Causes of Death in Hospitalized HIV Patients in the Early Anti-Retroviral Therapy Era.

OBJECTIVE: To establish the cause(s) of death among persons with HIV and AIDS admitted to the Fevers Unit of the Korle-Bu Teaching Hospital (KBTH) in 2007 and to determine whether they were AIDS-related in the era of availability of HAART. METHOD: Retrospective chart review of all deaths that occurred in the year 2007 among inpatients with HIV infection. Cause of Death (COD) was established with post mortem diagnosis, where not available ICD-10 was reviewed independently by two physicians experienced in HIV medicine and a consensus reached as to the most likely COD. RESULTS: In the year under review, 215 (97%) of the 221 adult deaths studied were caused by AIDS and HIV-associated illnesses. Of these, 123 (55.7%) were due to an AIDS-defining illness as described in CDC Category 3 or WHO stage 4. Infections accounted for most of the deaths 158 (71.5%), many of them opportunistic 82 (51.8%). Tuberculosis was the commonest COD. Clinical diagnosis of TB was accurate in 54% of deaths, but was not validated by autopsy in 36% of deaths. There were few deaths (14.5%) in patients on HAART. CONCLUSION: In a developing country like Ghana where HAART was still not fully accessible, AIDS-related events remained the major causes of death in persons living with HIV. Total scale-up of the ART programme with continuous availability of antiretrovirals is therefore imperative to reduce deaths from AIDS and HIV associated illnesses. There is need for interventions for early diagnosis as well as reduction in late presentation and also better diagnostic tools for tuberculosis.

The genetics of renal oncocytosis: a possible model for neoplastic progression.

Renal oncocytosis is a rare condition characterized by the presence of numerous oncocytomas and oncocytic changes in the renal tubules. Other than oncocytomas associated with the Birt-Hogg-Dube (BDH) syndrome, the genetics of oncocytosis is not known. Whether oncocytomas and oncocytosis are similar to BDH syndrome, in which the tumors diploid (as most oncocytomas are), or show chromosomal losses may be significant regarding the observation that in oncocytosis, there frequently is morphological evidence of progression to chromophobe carcinoma. Here we report on the case of a 69-year old male who underwent a staged procedure of partial nephrectomy on the left side and right radical nephrectomy for multiple renal tumors. The tumors were studied by routine hematoxylin and eosin morphology, immunohistochemistry, cytogenetics, and loss of heterozygosity analysis. Both kidneys had numerous oncocytic neoplasms morphologically progressing from oncocytomas to hybrid tumors with chromophobe carcinoma. Genetic studies demonstrated progression from normal cytogenetics to chromosomal losses similar to those in some oncocytomas and in chromophobe carcinomas. The genetics of this apparently nonfamilial oncocytoma differs from that of BDH syndrome and is characterized by losses involving chromosomes 1, 14, 21, and Y. To our knowledge, this is the first report of the genetic and cytogenetic findings in oncocytosis not related to BDH syndrome and may suggest a possible model of progression from oncocytoma to chromophobe renal cell carcinoma.

[Effect of a mixed E. coli O-111 (RNA-azopositive and RNA-azonegative strains) and Coxsackie B3 viral infection on oxygen demand and on the succinate dehydrogenase activity of an HEp-2 cell culture according to polarographic study data]. / Vliianie smeshannoi infektsii E. coli O-111 (RNK-azopozitivnyi i RNK-azonegativnyi shtammy) i virusov Koksaki B3 na potreblenie kisloroda i aktivnost' suktsinatdegidrogenazy kul'tury kletok HEp-2 po dannym poliarograficheskogo issledovaniia

The authors determined polarographically the intensity of oxygen consumption and the activity of succinic dehydrogenase of the HEp-2 cell culture infected with the association of the Cocksackie B3 with the RNA-asopositive and RNA-asonegative strains of E. coli O--111, in comparison with the uninfected and separately infected virus or control bacteria. The results were recorded 2, 6, 12, 18 and 24 hours after the infection of the cell cultures. Mixed virus-bacterial infection intensified the oxygen consumption and the activity of succinic dehydrogenase by the HEp-2 cells, followed by a profound respiratory depression. The same effect was produced by the infection of cells by the virus alone. Less pronounced was the action of bacterial component. A change in the cell repiration of the infected cultures was independent of the RNA-ase activity of bacteria. Under conditions of mixed infection the intensity of the changes in oxygen consumption and of the succinic dehydrogenase activity was determined by the viral component of the association.