Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023473 (chronic myeloid leukemia)
 18,916 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In 16 patients with chronic myelocytic leukemia an attempt to retard the myeoblastic transformation was carried out by means of repeated BCG administration in the period of remissions resulting from chemotherapy. Vaccinations were repeated at intervals of 4 weeks with doses of 2 mg of Mycobacteria by scarification. The time of uninterrupted remissions maintained with BCG vaccinations only ranged from 2 to 28 months, on the average 7.4 months. In this group 2 patients died and the duration of follow-up in the remaining cases ranges from 16 to 106 months, average 43.5 months. The survival time in the group of 16 patients with the same disease, who died after treatment with cytostatics only, was shorter ranging from 12 to 83 months, 32 months on the average. In one patient BCG vaccination was followed by tuberculosis of a supraclavicular lymph node.
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PMID:BCG immunotherapy in chronic myelocytic leukemia. 106 60

Twenty-two patients (16 male, six female; median age 34 years, range 16-49) with acute myeloid leukemia (1st complete remission (CR), n = 9), acute lymphocytic leukemia (1st CR, n = 5), chronic myeloid leukemia (chronic phase n = 5, accelerated phase n = 1), malignant lymphoma (n = 1) and myeloma (n = 1) were transplanted with unmanipulated donor bone marrow after standard conditioning including the monoclonal antibody Campath-1G daily from day -4 to day 0. No further graft-versus-host disease (GVHD) prophylaxis was given. All patients engrafted and neither graft failure nor rejection were observed. Acute GVHD grade I (skin) was seen in 12 out of 21 patients at risk. Acute GVHD grade II (skin) occurred in two patients. Severe GVHD (grade III, IV) of the gut, liver and skin developed in two patients. The overall incidence of severe acute GVHD (II-IV) was 19% of the patients at risk. Chronic GVHD (skin only) was seen in eight patients (42%) (six of extensive severity). A total of 14 patients died, the causes being relapse (four), direct cytotoxic drug toxicity (one), a GVHD (two), disseminated varicella zoster (one), systemic tuberculosis (one), interstitial pneumonitis (three) and veno-occlusive disease (two). These results indicate that the intravenous administration of Campath-1G may have reduced the incidence of severe acute GVHD without the occurrence of graft failure. However, the incidence of chronic GVHD does not appear to have decreased.
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PMID:In vivo use of Campath-1G to prevent graft-versus-host disease and graft rejection after bone marrow transplantation. 160 Apr 13

At the Clinic for Hematology of the Military Medical Academy in Belgrade two patients had been treated from November, 1983 to July, 1986, in whom the existence of chronic myelogenous leukemia (CML) was established with negative Ph'-chromosome, as well as the existence of acquired partial erythrocyte aplasia (APEA). In the male patient of 58 years of age and the female patient of 71, APEA was established at the same time as CML. The maladies showed to be refractory to antileukemia (busulfan, hydroxyurea) and immunosuppressive (corticosteroid, androgen) therapy in both of the patients, while in the first patient splenectomy was also without effect on the course of the disease. Serumal inhibitors of erythropoiesis were not registered. After 18 months of disease duration one patient had a blastic transformation of CML into acute myeloblastic leukemia (AML) of the M1 form, and death appeared under the clinical manifestation of sepsis during iatrogenic aplasia of the bone marrow. The other patient died 32 months after start of illness because of intracranial hemorrhage, without signs of HML metamorphosis. In the discussion, previous illnesses are considered--kidney tuberculosis and polyarthralgias--as well as the applied treatment of these illnesses (antituberculotics and nonsteroid antirheumatics) as possible etiological factors in the appearance of APEA. The mutual link between APEA and CML, though exceptionally rare, is possible, and erythroblastopenia can precede or occur simultaneously with CML or during its treatment. APEA is usually the sign of CML terminal metamorphosis into acute leukemia, though it sometimes coexists with CML as an independent malady.
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PMID:[Erythrocyte cell aplasia in chronic myeloid leukemia--coincidence or pathogenic link]. 212 May 56

Patients with chronic myeloid leukemia (CML) tend to suffer from non-reactive form of tuberculosis (TB) and often dissemination and death are the consequence when the blast crisis occurs. In those patients the eradication of pulmonary TB is essential to prolong their life. In a 58-year-old man with a tuberculoma and CML, right upper lobectomy was performed and was discharged 2 weeks later uneventfully. He succumbed to blast crisis 59 months after the onset of CML with no autopsy finding of recurrence nor dissemination of TB. The lobectomy in this patient was effective in preventing dissemination of TB. Controversy exists as to the indication for surgery but this case illustrates the effectiveness of surgery preventing the dissemination of TB in patients accompanying CML.
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PMID:[Indication for surgery in a patient with tuberculoma accompanied by chronic myeloid leukemia]. 224 39

We report 3 patients with chronic myeloproliferative syndromes and active tuberculous infection. The first patient had chronic myelocytic leukemia. In this patient, primary tuberculosis was localized in the lung. In spite of tuberculostatic treatment, he developed laterocervical lymphadenopathy and a tuberculous abscess in right lower limb. The second patient had agnogenic myeloid metaplasia. In this patient splenic tuberculosis (TBC) with subsequent pulmonary involvement were diagnosed. The third patient had idiopathic thrombocytopenia with pulmonary tuberculous infection. In two patients, tuberculosis was diagnosed some time after the diagnosis of hematologic disease, while in the third one both conditions were simultaneously identified. One of the patients died of complications of alkylating therapy, and the other two are still alive. In none of the three patients there has been evidence of active tuberculous infection after therapy, although their course has been slow and two have required associated surgery to eradicate the infection. We review the hematologic conditions which can develop during tuberculosis, the incidence of this infection during chronic myeloproliferative syndromes, the possible pathogenetic relation between both conditions, and the clinical presentation of tuberculosis in these patients, which usually is disseminated in character.
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PMID:[Chronic myeloproliferative syndromes and tuberculosis: apropos of 3 cases]. 235 80

Seven cases of miliary tuberculosis in patients with hematologic disease were analyzed clinicopathologically. Mean age of the patients was 65 years, and the hematologic diseases were CML, AML, ALL, MDS and malignant lymphoma. Diabetes mellitus was present as a complication in three patients. Miliary tuberculosis was found in 5 cases during the first admission to our hospital owing to hematologic problems. In 4 of 6 cases, fever had started more than two months before admission, consequently, the tuberculosis probably began about that time. After admission, chemotherapy was administered in 5 cases, and steroid in 6 cases for hematologic disease. The mean total quantity of steroid administered was 2,134 mg of prednisolone and average treatment duration was 69 days. The chest roentgenographic shadow was so atypical that miliary tuberculosis was suspected in only one case. The initial chest roentgenogram showed hilar and mediastinal lymph node swelling as well as the shadow of pulmonary tuberculosis in two cases. It was thought that the hilar and mediastinal lymph node swelling could be explained by primary complex, although the patients were of advanced age, or by "secondary complex" reported by Terplan, K in 1940. The diagnosis of tuberculosis was made in two patients before their death by smear of aspirated fluid of cervical lymph node and by bone marrow cell block in one patients, and by pathological examination of mediastinal lymph node biopsy in the other patients. Tubercles were found from bone marrow cell block in 2 out of 5 patients and from bone marrow biopsy in 1 out of 3 patients, but the positive results were reported in 2 patients following death. Smears of sputum, gastric juice, urine, spinal fluid and pleural effusion were negative in all cases. One patient diagnosed as miliary tuberculosis also had pneumocystis carinii pneumonia. This case was treated with antituberculosis drugs for 20 days without improvement. Another patient diagnosed as miliary tuberculosis improved under treatment with antituberculosis drugs, but died of cytomegalovirus pneumonia. Autopsy in 5 cases revealed non-reactive miliary tuberculosis, and pulmonary hemorrhage probably due to DIC was present as a complication in two cases. In these cases, severe immunosuppression, which is a major precipitating factor of miliary tuberculosis, is thought to be induced by hematologic disease itself, chemotherapy, steroid or other underlying disease such as diabetes mellitus. Miliary tuberculosis in such compromised host is cryptic and progresses rapidly. Consequently, early diagnosis is very important. Retrospectively, the unexplained pyrexia was most important to suspect tuberculosis.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Clinicopathological study of miliary tuberculosis in patients with hematologic disease]. 237 32

Of 2,143 biopsy proven cancer patients seen at our hospital over a six year period, 4 (0.19%) patients developed active tuberculosis (TB) during anticancer therapy or shortly after its completion. The cancer diagnoses of those patients were non-Hodgkin's lymphoma, breast cancer, chronic myelogenous leukemia, and astrocytoma. Institution of antituberculous therapy was successful in three patients, however, the TB course was rapidly fatal in the fourth patient with non-Hodgkin's lymphoma despite therapy. The association between TB and neoplasia is emphasized. TB complicating malignant disorders represents complex problem regarding its early recognition and its managements.
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PMID:Tuberculosis in patients with malignant disease. 259 98

The molecular forms of adenosine deaminase (ADA) were studied in pleural effusions with high ADA activity. The molecular forms were separated by polyacrylamide gel electrophoresis (PAGE), and the molecular masses estimated by gel filtration. Effusions investigated were: tuberculosis (TB) (20 cases), lymphoma (3 cases), chronic myelogenous leukemia (1 case) and empyema (6 cases). Two ADA forms were identified, a small form (Smf-ADA) and a large form (Lmf-ADA). Without exception, the tuberculous effusions have shown only Lmf-ADA. All the other effusions contained both forms, the Smf-ADA being predominant. This was also the ADA pattern seen in normal lymphocytes. These findings may indicate different mechanisms of ADA release or origins of ADA in the various effusions. The Lmf-ADA may be secreted by activated T cells in TB, which would confirm the notion that ADA activity reflects cellular immunity. In contrast, in the nontuberculous cases the ADA probably leaked from damaged lymphocytes or neutrophils, hence the reflection of the cellular ADA pattern. The PAGE pattern may also be of value in distinguishing between TB and these other causes of high pleural fluid ADA.
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PMID:Molecular forms of adenosine deaminase in pleural effusions. 316 74

Eight patients with haematologic malignancies contracted fatal invasive aspergillosis during an outbreak. Five patients were neutropenic. Bronchofiberoscopic examination with microbiology specimen brush and bronchoalveolar lavage yielded Aspergillus fumigatus in only 2/5 patients examined. The specific diagnosis reached during lifetime in 5 patients was based on a combination of invasive procedures (lung biopsy in 2, percutaneous lung puncture in 1), the presence of a lung abscess (3 patients), seroconversion (1 patient), and purulent maxillary sinusitis caused by A. fumigatus together with repeated abundant growth of A. fumigatus in the sputum (1 patient). Six patients received amphotericin B. The infection was temporarily controlled only in 2 bone marrow transplant recipients whose granulocyte counts recovered. In 3/8 patients the pneumonia was of polymicrobial aetiology, Mycobacterium tuberculosis (2 patients), Pneumocystis carinii (1 patient), and Legionella pneumophila (1 patient) being the other microbes involved. 3/4 bone marrow transplant recipients with aspergillosis had been transplanted for chronic myeloid leukaemia, supporting the previously reported association of bone marrow transplantation for chronic myeloid leukaemia and the risk of invasive aspergillosis. Improved diagnostic methods for earlier definitive diagnosis of invasive aspergillosis as well as more efficacious and less toxic antifungal agents are needed to allow early treatment.
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PMID:Invasive pulmonary aspergillosis: a diagnostic and therapeutic problem. Clinical experience with eight haematologic patients. 332 14

A 55-year-old woman was diagnosed as having chronic myeloid leukemia in 1961. After 9 years with stable white blood cells, progression of the disease was noted (white cells up to 180 X 10(9)/l; splenomegaly to the umbilicus). Busulfan was given over 4 weeks resulting in a remission of 13 years duration. Progression was observed again in 1983, 22 years after the initial diagnosis of chronic myeloid leukemia. Therapy with hydroxyurea resulted in another remission of shorter duration. Two chromosome studies showed the Philadelphia chromosome in 100% of metaphases without additional aberrations. In 1985 blast crisis developed. The cause of death as determined at autopsy was an undiagnosed miliary tuberculosis. The presented case is of special interest since (1) it is a report of the longest surviving patient with chronic myeloid leukemia, and (2) in contrast to other cases with long survival, this patient did not show chromosomal mosaicism or any additional chromosomal aberrations.
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PMID:[24-year survival in chronic myeloid leukemia]. 347 6


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