Bone marrow lymphoid aggregates in malignant lymphomas.

AIM: To examine the usefulness of molecular analysis of IgH gene rearrangement in assessment of clonality in bone marrow biopsies with lymphoid aggregates (LA) and/or nodular lymphoid hyperplasia (NLH) in patients with different subtypes of malignant lymphomas. METHOD: Five hundred and twenty nine samples of bone marrow biopsies, taken in a staging procedure at the time of the initial presentation of illness, were processed routinely. Results were grouped in positive, negative, and cases with LA or NLH. In 43 samples with present LA/NLH, polymerase chain reaction (PCR) analysis of the CDR3 region of immunoglobulin heavy chain gene (IgH) for B-cell clonality was performed. RESULTS: Bone marrow malignant lymphoma infiltrates were present in 33.8% of lymphoma cases. The incidence of LA/NLH in bone marrow was 8.1%. LA/NLH were more frequently found in patients with extranodal disease and aggressive subtypes of B cell non-Hodgkin lymphoma (B-NHL), but there was no significant difference among the incidence according to the biological behavior of malignant lymphoma (P=0.232). Results of IgH-CDR3 region PCR analysis showed a monoclonal pattern in 1 case of Hodgkin lymphoma and in 1 control case, an oligoclonal pattern in 2 cases of extra nodal B-NHL, whereas all other had polyclonal. CONCLUSION: The results support our initial hypothesis that LA/NLH could be differentiated from malignant infiltrates in bone marrow staging procedure of malignant lymphoma by topographic pattern and histocytomorphology of LA/NLH. Surprisingly, our patients with aggressive B-NHL, nodal, as well as extranodal, had LA/NLH in bone marrow biopsies more often than patients with indolent B-NHL.

Classic Kaposi's sarcoma: a case report.

A 60-year-old male from the Mediterranean area presented with edematous right leg and livid nodules and macules on the skin of upper and lower extremities. Biopsy specimen obtained from the right upper leg showed a pathohistologic finding indicative of Kaposi's sarcoma. Polymerase chain reaction testing revealed HHV-8 in the skin lesion. Serology for HIV was negative. Additional examinations did not reveal dissemination of the disease. Negative HIV serology, normal laboratory findings and absence of immunosuppressant therapy in the patient's history confirmed the diagnosis of the classic form of Kaposi's sarcoma.

[Occurrence of chronic B-cell lymphocytic leukemia in Hodgkin's disease: case report]. / Pojava B-kronicne limfocitne leukemije u Hodgkinovoj bolesti: prikaz bolesnice.

We present a case of a female patient (79 years) with pathohistologic diagnosis of Hodgkin's lymphoma (HL) (stage IIIB, histologic type MC) for which she was treated with chemotherapy according to LVPP protocol (6 cycles) with good therapeutic response. Unexpectedly, 18 months after HL diagnosis leukocytosis occurred (19.4 x 10(9)/L) with 65% of lymphocytes with lymphoplasmocytic differentiation. Immunophenotype of these cells is typical for B-chronic lymphocytic leukemia (B-CLL) (CD5/CD19+, CD23-, CD38 +/-; with weak expression of monoclonal light chains lambda). Molecular analysis confirmed clonal immunoglobulin heavy chain gene (IgH) rearrangement of peripheral blood lymphocytes. The diagnosis of B-CLL imposed the question of the connection between two neoplasms of lymphocytic origin. Molecular analysis of lymph node biopsy taken at the time of lymphoma diagnosis revealed clonal population of B lymphocytes. That test undeniably proved coexistence of both diseases from the beginning. The latest PCR analysis of archive peripheral blood smears confirmed B lymphocyte clonality without diagnostic criteria for lymphoproliferative disease of CLL type. This finding etiologically excludes secondary leukemia. The possibility of untypical presentation of CLL in transformation to Richter's syndrome with morphologic characteristics of HL from the beginning stays unconfirmed. The hypothetical question that remains unanswered is: "Was it one disease in different clinical forms?"

Angiotensin I-converting enzyme is expressed by erythropoietic cells of normal and myeloproliferative bone marrow.

It is proposed that a locally active, intrinsic renin-angiotensin system (RAS) exists in the bone marrow (BM) and plays a role in regulating haematopoiesis. Angiotensin II type I receptor has been detected on erythroid burst-forming unit-derived cells; its antagonist losartan and angiotensin I-converting enzyme (ACE) inhibitors can suppress erythropoiesis. The possible role of ACE/RAS in BM was investigated by evaluating ACE expression in normal BM, several myeloproliferative disorders and myelodysplasia. Immunohistochemical studies showed that erythroid elements expressed ACE protein in both normal and disturbed haematopoiesis. The presence of ACE in erythroid cells suggests another mechanism for direct ACE inhibitor activity in erythropoiesis.