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PubMed2004

Gingival involvement in a patient with CD56+ chronic myelomonocytic leukemia.

Leukemic infiltration of the gingiva is most commonly reported to be associated with monocytic subtypes of acute myeloblastic leukemia (AML) but rarely with myelodysplastic syndromes (MDS). Here we report a case of CD56+ chronic myelomonocytic leukemia (CMML) who developed gingival involvement simultaneously when the leukocyte count elevated. At that time no increase in peripheral or bone marrow blasts were observed. Gingival hypertrophy regressed with the treatment of hydroxyurea. Three months later, bone marrow blast count elevated and the patient was treated with two courses of AML-like regimen and then one course of consolidation therapy. The patient is in complete hematological remission for one and a half years. Similar to other extramedullary involvements, gingival hypertrophy in CMML can be a harbinger of the disease entering a more aggressive phase requiring systemic chemotherapy.

Adult↗
PubMed1995

Interferon-alpha inhibits erythropoietin-induced proliferation, but not differentiation, and restricts erythroleukemia development.

The immature erythroid cell line J2E responds to erythropoietin (Epo) by proliferating and terminally differentiating into hemoglobin-synthesizing red blood cells. These cells produce a rapid, fatal erythroleukemia in mice characterized by hepatosplenomegaly and severe anemia. The aim of this study was to investigate the effects of murine interferons-alpha (MuIFN-alpha) on J2E cells in vitro and in vivo. Here we show that in culture MuIFN-alpha inhibited the Epo-induced proliferation of J2E cells but did not interfere with differentiation. When mice with J2E erythroleukemias were treated with MuIFNs in vivo, an extension of their life span was observed. Moreover, numerous necrotic lesions of infiltrating leukemic cells were detected in the spleens of these mice. Finally, ex vivo treatment of leukemic bone marrow cells with Epo and MuIFNs delayed mortality even further. It was concluded that MuIFNs (1) suppressed the proliferation of J2E cells in vitro but did not affect Epo-induced differentiation, and (2) inhibited the progress of erythroleukemias, especially in combination with Epo.

Animals↗
PubMed1996

Laparoscopic-assisted surgery of the spleen: clinical experience in expanding indications.

Between January 1993 and November 1995 laparoscopic surgery was used in 21 patients with a variety of splenic diseases, namely idiopathic thrombocytopenic purpura, congenital spherocytosis, lymphoma, leukemic infiltrative disease, splenic infarction, trauma, or splenic cyst. Total splenectomy was carried out laparoscopically in 16 patients. Conversion to open splenectomy was necessary in two other patients because of intractable bleeding. Two patients with a splenic cyst underwent laparoscopic unroofing of the cyst. Conservative hemostasis of a spleen injury grade II was carried out in a child after blunt trauma. The total mean duration of the laparoscopic procedures was 158 min and the mean blood loss volume was 350 ml, both conversions being excluded. Postsurgical recovery was excellent and the average hospital stay was 5 days, including the patients with conversion. There were no significant postoperative complications. Our observations indicate that an increasing number of surgical diseases of the spleen can be managed adequately by a less invasive laparoscopic approach. However, the criteria for using this procedure are in an expanding phase and are still mainly dependent on the surgeon's technical experience.

Adolescent↗
PubMed1978

Acute myelogenous leukemia following immunosuppressive therapy for rheumatoid arthritis.

A 51-year-old woman had acute myelogenous leukemia following log-term cyclophosphamide therapy for rheumatoid arthritis. After standard methods of management had failed, the rheumatoid arthritis showed considerable improvement in response to approximately 25 mg cyclophosphamide per day over a four-year period. At the end of this period, pancytopenia developed, and cyclophosphamide was discontinued. A bone-marrow aspirate showed nonspecific changes. However, four months later because of severe progressive pancytopenia, another bone-marrow examination was performed; it showed acute myelogenous leukemia. Therapy failed to induce a remission, and two months after diagnosis the patient died of aspergillosis. Autopsy confirmed the presence of leukemic infiltration of bone marrow, lymph nodes, liver and spleen. These findings suggest a possible leukemogenic role of cyclophosphamide in this case and suggest that caution should be exercised in treating non-fatal diseases with antitumor drugs.

Arthritis, Rheumatoid↗
PubMed1988

Hairy cell leukemia and anti-leukocyte common antigen.

Thirty-three bone marrow biopsies from 15 patients with hairy cell leukemia (HCL) were evaluated morphologically and immunohistochemically by use of the peroxidase-antiperoxidase technique to demonstrate reactivity for leukocyte common antigen (LCA). Hairy cells in all biopsies showed a distinctive and characteristic pattern for LCA, which decorated the periphery of the cytoplasm but that left most of the cytoplasm and the nucleus unstained. Anti-LCA was particularly helpful in highlighting focal or subtle leukemic infiltrates. Hairy cells in biopsies from three patients had, on routine morphologic examination, a spindled and sarcomatoid appearance, but these too were strongly LCA positive. Treatment regimens were variable: five patients had splenectomy and received chemotherapy; five patients had splenectomy alone; and four patients had chemotherapy alone. Seven patients received interferon, and one patient received no treatment. In those six patients who had multiple biopsies as part of follow-up examinations, hairy cells as identified by anti-LCA were continuously present. Often in significant numbers, and were usually underestimated or not identified by routine examination. In those patients who received chemotherapy, qualitative alterations in the LCA reaction of hairy cells were observed.

Adult↗
PubMed1989

Effects of several commonly used fixatives on DNA and total nuclear protein analysis by flow cytometry.

Five commonly used fixatives (AZF, B-5, Bouin's, formalin, and Zenker's) were evaluated for their effect on the flow cytometric analysis of DNA and total nuclear protein (TNP) in solid tumors. Data were obtained with the use of colonic adenocarcinoma, squamous carcinoma of the lung, mammary adenocarcinoma, and spleen with a plasma cell leukemic infiltrate. The parameters examined were G0-G1 DNA staining intensity, %G0-G1, percent coefficient of variation (%CV), percent debris, and TNP staining intensity. The results showed that variations in the fixation of solid tumor significantly affected flow cytometric-derived parameters. In this study, paraffin-embedded tissue (PET) fixed in 10% (v/v) neutral buffered formalin (NBF) produced the best results, with a %CV below 4.7, whereas fixatives such as Zenker's and B-5 produced poor %CVs (above 6.0) or uninterpretable TNP and light scatter data. These data suggest that a portion of all tissue samples be fixed in NBF to allow for subsequent analysis by fixative-sensitive assays such as DNA in situ hybridization and flow cytometry.

Adenocarcinoma↗
PubMed1991

HTLV-I associated myelopathy (HAM) after blood transfusion in a patient with CD2+ hairy cell leukemia.

Hairy cell leukemia complicating hemolytic anemia developed in a 46-year-old woman. Morphologically and cytochemically typical hairy cells were found to express both CD20 and CD2 antigens. Expression of surface IgG of kappa-chain type and the rearrangement of Ig but not T-cell receptor beta genes confirmed a B-cell origin of the leukemia. Blood transfusion was followed by disappearance of the hemolysis and a marked improvement of the leukemia. However, the patient developed progressive spastic spinal paraplegia about seven months after transfusion and was diagnosed as having HTLV-I associated myelopathy (HAM) by the demonstration of HTLV-I antibodies in serum and cerebrospinal fluid. HTLV-I infection via the transfusion may have been involved in the hematologic improvement seen in this patient. Autopsy showed demyelination, vacuolar degeneration, gliosis, and perivascular cuffing in the white matter of spinal cord without evidence of leukemic infiltration.

Anemia, Hemolytic↗
PubMed1992

The "CD43 only" phenotype. An aberrant, nonspecific immunophenotype requiring comprehensive analysis for lineage resolution.

Paraffin section immunohistology of leukocytic proliferations is a routine method of immunophenotyping in many clinical laboratories. Furthermore, a relatively standard antibody screening panel that includes L26 (CD20), Leu22 (CD43), and UCHL1 (CD45RO) appears to be widely used. Although paraffin section immunophenotyping in general, and this panel in particular, have been shown to be very reliable in defining B-cell lineage, characterization of T-cell lineage is less definitive. This is related primarily to the relatively poor specificity of the commercially available T-cell-associated reagents. CD43 (Leu22) in particular has a broad immunoreactivity profile that has not been stressed adequately in some reports. Seventeen cases with a "CD43 only" phenotype were identified during the last several years while using the relatively standard screening panel mentioned above. These cases were quite heterogeneous with respect to cellular differentiation and most were not T-cell proliferations. Specifically, eight cases were extramedullary leukemic infiltrates (five myeloid, two monocytic, one mixed lineage), four cases were T-cell lymphomas, three cases were B-cell lymphomas and two cases were plasmacytomas. Although CD43 has demonstrable utility in a leukocyte screening panel, this report stresses the aberrancy and lack of specificity of the "CD43 only" phenotype. Caution is recommended in assigning a specific lineage to such cellular proliferations without additional immunologic or genotypic analysis. Recommendations for comprehensive diagnostic evaluation of these proliferations are provided.

Antigens, CD↗
PubMed1984

Urethan (ethyl carbamate) alone is carcinogenic for mouse skin.

Nine groups of 32 hairless mice (16 males and 16 females in each) were painted on the back skin with approximately 200 microliters solution of urethan twice a week for up to 58 weeks. The following treatments were given: acetone alone, propylene glycol alone, 10% urethan in acetone, 15% urethan in propylene glycol, 20% urethan in acetone, 30% urethan in propylene glycol, 40% urethan in acetone, 75% urethan in propylene glycol, and approximately 100% melted urethan. Histological examinations revealed no development of general epidermal hyperplasia or inflammatory reactions. Tumors developed in skin, liver and lymph nodes, and one mouse also developed leukemic infiltrations in kidneys and lungs. The rate and yield of skin tumors were registered and statistically analyzed. The number of other tumors occurring was also recorded. The results confirm that urethan is a tumorigen for the lung and several other organs, and that it is also a complete carcinogen for hairless mouse skin, even in a dose as low as 10% urethan in acetone. There is also a significant dose-response relationship.

Animals↗
PubMed1993

Case report: hypercalcemia in acute myeloblastic leukemia is caused by osteoclast activation.

Hypercalcemia in adult T-cell leukemia has been attributed to increased levels of 1,25-dihydroxyvitamin D (1,25(OH)2D), whereas in other types of leukemia, hypercalcemia has been blamed on direct skeletal invasion by malignant cells, ectopic parathyroid hormone (PTH) production or bone-resorbing cytokines. A 51-year-old man was studied who presented with back pain, circulating myeloblasts, and hypercalcemia. The bone marrow revealed acute myeloblastic leukemia. While the ionized calcium concentration was 8.17 mg/dL (normal, 4.73 to 5.21 mg/dL), the levels of PTH, PTH-related peptide, vitamin D, and thyroxine were normal or subnormal. Bone histomorphometry showed a decreased cortical width with intracortical erosion cavities dissecting into the marrow space. In cancellous bone, the osteoid area, osteoblast perimeter, and tetracycline fluorescence were sparse, whereas the osteoclast perimeter was increased. Persistent marrow fat, the general absence of trabecular narrowing, and the prompt response to calcitonin suggest that the osteoclasts caused the hypercalcemia and lytic lesions, rather than pressure atrophy or osteolysis by leukemic infiltration. Osteoclast activation and subsequent hypercalcemia may have been due to a locally produced cytokine, such as interleukin-1 beta or tumor necrosis factor.

Biopsy↗
PubMed1991

Plasmacytoid T-zone cell proliferation in a patient with chronic myelomonocytic leukemia. Histologic and immunohistologic characterization.

The term "plasmacytoid T-zone cells" has been used to describe distinctive cells that occur in clusters in the paracortex of some reactive lymph nodes. Recently, tumorous proliferations of these cells have been described in several patients with myelomonocytic leukemias. Neither the nature of these cells nor their relationship to myeloid leukemia has been conclusively established. We report the case of a 64-year-old woman with chronic myelomonocytic leukemia who developed lymphadenopathy that proved to be due to tumorous accumulation of plasmacytoid T-zone cells in the interfollicular regions of the lymph nodes. She underwent splenectomy because of symptomatic splenomegaly; the resected spleen also contained aggregates of plasmacytoid T-zone cells, in addition to extramedullary hematopoiesis. On treatment with busulphan and prednisone, the lymphadenopathy resolved and did not recur. The patient died 7 years later with blast transformation of her myelomonocytic leukemia and no recurrence of lymphadenopathy. The aggregates of plasmacytoid T-zone cells were architecturally and cytologically distinct from the leukemic infiltrates of myeloid cells in the spleen, and there was no evidence of differentiation of these cells into myeloid or monocytic cells. A panel of monoclonal antibodies on paraffin sections revealed no lineage-specific T- or B-cell markers (UCHL1-, L26-), and the plasmacytoid cells were positive for CD68 (KP1) and L60 (CD43), as well as faintly positive for 4KB5 (CD45RA) and MB1 (CD45R). They did not stain with antibodies to myeloid lineage antigens CD15, lysozyme, or myeloperoxidase. The combination of clinical, morphologic, and immunologic features of plasmacytoid T-zone cells in this case suggests that these cells may be of monocytic lineage but are not direct precursors of mature monocytic or granulocytic cells, and may not be part of the neoplastic clone in patients with myelomonocytic leukemia.

Antibodies, Monoclonal↗
PubMed1993

Rheumatic manifestations of neoplasia.

Recent literature on the rheumatic manifestations of neoplasia has again focused on the increased association of Sjögren's syndrome and rheumatoid arthritis with lymphoproliferative malignancies and leukemias. A series of 13 patients with monocytoid B-cell lymphoma, a recently described variant of low-grade B-cell lymphoma, and Sjögren's syndrome was reported. The skeletal manifestations of leukemias are extensively reviewed emphasizing that osteoarticular manifestations may predate the hematologic disease. A case of monoarthritis of the knee as a manifestation of chronic leukemia is presented in which synovial biopsy revealed a leukemic infiltrate. Recent studies looking at the association of polymyositis and dermatomyositis with malignancy challenge this link. Two cases of malignancy presenting with polyarthritis are reviewed, and in both cases the polyarthritis resolved with removal of the tumor. A case report and a series of synovial sarcomas are also reviewed. Hodgkin's disease can initially present with skeletal involvement; six cases are reviewed.

Humans↗
PubMed1995

Diffusely discordant In-111 WBC/Tc-99m SC bone marrow uptake. A possible chemotherapeutic effect.

In-111 WBC scintigraphy in a woman with relapsed acute lymphoid leukemia demonstrated normal uptake of white blood cells by the liver and spleen, but virtually absent bone marrow activity. Tc-99m SC imaging confirmed normal marrow function and distribution. A bone marrow biopsy revealed mildly hypocellular, regenerating marrow without leukemic infiltration. The effects of systemic cytotoxic chemotherapy on marrow reticuloendothelial function may have been responsible for this discordant uptake.

Bone Marrow↗
PubMed1980

Retroperitoneal processes involving the psoas demonstrated by computed tomography.

Twenty-five patients were found to have retroperitoneal pathology involving the psoas muscle including nine patients with inflammatory lesions, three with hematomas, seven with adenopathy, one patient with leukemic infiltration of the psoas, and five with retroperitoneal tumors. Computed tomography (CT) offers a unique method to investigate pathological processes that affect the psoas. In addition, the abdominal films on 24 of the patients were analyzed to correlate the value of radiography with that of CT. Computed tomography confirms the belief that the mere presence of a retroperitoneal mass will not necessarily obliterate the psoas.

Abscess↗
PubMed1978

Acute renal failure in patients with acute leukemia.

Acute renal failure may be a contributory cause of death in patients with acute leukemia. The purpose of this study was to define the causes and course of acute renal failure in group of patients with acute leukemia in order to identify preventive measures and reversible aspects of the renal insufficiency. Among 88 patients with acute leukemia whose courses were followed to the time of death, ten developed acute renal failure. Etiologic factors of the renal failure were uric acid nephropathy, sepsis with complicating hypotension and hypovolemia, and the administration of nephrotoxic antibiotics. In one patient ureteral obstruction from clots was responsible for renal failure, while in another patient disseminated aspergillosis led to renal failure. Other causes of acute renal failure in persons with acute leukemia, but not observed in this patient group, are hypercalcemia and leukemic infiltration of the kidneys.

Acute Disease↗
PubMed1980

Prolonged and concurrent lactic acidosis and hypoglycemia in a patient with monocytic leukemia.

Lactic acidosis or hypoglycemia occasionally occurs in patients with neoplastic diseases. We have described a patient with monocytic leukemia who had both, apparently as a result of marked leukemic infiltration of the liver. These metabolic anomalies were greatly ameliorated by chemotherapy. Thus, in leukemia and other malignant disorders in which significant liver infiltration is present, these metabolic derangements should be looked for, as their presence may call for a prompt and intensive treatment.

Acidosis↗
PubMed1986

Children cured of acute lymphoid leukemia. Long-term follow-up studies, including progeny.

The subject of analysis is a group of 111 children with acute lymphoid leukemia (ALL) whose remission has lasted at least 4 years since stopping treatment. Patients were observed from 4 to 18 years after ALL therapy. No symptoms of disease were observed in 110 children; one child had leukemic infiltration of the testes during the fifth year after stopping treatment. In this group of children no changes in physical development have been recorded, but a growth deficiency is sometimes noted. No symptoms of intrinsic organ lesions have been ascertained in most of the patients. All of the patients, except one with schizophrenia, lead normal lives and either attend school or go to work. Seven patients have healthy children, who were born 6-24 years after the beginning of the disease and 3-16 years after cessation of therapy.

Adolescent↗