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PubMedDate not supplied

Radiation treatment of testicular relapse in acute lymphoblastic leukemia.

Ten patients with testicular relapse among 128 cases of acute lymphoblastic leukemia are reported. At the time of the initial diagnosis of leukemia all patients with later testicular relapse showed one or more risk factors as predictive for leukemic infiltration of the testicles. All patients except one, who underwent orchiectomy and died 11 weeks after surgical intervention, received radiation therapy with doses ranging from 12 to 20 Gy and chemotherapy. The local control was excellent. Average survival time from testicular relapse to death was 68 weeks in 8 of 9 patients treated by irradiation and chemotherapy. One patient is still alive without signs of disease after 6 years.

Adolescent↗
PubMed1988

Fine needle aspiration cytology (FNAC) of the testes in childhood acute lymphoblastic leukemia and non-Hodgkin's lymphoma: preliminary report.

Eighteen patients with childhood acute lymphoblastic (ALL) or non-Hodgkin's lymphoma (NHL) in remission and 2 patients with ALL in suspected testicular relapses were studied by testicular fine needle aspiration cytology (FNAC). Well-preserved testicular cells, both singly and in small clusters, were considered indicative of an adequate aspiration. Of 18 patients in remission, 17 had at least one adequate sample from each testis and one showed evidence of leukemic infiltrate. None of these patients experienced a relapse during a median follow up of 4 years. In 2 other patients with clinically suspected testicular relapses, the smears from fine needle aspirates contained numerous malignant lymphoid cells that could be readily distinguished from seminiferous tubular cells. The observations indicate that FNAC is a promising new approach to study testicular conditions in childhood ALL and NHL. A larger prospective study and accumulation of additional follow-up data is required before a definitive evaluation of the technique can be made.

Adolescent↗
PubMed1994

Evidence against the role of hepatitis C virus in severe liver damage occurring early in the course of acute leukemia in children.

Severe liver damage revealed by a sharp transaminase elevation may be seen in patients with leukemia. This may be due to several possible causes, including viral hepatitis, chemotherapy-induced hepatotoxicity and leukemic infiltration. HCV infection may be suspected to play a relevant role as these patients are often heavily transfused after the onset of their hematologic disorder. We have therefore examined the role of HCV in 15 children with leukemia who developed severe liver damage shortly after the diagnosis of leukemia. All patients were tested for HCV-RNA by the polymerase chain reaction at the time of peak SGPT elevation and for anti-HCV on serial serum samples taken thereafter. Only one patient (6.6%) showed hepatitis C viremia and none developed confirmed anti-HCV positivity during follow-up, suggesting that HCV had not played a major role in causing these severe episodes of liver necrosis. This is in agreement with observations made in non-immunocompromised patients in whom fulminant hepatitis is only exceptionally due to HCV.

Acute Disease↗
PubMed1990

Hepatic fibrosis in juvenile chronic granulocytic leukemia: an unusual finding in three cases.

We present 3 cases of juvenile chronic granulocytic leukemia in which there are histological changes in the liver of both portal and bridging fibrosis, with fibrosis around central veins, the latter being confirmed by quantitative measurement. We stress the histological differences from cirrhosis, nodular regenerative hyperplasia, and veno-occlusive disease and describe the evidence which favors an etiology from the leukemic infiltration rather than chemotherapy.

Cell Movement↗
PubMedDate not supplied

MR imaging of central diabetes insipidus: a pictorial essay.

Central diabetes insipidus (DI) can be the outcome of a number of diseases that affect the hypothalamic-neurohypophyseal axis. The causes of the condition can be classified as traumatic, inflammatory, or neoplastic. Traumatic causes include postoperative sella or transection of the pituitary stalk, while infectious or inflammatory causes include meningitis, lymphocytic hypophysitis, and granulomatous inflammations such as sarcoidosis and Wegener's granulomatosis. Various neoplastic conditions such as germinoma, Langerhans cell histiocytosis, metastasis, leukemic infiltration, lymphoma, teratoma, pituitary adenoma, craniopharyngioma, Rathke cleft cyst, hypothalamic glioma, and meningioma are also causes of central DI. In affected patients, careful analysis of these MR imaging features and correlation with the clinical manifestations can allow a more specific diagnosis, which is essential for treatment.

Adolescent↗
PubMedDate not supplied

Leptomeningeal disease in pre-leukemic syndrome: cytogenetic abnormality versus cellular morphology.

Refractory anemia with excess blasts in transformation (RAEB-T) is a pre-leukemic syndrome that can progress to acute myelogenous leukemia (AML). Although leptomeningeal disease in AML is rare and it is commonly associated with specific cytogenetic abnormalities, it has not been documented in RAEB-T. We report a woman who experienced seizures and had subarachnoid enhancement on MRI suggestive of leukemic infiltrates in the leptomeninges. Her bone marrow aspirate revealed 6.6% blasts and the presence of Auer rods, findings consistent with a diagnosis of RAEB-T. Subsequent cytogenetic analysis detected an uncommon deletion of chromosome 11q23, and the breakpoint on chromosome 11 is identical to that seen in AML patients having leptomeningeal disease and translocation between chromosome 9 and 11. Although RAEB-T is not considered as leukemia and is thought unlikely to involve the central nervous system, the presence of leptomeningeal disease and 11q23 deletion in our patient suggests that cytogenetic abnormality may be an important determinant of neurological complications, regardless of a diagnosis of RAEB-T or AML which is based on cellular morphology.

Aged↗
PubMed2005

[Non germinal cell testicular tumors].

OBJECTIVES: We report a review of all patients with testicular tumors undergoing surgery in our Hospital over a 13 year period. There were 151 cases, 50 of them were reported as non germ cell tumors (33%). METHODS/RESULTS: 42% of them were haematopoietic tumors, lymphomas and leukemias. 30% of them were non neoplastic tumors, including vascular tumors and granulomatous orchitis. 12% were identified as Leydig or Sertoli cell tumors. 10% were metastases. CONCLUSIONS: Non germ cell tumors were more frequent in adults (78%) than in children (22%). Among children, 82% of the neoplasias were leukemic infiltration of the testicle.

Adolescent↗
PubMed2002

Methotrexate-related nonnecrotizing multifocal axonopathy detected by beta-amyloid precursor protein immunohistochemistry.

We describe a 64-year-old woman with biphenotypic leukemia involving the meninges who received 2 doses of intrathecal methotrexate. Soon after treatment, the patient developed postural rigidity and a marked decline in mental status. The patient died of respiratory failure 1 month after methotrexate treatment was initiated. At autopsy, the brain was grossly normal. Routine microscopy showed no evidence of leukemic infiltrates or necrotizing lesions. However, when stained with beta-amyloid precursor protein, multifocal axonal injury was evident in the brain, spinal cord, and nerve roots. Our findings show that immunohistochemical staining for beta-amyloid precursor protein can effectively demonstrate axonal injury associated with methotrexate neurotoxicity, even when conventional staining procedures are negative. This technique may therefore reveal a possible pathologic substrate for some of the neurological complications seen in patients with methotrexate neurotoxicity.

Amyloid beta-Protein Precursor↗
PubMed1975

Multiple myeloma and acute leukemia associated with alkylating agents.

Rapidly fatal acute myelomonocytic leukemia developed in five patients with multiple myeloma who were treated with melphalan for 28 to 54 months. In each patient, multiple myeloma responded to therapy and progress was satisfactory until the development of acute leukemia. At postmortem examination, leukemic infiltration of organs was seen, and there was little or no evidence of myeloma. Consideration of these cases and a review of the literature suggest that these circumstances represent the development of acute myelomonocytic leukemia rather than plasma cell leukemia; there also appears to be an increased incidence of acute leukemia in multiple myeloma, probably related to the alkylating agent.

Acute Disease↗
PubMed1975

[The "juvenile" type of chronic myelogenous leukemia (author's transl)].

The juvenile type of chronic myelogenous leukemia (CML) is characterized by hemorrhagic diathesis, hepatosplenomegaly, generalized enlargement of lymph nodes, reduced erythro- and thrombopoiesis, leukemic infiltration of bone marrow, and decreased activity of leukocyte alkaline phosphatase. The disorder differs from the adult type by the early manifestation of anemia and thrombocytopenia, the minor degree of leucocytosis, the failure to demonstrate the Philadelphia chromosome, and the presence of fetal markers in the patients' erythrocytes. The persistence of fetal markers in erythrocytes and the clinical manifestation in infancy and early childhood suggest that the disease is congenital in origin. The occurrence of CML of the juvenile type in an 8-year-old boy, which is reported in this paper, favors a postnatal acquisition of the disorder. The significance of hematological and cytogenetic findings and new aspects of nosological classification are discussed.

Adolescent↗
PubMed2000

[Perforation of small intestinal during hematologic recovery in an elderly man after induction therapy for acute lymphoblastic leukemia L3].

A 67-year-old man with a 7-month history of dilated cardiomyopathy was admitted to our hospital because of general fatigue, shortness of breath, and anemia on laboratory examination. Increased blasts were observed in the bone marrow. The blasts were characterized by large cells with abundant, intensely basophilic, vacuolated cytoplasm, round nuclei, and prominent nucleoli. Chromosome analysis revealed a nonrandom t(8;22)(q24;q11) chromosomal abnormality, and surface-marker analysis disclosed a positive immunophenotype for CD10, CD19, CD20, CD38, HLA-DR, FMC7, and IgM-lambda. These findings yielded a diagnosis of L3 acute lymphoblastic leukemia. The patient was treated with chemotherapeutic agents. On the 39th hospital day, during hematologic recovery after induction therapy, abdominal pain developed. Abdominal X-ray films disclosed ileus with dilatation of the small bowel and Kerckring's folds. Conservative treatment was begun but the patient died. At autopsy, intestinal perforations were observed at a site 55 cm proximal to the ileocecal junction. A specimen of perforated tissue revealed a diffuse infiltration of leukemic cells through the small bowel wall. However, bone marrow specimens showed no signs of aggravation of leukemia.

Aged↗
PubMed2001

[Preferential infiltration of liver sinusoids in acute lymphoblastic leukemia].

We report a case of acute lymphoblastic leukemia (ALL) presenting as severe jaundice. The patient, a 59-year-old man, was found to have abnormal liver function, including an elevated total bilirubin level (13.5 mg/dl) with hepatosplenomegaly, but no detectable lymphadenopathy. A liver biopsy and bone marrow examination revealed a lymphoid neoplasm. Pathologic features included invasion of an abnormal clone into the sinusoidal region of the liver, diffuse bone marrow involvement (41.6% of all nucleated cells) and splenomegaly. Small numbers of malignant cells were also detected in the peripheral blood. B-cell markers, such as terminal deoxynucleotidyl transferase (TdT), CD10, CD19, CD20 and HLA-DR were positive, and CD2, CD3, CD4, CD5, CD7, CD8, kappa, lambda, cytoplasmic mu and myeloperoxidase were negative. Cytogenetic analysis detected hyperdiploidy. In this case, a dose-attenuated CHOP regimen attained complete remission. To date, preferential infiltration to liver sinusoids has been noted in hepatosplenic gamma/delta T-cell lymphoma, other NK/T-cell malignancies, and some cases of hairy cell leukemia. Severe jaundice due to preferential infiltration of leukemic cells into liver sinusoids is rather uncommon as a presenting feature of ALL.

Humans↗
PubMed2002

[Echocardiographic assessment of circulation system in patients during and 3-5 years after all therapy in childhood].

Circulatory disturbances may occur during and after the treatment of acute lymphoblastic leukemia (ALL). The reasons are: leukemic infiltrations of the heart, anaemia, renal disturbances, infections, cardiotoxic drugs, especially anthracyclines (Atc). The aim of the study was echocardiographic assessment of circulatory system in patients during and 3-5 years after ALL therapy in childhood. The study group (group B) consisted of 20 children, aged 1-16 years, who underwent Atc treatment with cumulative doses 155.8-330 mg/m2 and cardioprotective agent--dexrazoxane. In this group echocardiography was performed before the treatment as well as after 1, 6, 12 months and 3 years. The retrospective group (R) consisted of 36 persons aged 12-24 years, examined 3-5 years after the completion of ALL treatment, who had undergone the treatment with Atc in doses 148.6-416.7 mg/m2 without cardioprotection. The control group (K) consisted of 28 healthy volunteers, aged 9-25 years. In all subjects echocardiography was performed, standard measurements taken, systolic and diastolic indices of left ventricle (LV) function calculated. In patients during and 3-5 years after the treatment neither LV dilatation nor abnormal wall-thickness was found. The systolic indices remained normal. In the group B echocardiographic indices did not change significantly during 3 years of treatment and did not correlate with growing cumulative Atc doses. In this group isovolumetric relaxation time (IVRT) was significantly longer, what emphasized the need of further clinical and echocardiographic follow-up.

Adolescent↗
PubMed1992

[Adult T-cell leukemia with various pulmonary complications].

A 59-year-old male, born in Wakayama prefecture, was admitted to our hospital because of cervical lymph node swelling, huge mass lesions in both liver and head of the pancreas, and multiple nodular shadows in the left lung. Lymph node biopsy revealed a necrotic lesion containing tuberculous bacilli with no epithelioid cells or giant cells. Adult T-cell leukemia (ATL) was diagnosed by the presence of atypical lymphocytes with a convoluted nucleus and positive anti-ATL antibody. During successful treatment of Mycobacterium tuberculosis with ethambutol, isoniazid and rifampicin, ATL transformed to the blastic phase. The new pulmonary infiltrates improved after treatment with both combination chemotherapy for ATL and antibiotics. However, new infiltrative shadows appeared in both lungs, and were resistant to treatment and the patient died of acute respiratory failure. Histological examination of the lung at autopsy showed interstitial fibrosis with infiltration of leukemic cells and cytomegalovirus infection.

Cytomegalovirus Infections↗
PubMed1992

Response assessment in chronic lymphocytic leukemia after fludarabine plus prednisone: clinical, pathologic, immunophenotypic, and molecular analysis.

The goals of this study were to evaluate the response to treatment in chronic lymphocytic leukemia (CLL) according to clinical, pathologic, immunophenotypic, and molecular features, as well as to address the clinical significance of each finding. One hundred fifty-nine CLL patients with either advanced Rai stage III or IV (81 patients) or progressive Rai stage 0 to II (78 patients) were treated with fludarabine (30 mg/m2/d intravenously every day for 5 days) plus prednisone (30 mg/m2/d orally daily for 5 days). Thirty-six patients were previously untreated. The response rates were 12% complete response (CR), 30% nodular complete response (nCR), and 18% partial response (PR). In all patients who achieved a complete response (both CR and nCR) less than 30% of nucleated cells were lymphocytes on marrow aspirate differential analysis; however, nCR patients had residual nodular and/or interstitial lymphocyte involvement on marrow biopsy examination. There was no evidence of leukemic infiltration on marrow biopsy examination in CR patients. With a median follow-up of 35 months, comparison of time to progression in the CR and nCR groups at 2 years showed a projected 87% versus 55% progression-free survival (P less than .03). Residual disease assessment by flow cytometry using simultaneous dual-color staining on blood and marrow lymphocytes was also performed on each patient. Residual disease was determined by the expression of CD5 on B lymphocytes and the monoclonality of surface light-chain expression. After six courses of fludarabine plus prednisone, no residual disease was detected by flow cytometry in 89% of the CRs, 51% of the nCRs, and 19% of the PRs. Clinical residual disease in PR patients with no residual disease detectable by flow cytometry was limited to lymph-adenopathy. Time to progression at 2 years was longer in CR and nCR patients having no residual disease detected by flow cytometry (84% v 39% 2-year progression-free survival, P less than .001). Posttreatment lg gene rearrangement analysis using JH, J kappa, and C lambda probes demonstrated no rearranged bands and a return to the germline configuration in five of seven CRs and two of eight nCRs studied. The molecular studies were concordant with the dual-parameter immunophenotype results and none of the patients who reverted to a germline DNA pattern after treatment have experienced relapse. The absence of detectable minimal residual disease by bone marrow biopsy, dual-color flow cytometry, and lg gene rearrangement analysis is achieveable in CLL with fludarabine and is predictive of the response duration.

Adult↗
PubMed1992

Combined therapy with all-trans-retinoic acid and high-dose chemotherapy in patients with hyperleukocytic acute promyelocytic leukemia and severe visceral hemorrhage.

Acute promyelocytic leukemia (APL) is associated with a high incidence of disseminated intravascular coagulation (DIC) and early hemorrhagic death. The risk of early fatal hemorrhage is increased when high peripheral-blood blast count and severe DIC accompanied by visceral hemorrhage are present at diagnosis. Progressive cytolysis induced by daily increased doses of chemotherapy, or differentiation all-trans-retinoic acid (ATRA) therapy have been proposed for initial control of DIC, but both are dangerous in hyperleukocytic APL patients. We report our results obtained in three high-risk APL patients treated with a combination of conventional chemotherapy and ATRA. All patients had documented hyperleukocytic APL [M3 or M3-variant subtype, (15, 17) translocation] with DIC, and all had critical clinical course before treatment. Patient 1 presented with cerebral hemorrhage, patients 2 and 3 had acute respiratory failure probably due to pulmonary leukemic infiltration and pulmonary hemorrhage. In order to minimize the severity of DIC during chemotherapy-induced acute cytolysis, ATRA (45 mg/m2 per day) was started on the first or second day of chemotherapy and withdrawn when complete remission (CR) was achieved. Despite adverse clinical features, CR was obtained in these three high-risk patients. Patient 1 showed no increase of cerebral bleeding during therapy. Patients 2 and 3 required transient intensive care, with mechanical ventilation from day 4 to day 11 for one of them. Differentiating granular cells were present in peripheral blood of all patients from the day 5, 12 and 8 of cytotoxic therapy. For the three patients, the number of days with white blood cell count < 1 x 10(9)/l was only 2, 7 and 11 days respectively. These results suggest that differentiation therapy with ATRA may be useful even in hyperleukocytic APL patients, when ATRA is used in combination with chemotherapy. The mechanisms of this putative beneficial effect are discussed.

Adult↗
PubMedDate not supplied

[Neuroleukemia in suckling mice].

The whole skull and spinal column were histologically studied in 55 suckling mice (intact and with transplantable leukemia). It was stated that the lesion of the vertebral canal prevailed due to the extensive growth of leukemic infiltrates in the bodies of the vertebra which had incompletely formed cortical plate of the bone tissue. Such age-dependent unfinished formation of the bone marrow tissue may predispose a rapid development of neuroleukemia.

Animals↗