[Pneumocystis carinii pneumonia in HIV infection. Diagnosis and therapy].
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Biomedical subjects
Publications and source records attributed to H J Stutte.
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Fifty consecutive AIDS autopsy cases were evaluated. All subjects showed one or more opportunistic infections and malignancies included in the AIDS case definition with cytomegalovirus and Kaposi's sarcoma being most prevalent. Mycobacterial and cryptococcal infections occurred only infrequently. Most patients of our series after successful treatment of Pneumocystis carinii pneumonia or cerebral toxoplasmosis later succumbed to less treatable conditions like disseminated cytomegalovirus or fungal infections or malignant lymphoma. In the absence of specific treatment for the HIV infection leading to these lethal complications special emphasis must be put on the prevention of HIV transmission and spread.
Hitherto it has generally been assumed that splenic haematopoiesis in adult humans occurs very infrequently and is predominantly associated with haematological disorders. In the present study of patients with cirrhosis of the liver, a marked splenic haematopoiesis was a constant finding. Moreover, low-level splenic erythro- and granulopoiesis was highly prevalent even in haematologically normal controls, while splenic thrombopoiesis was conspicuously absent in both groups. We suggest that splenic haematopoiesis results from entrapment and proliferation of circulating haematopoietic precursor cells in the splenic red pulp. This would account for the presence of splenic haematopoiesis in normal controls as well as in patients with cirrhosis of the liver. In the latter, stimulation of bone marrow haematopoiesis and increased splenic pooling of haematopoietic precursor cells may contribute to the marked increase of splenic haematopoiesis observed.
140 spleens involved by untreated Hodgkin's disease were studied utilizing conventional histological methods. Regardless of the subtype of Hodgkin's disease, infiltrates of neoplastic cells were present either in the periarteriolar lymphoid sheath, the marginal zone or in both locations. Initially, infiltrates were confined to the splenic white pulp, later larger nodular foci of Hodgkin's disease developed by coalescence of several infiltrates. Neoplastic cells in Hodgkin's disease may reach the spleen by both retrograde lymphatic spread or the splenic artery; the presence of neoplastic cells in both T- and B-cell areas of the splenic white pulp implies a preference for Hodgkin's disease in the spleen with regard to a suitable microenvironment. This may be provided by certain macrophage subpopulations.
Cytomegalovirus (CMV) was assayed by in situ hybridization with commercially available biotin-labeled CMV-DNA probes in 45 formalin-fixed paraffin-embedded autopsy specimens with Kaposi's sarcoma from 14 cases of the acquired immune deficiency syndrome (AIDS). In seven of the 14 cases, a few scattered hybridizing cells were detected in Kaposi's sarcoma, but not all specimens from the same case showed such cells. Most of the positive cells were peculiarly swollen and not typical of Kaposi's sarcoma cells. All positive cases had at least some CMV-infected organs with typical cytomegalic cells containing nuclear inclusions while five of the 7 negative cases revealed no CMV-infected tissue by conventional light microscopy. Our results suggest that this in situ hybridization procedure using biotin-labeled DNA probes only reveals generalized CMV infection that is a consequence of impairment of immune mechanisms in AIDS patients.
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Lymph nodes from eight LAS and six AIDS patients were studied by routine histology, immunohistochemistry, and ultraimmunohistochemistry. LAS lymph nodes show a peculiar follicular hyperplasia with a characteristic increase of proliferating dendritic and interdigitating reticulum cells. In AIDS, these cells are reduced and the expression of proliferation-associated antigens is diminished. The immunohistochemical analysis of dendritic and interdigitating reticulum cells and of proliferation-associated antigens in lymph nodes thus allows a clear distinction between LAS and AIDS and may have important prognostic implications.
Twenty-one cases (25 biopsies including 9 frozen biopsies) of Kaposi's sarcoma associated with the acquired immune deficiency syndrome (AIDS) were examined immunohistochemically, lectin-histochemically, and enzyme histochemically to ascertain the histogenesis of the lesion. The Kaposi's sarcomas were histologically subtyped according to a modified Schmid's classification (granulation tissue-like-, angiosarcoma-like- and spindle cell type). In almost all lesions, many atypical vasoforming cells and at least some spindle cells without definite evidence of vasoformation by conventional microscopy were positive for factor VIII-related antigen, BMA 120 (a new monoclonal antibody to an endothelial cell-specific antigen), Ulex europaeus I (UEA-I), alkaline phosphatase and ATPase. Linear reaction products for BMA 120 and UEA-I, suggesting the luminal surface of immature vascular channels, were sometimes recognized in the positive spindle cells. Electron micrographs confirmed endothelial characteristics, such as irregular and fragmented but distinct basal lamina and numerous pinocytotic vesicles, in both the UEA-I- and ATPase-positive spindle cells. Among spindle cells negative for the endothelial markers, there were many macrophages as a stromal reaction to tumor tissue, identified by monoclonal antibodies to macrophages (KiM 6, 7, 8 and EBM 11), acid phosphatase and alpha-naphthyl acetate esterase. The results of the immuno- and enzyme histochemical investigations did not correlate with the different histologic types of Kaposi's sarcoma. However, our results strongly suggest that tumor cells of Kaposi's sarcoma are derived from vascular endothelial cells rather than lymphatic endothelium.
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In rats chronic hypoxia causes extramedullary haematopoiesis mainly localized in the spleen. It is not known how splenic erythropoiesis develops and how it regresses after termination of hypoxia. In this study the spleen of rats exposed to chronic hypoxia was studied by light and electron microscopy; the findings were compared to relevant peripheral blood values. Splenic erythropoiesis begins almost immediately after exposure to hypoxia and reaches its maximum after 2-4 weeks. It occurs mainly in the splenic cords drawing upon local erythroblasts and is accompanied by an increase in splenic weight as well as a decrease in splenic iron stores. After termination of hypoxia marked phagocytosis by splenic cord macrophages diminishes the number of erythroblasts and of erythrocytes with a concomitant increase in splenic iron stores. Thus, splenic erythropoiesis appears to be inhibited as part of a rebound phenomenon and returned to normal by phagocytosis of erythroid cells within 4 weeks after cessation of the hypoxic stimulus.
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