Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Scabies was first found in a 71-year-old female who had been diagnosed as having leukemic transformation of primary myelofibrosis and had undergone treatment for the disease. She was admitted to the hospital in December 1986, because of abdominal fullness and a generalized subcutaneous tumor that proved to be myeloblastoma. For treatment of the underlying disease, the regimen of the combination of vindesine, cyclophosphamide, 6-mercaptopurine, and prednisolone was selected. She developed cardiac failure and fell into a coma one month after starting the anticancer therapy. She was put on artificial respiration and on additional steroid therapy as well. Dexamethasone was administrated at 16 mg/day. Since the myeloblastomas found on admission regressed, the steroid therapy was continued. She was in coma for a few days before her skin lesions turned red and formed a grayish crust in the lower abdominal region. Several days later, the doctor responsible for the treatment of this patient developed pruritus and exanthema on both arms, and soon many nurses in the same hospital-ward developed similar symptoms. At approximately the same time, the patient with myelofibrosis was diagnosed as having Norwegian scabies: the crusted skin lesions revealing many Sarcoptes scabiei mites. Two doctors (2/18), 17 nurses (17/19) and 3 other patients (3/51) were found to have contracted scabies, and we recognized the hospital spread of the infection. The first patient was isolated in a private room, and we avoided direct contact with her. The persons with scabies were treated with crotamiton liniment. The first scabies patient died of cardiac failure 1 month after falling into a coma.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Hospital spread of scabies from an immunocompromised patient with Norwegian scabies]. 176 99

The evolutive patterns, actuarial survival and causes of death of idiopathic myelofibrosis were analysed in a series of 60 patients. The median age of the patients was 64 years; 41 were males and 19 females. In the initial bone-marrow biopsy studies 25 patients were in stage MF/C, 17 in MF/O- and 18 in MF/O+. When performing this analysis, 32 patients were dead, 19 were still alive and 9 had been lost after a median follow-up of 6 months. The median survival of the whole series was 57 months. Four major evolutive patterns were recorded: 1) blastic crisis (7 cases), 2) portal vein hypertension (4 cases), 3) liver insufficiency due to massive myeloid metaplasia of the liver without signs of portal vein hypertension (5 cases); in 2 of them this pattern followed splenectomy), and 4) heart failure ascribable, at least partially, to post-transfusion haemochromatosis (3 cases). The blastic crisis appearing in 7 patients presented after a median follow-up of 19 months, and 6 of these patients have died after a median of 5 months since the diagnosis of the blastic crisis. In the 16 patients who died without any characteristic evolutive pattern, the following causes of death could be registered: septic shock (6 cases), intracranial haemorrhage, haemoperitoneum and acute renal failure (1 case each), whereas the cause of the deceased was unclear in the remaining 7 patients.
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PMID:[Idiopathic myelofibrosis: clinical course, survival, and causes of death in a series of 60 patients]. 219 99

The patient is a 71-year-old female who underwent splenectomy due to splenomegaly 32 months after diagnosed as having primary myelofibrosis. On examination she was found to have massive skin nodules, lymph nodes swelling and an enlarged liver with an abnormal hematologic profile as follows: RBC count 3.68 x 10(6)/microliters; WBC count 151 x 10(3)/microliters with 11% blasts; and platelet count 42 x 10(3)/microliters. The bone marrow aspirate showed a hypocellular marrow with 19.2% blasts. Histological examination of the skin nodules revealed that they were myeloblastomas, thus suggesting leukemic transformation of primary myelofibrosis. Her WBC count dropped to about 20 x 10(3)/microliters through treatment with vindesine, cyclophosphamide, 6-mercaptopurine and prednisolone, but it did not drop further. Treatment with dexamethasone remarkably regressed the myeloblastomas, but she died of heart failure 4 months after diagnosis of leukemic transformation of primary myelofibrosis. The autopsy findings showed the formation of numbers of myeloblastomas in both the systemic fatty tissue and dura mater as well as extramedullary hematopoiesis in liver and lymph nodes. A rapid development of splenomegaly in a patient with primary myelofibrosis seems to be associated with leukemic transformation.
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PMID:[Blastic crisis of primary myelofibrosis associated with multiple myeloblastomas ]. 231 11

A 52-year-old male with idiopathic myelofibrosis of 8 years' duration developed pericardial tamponade during recovery from acute tubular interstitial nephropathia following septicaemia. Splenectomy had been performed 7 yr previously. The tamponade was relieved by pericardiocentesis and its recurrence was prevented by a minor pericardiectomy. Pathological examination, including staining for factor VIII-positive cells, demonstrated extramedullary haematopoiesis in the pericardium. In patients with myelofibrosis and increased silhouette on X-ray film, with or without clinical heart failure, echocardiographic examination is recommended in order to identify a possible pericardial effusion.
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PMID:Pericardial haematopoiesis with tamponade in myelofibrosis. 399 93

We report a rare case of idiopathic myelofibrosis transformed to acute myelomonocytic leukemia associated with non-Hodgkin's lymphoma. A 64-year-old woman was admitted to our department because of anemia and leukocytosis. On admission, anemia and hepatosplenomegaly were noted. The hemoglobin content was 6.8 g/dl, and WBC count was 26,200/microliters with an increased number of immature neutrophils. Bone marrow biopsy revealed an increased amount of reticulin fiber. Because she had no disease which causes secondary myelofibrosis, idiopathic myelofibrosis was diagnosed, and she was treated with prednisolone, anabolic steroid and blood transfusion. Fifteen months after the diagnosis of myelofibrosis, blast increased in her peripheral blood and her spleen and liver enlarged remarkably. A tumor of right parotid region was recognized at the same time. The pathological diagnosis of biopsied tumor was non-Hodgkin's lymphoma. The cytochemical study of blasts in her peripheral blood showed that she had acute myelomonocytic leukemia. In spite of intensive chemotherapy, she died from heart failure, respiratory failure and renal insufficiency.
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PMID:[Idiopathic myelofibrosis transformed to acute myelomonocytic leukemia associated with non-Hodgkin's lymphoma]. 807 93

Between 1992 and 1999, 5 patients with chronic idiopathic myelofibrosis (MF) underwent splenectomy at our hospital. The median age at the time of splenectomy was 63 years (range, 58-69 years), while the median interval from diagnosis of MF to splenectomy was 38.2 months (range, 3.7-87.2 months). Reasons for splenectomy included symptomatic splenomegaly in 5 patients, transfusion-dependent anemia in 5, and refractory thrombocytopenia in 3. Although most of the patients with transfusion-dependent anemia and thrombocytopenia showed some improvement at 1 month after splenectomy, the response was durable in only 2 patients at 6 months. Post-surgical thrombocytosis of 1020 x 10(9)/l was observed in one patient. Blast cell counts in peripheral blood increased after splenectomy in 4 patients. Leukemic transformation occurred in one patient 5 months after splenectomy. Four patients eventually died (2 of infection, 1 of acute myelocytic leukemia, and one of heart failure). Overall median survival was 54.7 months (range, 10.9-110.0 months) and 10.2 months (range, 6.0-33.6 + months) from diagnosis and time of splenectomy, respectively. We confirmed the palliative role of splenectomy in advanced-stage MF, but sufficient consideration should be given to late complications including blastic transformation.
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PMID:[Splenectomy in 5 patients with idiopathic myelofibrosis]. 1157 2

Agnogenic myeloid metaplasia is a hematologic disorder accompanied by extramedullary hematopoiesis (EMH) affecting various organs. Lung involvement however is rare. We present the case of a 76-year-old woman with myelofibrosis, recurrent pleural effusions, pulmonary hypertension, and serious right cardiac failure. An open lung biopsy confirmed pulmonary EMH. She underwent low-dose (200 cGy) whole-lung radiotherapy in 4 fractions of 50 cGy each. Her clinical and hemodynamic parameters improved. We conclude that low-dose whole-lung radiation may be efficacious for the palliative treatment of pulmonary EMH.
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PMID:Whole-pulmonary low-dose radiation therapy in agnogenic myeloid metaplasia with diffuse lung involvement. 1192 Oct 22