (phytohemagglutinin plus interleukin 2) which allow clonal expansion of most T lymphocytes. A total number of 101 T cell clones (37 CD4+ and 64 CD8+) from PB of AIDS patients and of 188 T cell clones (115 CD4+ and 73 CD8+) from PB of four normal controls were obtained and tested for their helper function as well as for their capacity to release lymphokines. Unstimulated CD4+ TCC from patients with AIDS showed enhanced helper function for IgG synthesis in vitro in both autologous and normal allogeneic B cells in comparison to clonable CD4+ T cells of normal donors. Such activity was further potentiated by addition to the cell cultures of anti-CD3 monoclonal antibody. The majority of CD4+ T cell clones from AIDS patients showed a reduced ability to produce interleukin 2 and interferon-gamma in response to activation with phytohemagglutinin. However, most of them released greater amounts of soluble factor(s) able to promote B cell proliferation of anti-IgM-activated normal B cells and to induce the differentiation of normal B lymphocytes into IgG-secreting cells. These data demonstrate that most surviving CD4+ T cells in PB of patients with AIDS belong to a T cell subset producing B cell growth and differentiation factors, which may contribute to the B cell hyperactivation seen in AIDS patients.

Acquired Immunodeficiency Syndrome↗