Search PubMed⌕ Search

Biomedical subjects

V V Joshi

Publications and source records attributed to V V Joshi.

At least 73 records · Page 4Linked to original sources
PubMed1989

Conduction system in children with acquired immunodeficiency syndrome.

Six children died of acquired immunodeficiency syndrome (AIDS), four of them females, ages 7 months, 13 months, 2 years 8 months, and 4 years; and two of them males, aged 2 1/2 and 7 years. They were born to IV drug-addicted parents. The conduction system (CS) and the entire heart were studied by serial section. In all cases the heart was hypertrophied and enlarged; one had total thrombotic occlusion of the right coronary artery with extensive infarction of the ventricular septum. Vascular changes also were found in all hearts, involving small arteries, arterioles, and venules. In the arteries, they involved the intima, media, and adventitia, and perivascular areas in a degenerative and inflammatory process. The elastic tissue was especially affected. A nonspecific myocarditis was present in four cases and epicarditis in all. Changes in the summit of the ventricular septum were present in four cases, consisting of increased fibrosis and arteriolosclerosis. The CS changes varied in location, showing either vasculitis, myocarditis, or fragmentation of the bundle with lobulation and fibrosis. The changes in the conduction system were not as severe as the changes in the surrounding myocardium. In one case the ECG was abnormal, showing left hemiblock. This corresponded to the finding of fibrosis, vacuolization of cells, and space formation in the left bundle branch.

Acquired Immunodeficiency Syndrome↗
PubMed1988

Dilated cardiomyopathy in children with acquired immunodeficiency syndrome: a pathologic study of five cases.

Clinicopathologic features with special reference to the heart are presented in five fatal cases of acquired immunodeficiency syndrome (AIDS) in children. Three children showed clinical evidence of cardiovascular compromise or congestive heart failure. Autopsy was performed in all cases. The enlarged heart showed biventricular dilatation with grossly unremarkable valves and coronary arteries and absence of mural thrombi. Microscopic examination of the heart revealed primarily myopathic abnormalities with hypertrophy of the myocardium and only rare foci of sparse inflammatory infiltrate. The pathogenesis of dilated cardiomyopathy in these children with AIDS is not known. Infection, immunologic factors, anemia, deficiency of nutritional factor(s), and longer survival may be related to the pathogenesis. Pediatricians should be alert to the possibility of cardiac involvement in pediatric AIDS.

Acquired Immunodeficiency Syndrome↗
PubMed1988

Congenital acquired immunodeficiency syndrome and congenital toxoplasmosis: pathologic support for a chronology of events.

We report a case of congenital acquired immunodeficiency syndrome (AIDS) with congenital opportunistic toxoplasmosis. The thymic histopathology was that seen in childhood AIDS cases and not that seen in primary congenital toxoplasmosis. The toxoplasma infection was selectively localized to the brain and the serum titers were paradoxically low as reported in most adult cases of AIDS with secondary infection by the parasite. These findings strongly suggest that the infection by the human immunodeficiency virus (HIV) preceded the toxoplasma infection in the fetus.

AIDS Serodiagnosis↗
PubMed1988

Primary lymphoma of the central nervous system in children with acquired immunodeficiency syndrome.

Three children with acquired immunodeficiency syndrome and primary lymphoma of the CNS are described. All three children had clinical signs of focal mass lesions and progressive neurologic deficits. In one child the deterioration was extremely rapid. New lesions appeared on serial CT scans every few days, simulating an infectious process and leading to death within 3 weeks. Results of neuroradiologic studies in these patients demonstrated multicentric lesions that were often periventricular. On CT scans, the lesions were hyperdense before contrast and were enhanced with contrast medium. Double-dose delayed contrast CT scans and magnetic resonance imaging studies were more sensitive in indicating additional lesions. Histologically, all three tumors were B cell neoplasms; two lymphomas were large cell type, whereas one was small cell, noncleaved (Burkitt-like). Primary CNS lymphoma occurred with an incidence of 1/26 (4%) in our autopsy series and 3/100 (3%) of all pediatric cases of human immunodeficiency virus-type 1 infection, living and dead, that have been seen at the Children's Hospital of New Jersey. By comparison, opportunistic and reactivated latent CNS infections were less common in this same population and never appeared clinically as mass lesions. Therefore, in our experience, primary lymphoma is the most common cause of focal or multifocal mass lesions in the brains of children with acquired immunodeficiency syndrome. This tumor may be radiosensitive. In most cases, early biopsy is probably necessary to establish the diagnosis.

Acquired Immunodeficiency Syndrome↗
PubMed1987

Polyclonal polymorphic B-cell lymphoproliferative disorder with prominent pulmonary involvement in children with acquired immune deficiency syndrome.

Four cases of pediatric Acquired Immune Deficiency Syndrome (AIDS) with lymphoproliferative disorder are described and other lymphoid lesions in previously reported cases of pediatric AIDS are reviewed. The lymphoproliferative disorder was characterized by polyclonal, polymorphic B-cell content without evidence of cellular atypia, necrosis or prominent mitotic activity but with predominantly extranodal systemic and prominent pulmonary involvement. Since the lesion has overlapping features it is considered to be intermediate between benign and malignant lymphoproliferations and designated as polyclonal, polymorphic B-cell lymphoproliferative disorder (PBLD) of pediatric AIDS. The PBLD is part of a spectrum of lymphoid lesions in pediatric AIDS consisting of follicular lymphoid hyperplasia of nodal and extranodal sites, pulmonary lymphoid hyperplasia/lymphoid interstitial pneumonitis complex (PLH/LIP complex) in cases previously reported by the authors, and also malignant lymphoma reported by others. It is possible that Epstein-Barr virus (EBV) by itself or in synergism with human T-lymphotropic virus-type III (HTLV-III) is related to pathogenesis of PBLD in children with AIDS.

Acquired Immunodeficiency Syndrome↗
PubMed1987

Arteriopathy in children with acquired immune deficiency syndrome.

Pathologic features of the arteries of different organs (heart, lungs, kidneys, spleen, intestine, brain) seen at autopsy in 6 children with acquired immune deficiency syndrome (AIDS) are described. Small and medium-sized arteries, which were the most commonly involved, showed intimal fibrosis with fragmentation of elastic tissue, fibrosis and calcification of media with variable luminal narrowing, and a vasculitis or perivasculitis that was seen only in the brain in association with AIDS encephalopathy. In 1 case aneurysms of the right coronary artery with thrombosis and myocardial infarction were seen. Vascular inflammation, seen only in the brain, may be related to the agent associated with AIDS encephalopathy. The fibrocalcific arterial lesions most closely resemble idiopathic arterial calcification of infancy, but because of differences in age incidence, clinicopathologic and immunologic features, and the size and distribution of the involved arteries, the arterial lesions of pediatric AIDS appear to constitute a distinctive arteriopathy. Infection, secondary to immunodeficiency and resulting in increased exposure to endogenous and exogenous elastases, may be the pathogenesis. Luminal narrowing caused by arterial lesions may play a contributory role in the pathogenesis of the atrophy, cell depletion, scarring, and necrosis or infarction found in organs of children with AIDS. Pediatricians should be alerted to the possibility of arterial involvement in pediatrics AIDS.

Acquired Immunodeficiency Syndrome↗
PubMed1986

Pathologic features of AIDS encephalopathy in children: evidence for LAV/HTLV-III infection of brain.

The neuropathologic findings in 11 children with a new CNS disorder that occurs in children with the acquired immunodeficiency syndrome (AIDS) and is postulated to be due to LAV/HTLV-III, the virus that causes AIDS, are reported. The children, who ranged in age from 4 months to 11 years, died of AIDS complicated by progressive encephalopathy. Ten of the children either had positive serum antibody for LAV/HTLV-III or had received blood products from donors later found to be antibody-positive. Examination of the brains of these children at autopsy revealed a unique constellation of findings, including varying degrees of diminished brain weight in all cases, inflammatory cell infiltrates in nine brains, multinucleated cells in eight, three of which also contained multinucleated giant cells, vascular calcification in ten, vascular and perivascular inflammation in five, and white matter changes in nine. Inflammatory and vascular lesions were most prominent in basal ganglia and pons. LAV/HTLV-III retroviral particles, associated with multinucleated giant cells, were observed in two brains on electron microscopic examination. These two and one additional brain had evidence of the LAV/HTLV-III genome by hybridization studies. Only one brain had a recognizable opportunistic infection.

Acquired Immunodeficiency Syndrome↗
PubMed1986

Pathology of opportunistic infections in children with acquired immune deficiency syndrome.

Opportunistic infections (OI) were diagnosed by histology and culture of biopsy and autopsy material in 15 children with the acquired immune deficiency syndrome (AIDS). The opportunistic pathogens included Pneumocystic carinii, Toxoplasma gondii, Candida species, Aspergillus species, Mycobacterium avium-intracellulare, cytomegalovirus, and herpes simplex virus. Seven of 15 patients also had multiple systemic infections with common pathogenic bacteria. Accurate diagnosis of OI in AIDS is of importance in the decision regarding the choice of appropriate antimicrobial therapy. Careful histologic assessment of the biopsy specimens; awareness of unusual features such as paucity of organisms and inflammatory reaction, "histoid" variety of reaction, lack of granuloma formation, and resemblance to Whipple's disease in certain OI; and demonstration of causative organisms by appropriate special stains and/or culture are essential in the evaluation of these patients.

Acquired Immunodeficiency Syndrome↗
PubMed1986

Cystic lung disease in Down's syndrome: a report of two cases.

Previously unreported lung disease found at autopsy in 2 young infants with Down's syndrome and congenital heart disease (complete atrioventricular canal malformation with left-to-right shunt) is described. The perinatal and neonatal period was unremarkable, and there was no history of mechanical ventilation or administration of high concentration of oxygen for extended periods. In 1 of the cases respiratory symptoms and hyperinflation with focal cystic changes in the lung fields on chest X-ray were noted at 5-7 months of age. Pathologically there was cystic dilatation of alveoli with focal cuboidal metaplasia of alveolar epithelium and mild to moderate focal alveolar septal fibrosis. Wilson-Mikity syndrome, congenital pulmonary lymphagiectasia, bronchopulmonary dysplasia, and idiopathic interstitial fibrosis of lungs were ruled out on clinical and/or pathologic grounds. Factors such as compression of bronchi by enlarged pulmonary arteries or cardiac chambers, peribronchiolar accumulation of fluid, pulmonary hypoplasia occurring in Down's syndrome, and episodes of pulmonary arterial hypoperfusion associated with severe congenital heart disease may be related to the pathogenesis of the lesion.

Cysts↗
PubMed1986

Atypical mesoblastic nephroma. Pathologic characterization of a potentially aggressive variant of conventional congenital mesoblastic nephroma.

A case of an aggressive variant of conventional congenital mesoblastic nephroma (CMN) occurred in a 10-month-old male infant. The tumor proved to be fatal, with two abdominal recurrences, but no metastases were found. Of the various terms used to designate the tumor, atypical mesoblastic nephroma (AMN) is preferred. We reviewed 17 previously reported cases to attempt pathologic characterization of AMN. The features that distinguish AMN from CMN are as follows: (1) atypical gross features consisting of one or more of the following: fleshy areas, foci of hemorrhage, necrosis, involvement of adjacent structures other than connective tissue; and (2) high cellularity and mitotic index. Aggressive behavior was noted at surgery or on follow-up in seven of the 18 cases. It was characterized by one or more of the following: (1) invasion of adjacent structures, such as adrenal gland, spleen, colon, and diaphragm (three cases); (2) one or more recurrences (four cases); and (3) metastasis (two cases). Atypical mesoblastic nephroma should be recognized as a potentially aggressive lesion separate from CMN.

Combined Modality Therapy↗