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PubMedDate not supplied

[Polycythemia vera, complicated by myocardial infarction].

In an autopsied female primary polycythemia was definitely diagnosed only after histological examination. A classical form of Vaquez-Osler disease was characterized by pronounced normo-, granulo- and megakaryocyte hyperplasia of the bone marrow, spleen and liver myelosis with an admixture of atypical megakaryocytes and splenomegaly. There was a complication in the form of two coronary arteries thrombosis. Lethal outcome resulted from myocardial infarction.

Aged↗
PubMed1994

[Combined endocrine autoimmune syndrome--incidence, forms of manifestation and clinical significance].

UNLABELLED: In a retrospective case finding study we collected data from patients with polyglandular autoimmune syndrome type II (PGAS Type II) who had been treated in our endocrine outpatient clinic between 1975 and 1989. 31 adult patients (25 females and 6 males) fulfilled the criteria for PGAS Type II (association of autoimmune endocrine disease with at least one other--usually endocrine--autoimmune disease or autoantibodies against another organ). Among these patients, 18 had hypothyroidism due to autoimmune thyroiditis, 8 were hyperthyroid (Graves' disease), and 4 had silent autoimmune thyroiditis (without thyroid dysfunction). Insulin dependent (type I) diabetes mellitus (IDDM) was seen in 11, Addison's disease in 7, primary hypogonadism in 5, vitiligo in 6 and pernicious anemia in 5 cases. The presence of antiparietal cell antibodies was demonstrated in 21 of 30 investigated patients. These patients also showed other evidence of autoimmune gastritis, such as increased gastrin (in 10 out of 13), diminished vitamin B12 levels (6 out of 13), atrophic gastritis (9 out of 9), pernicious anemia (6 out of 30) and funicular myelosis (2 out of 30). CONCLUSION: The most common endocrine diseases in our patient group were autoimmune thyroid diseases (97%) followed by IDDM (35%) and Addison's disease (23%). A high percentage (70%) of our subjects had elevated titers of antiparietal cell antibodies. Polyglandular autoimmune syndrome must be suspected in all patients with autoimmune endocrine disease, especially in the presence of relatives suffering from PGAS. Patients at risk should be screened regularly by measuring thyrotropin (ultrasensitive assay), fasting blood glucose levels, and by checking red blood count and antiparietal cell antibodies.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1976

[Search for embryonic antigens in the serum of leukemia patients].

The authors examined patients with blastic leucosis, myelosis and lympholeucosis for the presence of specific embrional antigens by immunodiffusion, using antisera, obtained after immunization of rabbits with extracts from human embryos and absorbed with tissue extracts from a normal adult. There were no specific embryonal components in the patients with leucemic sera or in the women from the control group.

Adult↗
PubMed1993

[Treatment of the leukostasis syndrome in chronic lymphadenosis using leukapheresis].

The authors draw attention to the leukostasis syndrome which develops in haematological patients in case of enormous leucocyte proliferation. It occurs most frequently in chronic myelosis but may occur also in other types of leukaemia. The diagnosis is not easy. Most frequently disorders of the microcirculation develop in the lungs and brain. These are frequently very urgent clinical situations which can be resolved by leukapheresis. The authors described a patient where during chronic lymphadenosis proliferation of lymphocytes occurred to values of 1432 x 10(9)/l. After leukapheresis and cytostatic treatment rapid improvement of the condition occurred and the leucocyte values were approximately 30 x 10(9)/l. The patient's condition improved for a long period of time and became stabilized.

Humans↗
PubMed1993

[Interferon therapy in essential thrombocythemia].

Interferon-alpha (IFN-alpha) exhibits a clear platelet reductive effect in patients with essential thrombocythemia as well as in other chronic myeloproliferative disorders with thrombocytosis. In a total of 51 patients with chronic myeloproliferative disorders with thrombocytosis we analyzed the effect of IFN-alpha in respect to platelet reduction, remission rates, induction- and maintenance dosage, long term tolerance and side effects. According to our classification CML 6, chronic mega-karyocytic granulocytic myelosis 5, essential thrombocythemia 26 and polycythemia vera 15 patients were treated. Treatment consisted of induction with 3 or 5 MU IFN-alpha daily followed by a maintenance therapy with 3 or 5 MU thrice weekly. Platelet reduction was found in all patients, CR (platelets < 450 G/l) in 78%. Within 2 months of induction therapy, CR in patients treated with 5 MU IFN daily was found in 75% compared to 52% in patients treated with 3 MU IFN daily. Dosage reduction in maintenance periode caused an increase of platelets to more than 450 G/l in 39% of patients. Out of 40 Philadelphia-negative chronic myeloproliferative disorders treated for more than 3 months in 10 patients treatment was disrupted after 5 to 18 months because of the following side effects: nausea, fatigue, vertigo, fever, headache, diarrhea, anorexia, heartburn, hairloss, myalgia, and thrombocytopenia. Due to the mutagenic effect of alkylating cytostatics and Radiophosphorus, IFN-alpha treatment represents a first line strategy for chronic myeloproliferative disorders with thrombocytosis especially in younger patients who are symptomatic and in those who suffered from episodes of bleeding or thrombosis.

Dose-Response Relationship, Drug↗
PubMed1993

[HLA-DR antigens and leukemias].

In 79 leukaemic subjects (42 with acute leukaemia, 37 with chronic myelosis) the authors assessed HLA-DR antigens 1-5.7 and their frequency. As compared with a group of 130 healthy subjects, no significant difference was found. The results do not support a possible relationship of HLA-DR antigens and leukaemia.

HLA-DR Antigens↗
PubMed1993

[Histopathology and molecular pathology of chronic myeloproliferative disorders].

Diagnosis of chronic myeloproliferative disorders (CMPD) can encounter difficulties due to overlaps and possible transitions between the different entities and their similarity to reactive myeloproliferations. In this study DNA analysis has been applied to improve differentiation of CMPD. All subtypes of CMPD analyzed, including chronic myeloid leukemia (CML), agnogenic myeloid metaplasia (AMM), polycythemia vera (PV), and essential thrombocythemia (ET), had in common that granulocytes and bone marrow cells were clonal in origin as shown by X-chromosome-linked DNA polymorphism in conjunction with methylation patterns. Reactive myeloproliferations, by contrast, revealed a polyclonal inactivation pattern. Clonality could not distinguish CMPD from cases of myelodysplastic syndrome (MDS) since the latter also exhibited clonal hematopoiesis. AMM belongs to the group of myeloproliferative syndromes. Up to now the cellular phase at onset of the disease (megakaryocytic myelosis) has not been analyzed for clonality of the hematopoietic cells. Granulocytes as well as bone marrow cells from the cellular phase and advanced stages of the disease revealed a monoclonal inactivation pattern of X-chromosomal genes. These results show that the cellular phase already represents a monoclonal, and hence probably a neoplastic, proliferation of a pluripotent stem cell. The monoclonality of granulocytes could also be demonstrated in patients with splenomegaly and strongly argues against a compensatory proliferation of regular hematopoiesis in this organ. Because of their clonal origin, peripheral granulocytes were used in all cases (n = 244) for the detection of bcr-gene rearrangement. Despite possible morphological overlaps between different types of CMPD, bcr-gene rearrangement proved to be specific for CML and could be applied to differentiate CML from other CMPD in cases of uncertain morphological diagnosis. It is concluded that CMPD represent clonal hemopoietic disorders that probably have specific underlying genetic defects. Thus, DNA analysis can substantially aid in the differential diagnosis of CMPD.

Base Sequence↗
PubMed1997

Lifetime treatment of mice with azidothymidine (AZT) produces myelodysplasia.

AZT has induced a macrocytic anemia in AIDS patients on long term AZT therapy. It is generally assumed that DNA elongation is stopped by the insertion of AZT into the chain in place of thymidine thus preventing the phosphate hydroxyl linkages and therefore suppresses hemopoietic progenitor cell proliferation in an early stage of differentiation. CBA/Ca male mice started on AZT 0.75 mg/ml H2O at 84 days of age and kept on it for 687 days when dosage reduced to 0.5 mg/ml H2O for a group, another group removed from AZT to see recovery, and third group remained on 0.75 mg. At 687 days mice that had been on 0.75 mg had average platelet counts of 2.5 x 10(6). Histological examination on 9 of 10 mice with such thrombocytopenia showed changes compatible with myelodysplastic syndrome (MDS). A variety of histological patterns was observed. There were two cases of hypocellular myelodysplasia, two cases of hypersegmented myelodysplastic granulocytosis, two cases of hypercellular marrow with abnormal megakaryocytes with bizarre nuclei, one case of megakaryocytic myelosis associated with a hyperplastic marrow, dysmyelopoiesis and a hypocellular marrow and two cases of myelodysplasia with dyserythropoiesis, hemosiderosis and a hypocellular marrow. Above mentioned AZT incorporation may have induced an ineffective hemopoiesis in the primitive hemopoietic progenitor cells, which is known to be seen commonly in the myelodysplastic syndrome.

Acquired Immunodeficiency Syndrome↗
PubMedDate not supplied

[Neurologic disorders in a patient with autoimmune hemolytic anemia].

Completely different entities might be with the same possibility in the baseline of interweaving of symptoms and signs of nervous system damage. One of them, the deficiency of vitamin B12 very frequently causes megaloblastic anemia and funicular myelosis. In the case of our patient, after the clinical picture of hemolytic anemia was revealed, by slow-progressive course was developed neurologic deficiency that, according to its features, could have the deficiency of cobalamin and folic acid in its etiologic background. On the basis of disease course, clinical finding, numerous clinical investigations so as the reaction to applied therapy it was assumed that the patient had besides confirmed autoimmune hemolytic anemia the pernicious anemia as the associated cause of anemic syndrome and the basic reason of the development of neurologic deficiency. Described is the frequent associated occurrence of pernicious anemia and antiglobulin positive hemolytic anemia, so as the significant association of pernicious anemia with the deficiency of immunoglobulins that was otherwise observed in our patient as the permanent IgA deficiency.

Adult↗