Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023467 (acute myeloid leukemia)
 35,200 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Histologic studies suggest that polymorphonuclear leukocytes (polys) may initiate, enable, and/or enhance the development of psoriasis. A man with long-standing psoriasis developed acute myelogenous leukemia. His psoriasis disappeared after treatment with daunorubicin and cytosine arabinoside. Smears of his peripheral blood showed essentially zero polys from day 10 to day 22 after start of chemotherapy. His psoriasis began to reappear on day 14, became prominent by day 16, and persisted. Polys may not be requisite for the development and maintenance of psoriasis.
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PMID:Psoriasis without neutrophils. 232 25

A 16 year-old boy was admitted to our hospital in April 1985, because of bilateral submandibular swellings. Hematological examination revealed Hb was 7.3 g/dl, WBC was 89,000/microliters (76% blast), and platelet was 154,000/microliters. His bone marrow was hypercellular and consisted with 91% blasts. Myeloperoxidase staining was positive for 38% of blasts. Auer rods were seen in some of blasts. Thus, the diagnosis was M1 according to FAB classification. Cytogenetic studies of 20 marrow cells were performed and all cells had 46, XY, -1, -7, 3q-, 7q-, 17q+, +2mar. Eighty five percent of blasts expressed HLA-DR and 43% of blasts expressed CD2 and CD13 simultaneously. Thus, this leukemia was considered as the hybrid type of acute mixed leukemia by surface marker analysis. DBMP-85 regimen, the chemotherapy for AML, was started after admission and complete remission (CR) was attained in June 1985. After 4 courses of post remission chemotherapy, he discharged in December 1985 and was followed at our outpatient clinic without chemotherapy. His disease was relapsed in June 1986, and the combination chemotherapy with mitoxantrone, etoposide and Ara-C was applied to him but failed to attain CR. Then, LVP protocol, the chemotherapy for ALL, was started and CR was achieved. The blasts at relapse had morphologically myeloid features, and expressed HLA-DR, CD2 and CD13 as well as at diagnosis. Cytogenetic studies at relapse showed some karyotype except gaining 12p- anomaly. Therefore, same blasts were considered to emerge at relapse. Our case suggests that LVP therapy may be effective for AML expressing myeloid and lymphoid surface markers.
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PMID:[DBMP-85 was effective at diagnosis and LVP was effective at relapse in a case of acute mixed leukemia]. 236 35

Acute myeloblastic leukemia (AML) was diagnosed in a 54-year-old male who had been known to carry a chronic hepatitis B surface antigen (HBsAg) from June, 1983. Prompt remission was achieved with combination chemotherapy of BHAC-DMP. Follow-up maintenance and an intensification of this chemotherapy had been given for five years. He was readmitted to our hospital in March, 1988 because a mass was detected in the right lobe of the liver by ultrasonography. His serum alpha fetoprotein (AFP) level was found to be 180.1 ng/ml, and was diagnosed as having a hepatocellular carcinoma though there was no evidence of liver cirrhosis. A curative right hepatectomy was performed in May, 1988 after transcatheter arterial embolization and portal embolization. After resection of the tumor, the AFP level decreased to 10.7 ng/ml and no HbsAg was detected in the serum.
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PMID:[Hepatocellular carcinoma treated with a curative segmentectomy five years after complete remission of acute myeloblastic leukemia]. 254 80

We report a patient with acute nonlymphocytic leukemia (FAB classification: M 2) with trisomy 4, which is the first case in our country. A 42-year-old man was admitted to our hospital because of fever and general fatigue in May, 1988. His WBC count was 8,100/microliters with 90% of leukemic cells and bone marrow smear showed 76.1% leukemic cells. The chromosomal analysis of marrow cells by G-banding revealed 47, XY, +4. In spite of administration of chemotherapy complete remission was not obtained, and he died of septic shock and severe liver damage 4 months after making the diagnosis. Chromosomal abnormality of trisomy 4 has been reported to be associated with predominantly either M 4 or M 2, and to be less than 0.1% of incidence in ANLL, according to the Second MIC Cooperative Study Group. It is suggested that trisomy 4 may be caused by exposure to some environmental factors such as toxic substances, since this chromosomal abnormality has been reported in the last 10 to 20 years.
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PMID:[Chromosomal abnormality of trisomy 4 in a patient with acute nonlymphocytic leukemia (FAB: M2)]. 269 22

A 20-month-old child was treated for acute nonlymphocytic leukemia (ANLL) with basophilic differentiation. His leukemic cells also had the cytogenetic abnormality of t(9,11)(p22,q23). Although immature blasts responded well to induction therapy with etoposide, the leukemic cells that were more differentiated toward basophils were quite refractory to the drug. However, complete remission was finally achieved with a conventional multidrug regimen.
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PMID:Acute nonlymphocytic leukemia with basophilic differentiation and t(9,11)(p22,q23) in a child. 273 19

We report a case of factitious hyponatremia in a boy who had received a bone marrow transplant for acute myeloid leukemia. Following transplantation, he developed graft-versus-host disease and obstructive jaundice. The pseudohyponatremia was found to be due to hyperlipidemia, but there were some unusual features. The patient's plasma triglyceride concentration was not significantly raised, but he had an extremely elevated cholesterol concentration, probably due to the presence of lipoprotein-X. His plasma, when first separated at room temperature, was icteric and relatively clear but developed a dense turbidity on being frozen at -20 degrees C.
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PMID:Factitious hyponatremia in a patient with cholestatic jaundice following bone marrow transplantation. 352 99

Four patients with acute leukemias resistant to various ARA-C containing regimens and one patient with rapidly progressive malignant nonseminomatous tumor of the testis, who failed to conventional therapy were treated with HD ARA-C from december 1979 to september 1980. The drug was monitored by HPLC in plasma and in CSF. The first patient received only one course of HD ARA-C, developed fever and died of septicemia ten days later. The leucocyte count of her AML (FAB 2) decreased from 120,000/microliter to 30,000/microliter on the third day after HD ARA-C. Patient 2 reached CR criteria of the bone marrow for 23 days, then resistant AML (FAB 2) recurred. A male patient of 30 years was treated for recurrent acute undifferentiated leukemia (AUL) with a high cumulative dose of 176 gs of ARA-C. The repeated courses of treatment included a period of 50 days of CR. Toxicity was remarkable including pulmonal and cerebral dysfunction. A fourth patient with monocytic leukemia did not respond to HD ARA-C, neither did the patient with the malignant teratoma. Adverse reactions were tolerable. Only the third patient suffered from severe toxicity, pneumonitis, blurring vision, cerebral dysfunction and dermatitis. His pretreatment regimen had included X-ray prophylaxis to the skull. Since there was no possibility to prolong the remission duration in 1980, we decided not to treat further patients with HD ARA-C. Nowadays bone marrow transplantation offers some patients a capability of eradication of the leukemic disease.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Results of therapy with high-dose cytosine arabinoside]. 388 22

A 5-year-old boy developed an ependymoma; 3 years later, after chemotherapy and radiotherapy, he developed glioblastoma multiforme and acute myeloblastic leukemia. His maternal grandmother had died at a young age of colon cancer. Since ependymoma is not known to predispose to other cancers, the unusual sequence of malignant disease may have been due to combined therapy in a susceptible host.
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PMID:Ependymoma, glioblastoma, and acute leukemia in a child. 630 Jun 25

A 33 year old man, with pre-existing psoriasis and a family history of multiple occurrence of acute myeloid leukemia and other myeloproliferative disorders, developed steroid-responsive ulcerating skin lesions, pancytopenia, marrow hypoplasia, hyperglobulinemia and polyarthritis. An abnormal karyotype (47,XY + i(1q] was detected in the bone marrow, and comparison with a case previously reported by Lee et al. Suggested that this abnormality may be significant. His sister, who developed chronic leucocytoclastic vasculitis, had pre-existing psoriasis, variable mild leucopenia and marrow dysplasia. Review of available records of other affected family members documented the occurrence of steroid responsive pancytopenia, knee swelling and terminal lipoid pneumonia in a first cousin. Four other relatives died with acute myeloblastic leukemia and another died with myelofibrosis. Two healthy first degree relatives were subjected to laboratory investigations with essentially negative findings.
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PMID:Dermal necrosis and chromosome Iq abnormality in a man with a familial myeloproliferative disorder. 657 33

Adenocarcinoma of the pancreas developed in a young man who was a 10-year survivor of acute myeloblastic leukemia (AML). His extensive cytotoxic chemotherapy for AML is reviewed along with a discussion of its possible oncogenic effects. Other case reports of second malignant neoplasms (SMN) following acute leukemia are cited; available data suggest that the overall risk of SMN in AML may be in the range of 6%. While our patient's second malignancy may have been a chance association, his and other cases of pancreatic carcinoma in young survivors of hematologic neoplasia suggest that the cytotoxic treatment may have had a role in the pathogenesis of the pancreatic carcinoma.
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PMID:Pancreatic carcinoma in a ten-year survivor of acute myeloblastic leukemia. 695 11


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