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Biomedical subjects

G Costanzi

Publications and source records attributed to G Costanzi.

At least 19 recordsLinked to original sources
PubMed1992

AIDS-defining diseases in 250 HIV-infected patients; a comparative study of clinical and autopsy diagnoses.

OBJECTIVE: To evaluate the correlation between clinical and autopsy findings in 250 AIDS patients. METHODS: Clinical and autopsy diagnoses of AIDS-defining diseases in 250 AIDS patients who died in Milan between May 1984 and February 1991 were compared. RESULTS: Pneumocystis carinii (PCP) and oesophageal candidiasis were the most frequent clinical diagnoses, while cytomegalovirus (CMV) infection was observed in almost half of the autopsies. Forty-seven per cent of the diseases found at autopsy had not been diagnosed during life; CMV infection, mycoses, HIV-specific brain lesions, cerebral lymphomas and progressive multifocal leukoencephalopathy (PML) had a higher rate of non-diagnosis in life. CMV visceral infection accounted for the majority of the diseases not recognized in life. In contrast, clinically diagnosed PCP, oesophageal candidiasis and, to a lesser degree, brain toxoplasmosis were often not found at autopsy, possibly indicating a significant rate of recovery and prevention of relapse. Finally, bacterial pneumonia and sepsis, although not AIDS indicator diseases, were observed in approximately one-third of the autopsies. CONCLUSION: Considerable differences in the frequency and type of the AIDS-defining diseases diagnosed during life and at post mortem were found.

AIDS-Related Opportunistic Infections↗
PubMed1992

Hypophyseal pathology in AIDS.

One hundred and eleven pituitary glands of patients (93 males, 18 females; mean age 32 years, 5 months) who died of fully developed AIDS or ARC were examined under light microscopy with the aid of immunohistochemistry. On post mortem (p.m.) examination a wide series of multiorgan alterations was noticed. Microscopically various lesions in both adeno- and neurohypophysis were seen. These ranged from vessel damage to secondaries to systemic infections, neoplasms and functional derangements. Necrotic lumps due to recent infarction could appear in both parts of the gland, while old fibrous scars sustained a previously overcome necrosis. Different pathogens (mainly fungi) could be seen either within the gland or arising from its meningeal surroundings. Examples of tumour pathology were provided by microadenomas, gliosis/gliomas; the frequency of adenomas (11.7%) was similar to that typical of senility. The functional impairment was mainly connected with ACTH cell hyperplasia, which seems in keeping with corticoadrenal or ACTH-receptor damage.

AIDS-Related Complex↗
PubMed1990

High frequency of Epstein-Barr virus genome detection in Hodgkin's disease of HIV-positive patients.

Lymph nodes obtained from 7 HIV-positive and 20 HIV-negative patients with Hodgkin's disease were examined for the presence of Epstein-Barr virus antigens and genome. EBV antigens were observed in only 2 out of 20 HIV-negative patients, whereas lymph nodes of HIV-positive patients did not reveal evidence of EBV antigens. By in situ hybridization and Southern blot analysis, EBV genome was found in 5 out of 7 HIV-positive patients; the EBV genome was detected in the nucleus of Reed-Sternberg and Hodgkin's cells. EBV DNA was observed by in situ hybridization and Southern blot analysis in only 3 out of 20 HIV-negative patients with Hodgkin's disease. In both groups, Reed-Sternberg and Hodgkin's cells were negative for C3d EBV receptor. Our results show a statistically significant increased expression of EBV DNA in HIV-positive patients with Hodgkin's disease, as compared with HIV-negative patients with HD.

Adolescent↗
PubMed1989

Cell association of HIV in AIDS-related encephalopathy and dementia.

The presence of HIV gag and env proteins (HIV Ag) and virus replicating cells was studied by immunohistochemistry and in situ hybridization, respectively, in brain specimens from five HIV infected patients. HIV antigens were detected in 3 of 5 brains in micronodular areas characterized by increased cellularity and the presence of multinuclear giant cells. By double immunostaining, HIV Ag positive cells were shown to express markers common to macrophages and microglia i.e. Leu M5+, My4+, HLA-Dr+, RCA-1+, and to a lesser extent CD4+ (Leu3+). Another macrophage specific marker, KiM6, was found only on HIV+ cells in HIV infected specimens and not in uninfected, control brains. Medium-sized, virus replicating cells were found exclusively in micronodular areas, but in much smaller quantities than HIV Ag+ cells. Our observations provide further evidence to support the hypothesis that macrophages play an important role in CNS infection by HIV and additionally support the concept that reactive microglial originate from activated macrophages infiltrating the brain. Both direct effects of viral components and cell mediated reactions can be implicated from our findings as mechanisms involved in the pathogenesis of the CNS lesions.

Acquired Immunodeficiency Syndrome↗
PubMed1989

Morphogenesis, evolution and prognostic significance of lymphatic tissue lesions in HIV infection.

Morphological changes in lymph node biopsies of HIV-infected patients can be classified in four stages, based upon the degree of damage to follicular structures: (1) follicular hyperplasia, (2) follicular lysis, (3) follicular atrophy and (4) follicular and lymphocytic depletion. To define the relative usefulness of morphological, clinical and immunological findings for prognostic purposes, we followed the clinical evolution of 86 biopsied HIV+ patients for a period ranging from 1 to 56 months. A relatively good correlation between histological and clinical findings, at the time of biopsy, was observed. Statistical analysis confirmed the prognostic value of the histological features for clinical deterioration, progression to AIDS and survival. Moreover, histological findings gave more reliable prognostic information than clinical values. Our data suggest that lymph node biopsy can be utilized for prognostic purposes in the evaluation of the progression of the disease and effectiveness of antiviral therapeutic trials.

Acquired Immunodeficiency Syndrome↗
PubMed1989

HIV encephalopathy and lymphadenopathy: cells associated with viral antigens.

HIV associated subacute, micronodular encephalitis and lymphadenopathy were compared with regard to demonstrable HIV antigens and characterization of HIV antigen expressing cells. In the brain, both gag- and env-coded antigens were confined to cells of micronodular lesions with immunophenotype of monocyte/macrophages (KiM6+, 9.4+, CD4+/-). The micronodular lesions were also infiltrated by some lymphoid cells, predominantly CD8+. In lymphadenopathic nodes, gag-encoded antigens were demonstrable almost exclusively in follicles/germinal centres in association with follicular dendritic cells, whereas env-antigens usually were not found. Follicular involution was related to destruction of follicular dendritic cells and infiltration of CD8+ lymphocytes within the germinal centres. During follicular involution, HIV-gag antigens diminished in parallel with destruction of the network of dendritic reticulum cells. These findings indicate important tissue related differences in HIV expression. In addition, a possible participation of CD8+ cells in the pathogenesis of HIV induced tissue lesions is suggested.

AIDS-Related Complex↗
PubMed1988

Monoclonal antibodies to the human immunodeficiency virus p18 protein cross-react with normal human tissues.

The immunohistochemical reactivity of four monoclonal antibodies (MAbs): CVK, 49-5, 49-6 and 63-FH2, raised against the p18 protein of HIV-1 was assessed in tissues obtained from HIV-infected and uninfected individuals. As already reported, all the MAbs specifically labelled follicular dendritic cells (FDC) in lymph nodes from HIV-infected patients with lymphadenopathy, and cells of microglial nodules in the brain from patients with AIDS-related encephalopathy. However, cross-reactivity with normal uninfected tissues was also observed: epithelial cells of the skin, the thymus and tonsils with CVK, and astrocytes in the brain of 49-6 and 63-FH2. Such cross-reactivities suggest that 'molecular mimicry' could exist between p18 of HIV and normal constituents of human cells. This phenomenon could be relevant for the diagnostic use of anti-p18 MAbs on pathological specimens, and it could be of importance in the pathophysiology of HIV infection.

Antibodies, Monoclonal↗
PubMed1987

Brain pathology induced by infection with the human immunodeficiency virus (HIV). A histological, immunocytochemical, and electron microscopical study of 100 autopsy cases.

Neuropathological examination of brain tissue of 100 patients with infection by the human immunodeficiency virus (HIV), including 98 with clinically manifest acquired immune deficiency syndrome (AIDS), revealed distinct multifocal-disseminated and diffuse brain tissue lesions, which can be regarded as HIV-induced brain lesions: multifocal giant cell encephalitis (MGCE; 4) and progressive diffuse leukoencephalopathy (PDL; 25). These lesions were found in 38 brains, and in 17 in absence of infectious, necrotizing or inflammatory changes of other types. In 13 brains, a combination of MGCE with PDL was seen, suggesting a spectrum of HIV-induced brain lesions. MGCE is characterized by perivascular accumulations predominantly of rod cells, monohistiocytes and macrophages, all of which are strongly labeled with a monoclonal antibody to macrophages. Most conspicuous are multinucleated giant cells which are also labeled by anti-macrophage antibody, and which can be regarded as evidence of the local presence of HIV, as confirmed by electron microscopical detection of HIV particles in four MGCE brains, and by immunocytochemical detection of HIV proteins in two MGCE brains. PDL is characterized by a triad: diffuse myelin loss, astroglial proliferation, and infiltration by mono- and multinucleated macrophages. HIV-induced lesions can be morphologically differentiated from histopathological brain lesions known in immunosuppression, including what is called here nodular encephalitis ["subacute encephalitis" of the literature, in most cases attributable to cytomegalovirus (CMV) or toxoplasmosis], by their characteristic histopathology including the hallmark presence of multinucleated giant cells, by direct immunocytochemical and electron microscopical demonstration of HIV in the lesions, and by the absence of opportunistic agents (bacteria, fungi, Toxoplasma, CMV, HSV or papovaviruses). Diffuse poliodystrophy (diffuse proliferation of astroglia with swollen nuclei, occasionally minor neuronal loss and rod cell proliferation) was found in the cerebral cortex and other gray matter in half of all brains, including cases with gyral atrophy, and may be another correlate of HIV damage to the brain. Morphological delineation of HIV-induced brain lesions is a necessary prerequisite for a meaningful clinical definition of HIV-induced cerebral disease.

Acquired Immunodeficiency Syndrome↗