Biomedical subjects
Publications and source records attributed to N Suvajdzić.
We report the case of a littoral-cell angioma of the spleen, a recently described benign vascular tumour, whose imaging and pathological characteristics have been discussed only by a few authors. The diagnosis was made after elective splenectomy. The CT images, scintigraphy and histological specimens are presented, and differential diagnoses discussed.
BACKGROUND: Endoscopic ultrasonography (EUS) is an important tool for diagnosis and pretreatment staging of primary gastric lymphoma. The aim of the study was to evaluate the diagnostic importance of endosonography (EUS) in gastric lymphoma; to assess the depth of tumoral infiltration in low-grade gastric lymphoma of mucosa-associated lymphoid tissue (MALT) and to assess EUS response to medical treatment (Cyclophosphamid/Mabtera and/or anti-Helicobacter pylori therapy). METHODS: 26 patients with MALT gastric lymphoma were investigated by EUS. Six of them were evaluated after the eradication of Helicobacter pylori infection and 20 after and during the cyclophosphamide/Mabtera and anti H. pylori treatment. EUS staging was compared with histopathology. Tumours were staged according to the 2000 TNM and modified Ann Arbor classification. RESULTS: Six patients were treated with anti - Helicobacter pylori eradication therapy. Full regression of lymphoma was observed in 2 of 6 (33.3%) patients, which was endoscopicaly and histologicaly proved. EUS correlated with histology in all (6/6). In 20 patients treated with cyclophosphamide/Mabtera therapy, EUS revealed regression of lymphoma in 14 cases. Positive correlation with histology was found in 11 patients (11/14; 78%). The initial EUS showed an increased wall thickness more than 5mm in 24 of 26 patients (92%). The thickening was predominantly of mucosa and submucosa and in 11 patients extended the muscularis propria. After the therapy, the gastric wall thickening returned to normal in 14 patients, however, 3 of them still had positive histology findings. In 2 cases, during the follow-up, the EUS showed remained thickening of gastric wall, whereas biopsies were negative. Six months later histology revealed progressive low-grade MALT lymphoma in this cases. CONCLUSION: EUS appears to be a sensitive procedure for initial staging and assessment of treatment response and long-term follow up in patients with gastric lymphoma. The importance of EUS lies in abbility to detect relapse early, too.
BACKGROUND: Between January 1989 and July 1995, a prospective study of the therapeutic efficacy of the LALA 87 protocol in adult acute lymphoblastic leukaemia (ALL) has been conducted. METHODS: A total of hundred and twelve patients with ALL have been analysed. The median age of the patients was 40 years (range: 15-65), the gender ratio (M/F) was 66/46, and the morphologic FAB (French-American-British) profile was L1 in 30 (26.9%) patients, L2 in 71 (63.3%) and L3 morphology in 11 (9.8%) of the patients. The LALA 87 protocol includes five phases: induction, consolidation, reinforcement, maintenance and central nervous system (CNS) prophylaxis with intrathecal methotrexate and irradiation. The induction phase comprised daunorubicin 50 mg/m(2) (days 1-3), cyclophosphamide 600 mg/m(2) (days 1 and 8), vincristine 1.5 mg/m(2) (on days 1, 8, 15 and 22) and daily oral prednisone on days 1-21. Maintenance therapy was given for 2 years and consisted of different drugs as reinforcement, daily 6-mercaptopurine and weekly methotrexate. RESULTS: Complete remission (CR) was achieved in 81 (72.3%) of the patients. The causes of induction failure were partial response in 10 (8.9%), and hypoplastic death in 12 patients (10.7%), and 9 were non-responders (8.0%). Of the 81 patients who achieved CR, 62 relapsed (76%). Among the relapsed patients, 9 developed CNS disease in spite of CNS prophylaxis during induction chemotherapy. Median follow-up for the living patients was 110 months. Median disease-free survival (DFS) was 16 months; 19 patients are still in remission with an estimated 10-year DFS (24%). Adverse prognostic factors were >50 years of age, immunologic subtype and cytogenetic profile. CONCLUSION: The results support the strategy of applying more effort and other treatment modalities in the therapy of ALL.
Splenectomy is definitive treatment for idiopathic thrombocytopenic purpura (ITP) because it removes both the sites of autoantibody producing cells and also the major site of platelet destruction. The purpose of this study was to evaluate long term results of splenectomised patients with ITP and to determine predictor factors for good response. A 167 patients with chronic ITP (136 females, 31 males), median aged 35 years (17-74) was splenectomised after 2 to 160 months (Median 12) from diagnosis of ITP. Indications for splenectomy were: 6 weeks of steroid therapy with platelet count below 10 x 10(9)/l or 3 months with platelet count under 30 x 10(9)/l, or treatment with prednisone above 30 mg more of 6 months to increase platelet count over 30 x 10(9)/l, or repeated relapses. Postoperative complications developed in 16 patients (9.5%), 3 of them died (1.8%) due to thromboembolism and 17 patients discontinued later controls. During follow up to 172 months (Median 62) 111/147 splenectomised patients were in remission (75.5%), 99 in complete (above 100 x 10(9)/l), 12 in partial (50-100 x 10(9)/l) and 36 patients (24.5%) were relapsed (below 50 x 10(9)/l). Remission was achieved in 79/88 patients (89.8%) with good response to prednisone before splenectomy toward 32/62 patients (51.6%) with poor response to prednisone (p < 0.01). Remission was obtained in 9/11 patients (81.8%) who responded well to intravenous immune globulin (0.4 g/kg x 5 d) and only in 1/8 who did not (p < 0.05). Higher response rate was achieved in patients under 40 years of age (81.6%) than in older ones (63.4%) (p < 0.05). No difference was shown between sex and time intervals (3, 6, 12, 24, 36 or over 36 months) from diagnosis to splenectomy. Splenectomy is an effective treatment of refractory ITP with response rate of 75.5% after median follow up of 62 months. In our patients better results on splenectomy were associated with age less than 40 years, good responses to steroid, and intravenous immune globulin.
Monocytoid B cell lymphoma (MBCL) is an immunologically and morphologically well-defined low-grade lymphoma with a predilection for lymph nodes of the parotid region. We describe an association of MBCL with anti-myelin-associated glycoprotein (MAG) polyneuropathy in a 53-year-old male. The diagnosis of stage IV MBCL with nodular bone marrow infiltration, Sjögren's syndrome and sensorimotor polyneuropathy was made in October 1996. Serum immunoelectrophoresis demonstrated IgMkappa paraprotein. This was then cross-reacted with epitopes of MAG and sulphated glucuronyl paragloboside (SGPG) on myelin sheaths, and detected by thin layer chromatography and Western blot. Direct immunofluorescence of a sural nerve biopsy showed loss of myelin fibres, segmental demyelinization and IgM deposits on the myelin sheaths. The cerebrospinal fluid was normal. After six cycles of chemotherapy (ChlVPP protocol), all the patient's haematological parameters normalized accompanied by an improvement in neurological signs. The improvement of the polyneuropathy after chemotherapy indicates that the autoimmune anti-MAG and anti-SGPG antibodies resulted from the neoplastic lymphoid proliferation.
A 39-year-old woman with a history of travel to the Montenegrin coast presented with a 9-month long history of fever and weakness, and on examination was found to be emaciated with hepatosplenomegaly and pancytopenia. Marrow aspiration showed poor cellularity with abundant Leishman Donovan (LD) bodies in the macrophages. Bone marrow trephine biopsy revealed a marked myelofibrosis (Manoharan classification: grade III) with osteosclerosis. The impression smears of a trephine biopsy stained with Güiemsa also showed LD bodies. The patient did not exhibit evidence of any risk factors for visceral leishmaniasis (VL). She was treated with meglumine antimoniate (Glucantime) without any adverse effect. The spleen returned to a normal volume after 4 months and bone marrow trephine biopsy performed 6 months after initiation of the therapy had returned to normal. A diagnosis was difficult to establish as VL is rarely encountered in the continental parts of Yugoslavia, and with the presence of associated myelofibrosis it could easily have been mistaken for chronic idiopathic myelofibrosis. The association of myelofibrosis with visceral leishmaniasis has been reported in the literature only three times; we thus feel that documentation of this case is merited.
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We report a 34-year-old woman with sequentially occurring autoimmune diseases that are possibly triggered by numerous ovulation inductions. At the ages of 26-32 years, she experienced 27 uncontrolled ovulation induction cycles using clomiphene citrate (CC) or CC plus human menopausal gonadotropin plus human chorionic gonadotropin. She became pregnant at the ages of 27, 30 and 31 with subsequent pregnancy loss in the 28th, 8th and 10th week of gestation, respectively. Insulin-dependent diabetes mellitus (IDDM) developed at the age of 28. During the second year of ovulation induction, at the age of 27, she developed arthralgia that worsened and became migratory from the age of 31. Thrombocytopenia appeared at the age of 33. The diagnosis of systemic lupus erythematosus (SLE) and antiphospholipid syndrome (APS) was established at the age of 34. To the best of our knowledge, this is the first case of concurrent IDDM, SLE and APS in a patient associated with ovulation inductions. Excessive levels of estradiol achieved during the ovulation inductions could play a role in the expression of multiple autoimmune diseases in the susceptible woman.
Hepatosplenic candidiasis following granulocytopenic periods is a relatively recently recognised problem in immunocompromised patients, particularly in those with acute leukaemia. We present three patients in whom diagnosis of hepatosplenic candidiasis was suspected on the basis of ultrasonographic (US), computed tomographic (CT) findings and confirmed by laparoscopy and biopsy of liver lesions. All three patients were successfully treated briefly with amphotericin B, followed by a longer period of fluconazole. In one patient laparotomy and surgical evacuation of abscesses was performed. This condition could be more often recognised by careful follow-up of liver function test, C-reactive protein level, ultrasonography, CT and MRI after recovery from chemotherapy-induced neutropenia.
The extent of megakaryocytopoiesis (Mk-poiesis) and clinical outcome are evaluated in 14 patients with severe refractory chronic immune thrombocytopenia (rchr ITP). Three out of 14 patients died due to hemorrhage. The number of bleeding episodes and the number of treatment modalities proved to be both sensitive prognostic survival parameters (p < 0.05). Thirty two corticosteroid responsive chr ITP patients (chr ITPPR), 15 not treated patients (chr ITP(NT)) and 14 healthy volunteers (C) served as a control. There was a significant difference in the platelet count between the study groups (p < 0.05). The number of megakaryocytes and promegakaryoblasts per mm3 of bone marrow were significantly lower in rchr ITP patients (p < 0.05) than in chr ITP(PR) and in chr ITP(NT) group, thus implying an inadequate Mk-poiesis in rITP chr patients. From the data presented here it may be suggested that the inadequate Mk-poiesis is operating in rchr ITP.
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The Belgrade laboratory (b/b) rat has a hereditary hypochromic microcytic anemia because of defective transmembrane iron transport into erythroblasts. The present study was prompted by our previous work in which we showed that the b/b rat has hypomegakaryocytic thrombocytopenia associated with increased megakaryocyte size. To define the basic mechanism underlying this abnormality in the b/b rat we have studied both megakaryocytopoiesis and granulopoiesis in anemic b/b rats, chronically transfused b/b rats, iron-treated b/b rats, and controls. We have found decreased concentrations of megakaryocyte and granulocyte progenitors in the marrow of b/b rats. Full correction of the severe anemia by chronic transfusion resulted in normalization of megakaryocyte progenitors, small acetylcholinesterase positive cells, megakaryocyte size, and platelet counts, along with granulocyte progenitors. In contrast, the partial correction of anemia obtained by iron treatment resulted in improvement, but not normalization, of these parameters. These findings indicate that abnormal megakaryocytopoiesis in the b/b rat can be best interpreted as a consequence of hypoxia because of the severe anemia. Because we have recently shown that the number of erythroid progenitors in b/b rats is also low, we propose that abnormal megakaryocytopoiesis in this animal is a reflection of an acquired stem cell disorder induced by the prolonged hypoxia resulting from the severe anemia.
The aim of this work was to investigate T cell subset composition of peripheral blood cells in patients with acute myeloid leukaemia, acute lymphoblastic and chronic lymphocytic leukaemia, by enumerating T cells positive for receptors for sheep erythrocytes (E-RFC, A-RFC) using the method of E-rosette, and for CD3, CD4 and CD8 antigens, by indirect immunofluorescence technique, using the monoclonal antibodies of the OK series. The study was performed on 57 patients without therapy and 46 healthy persons. The results of enumeration of T cells and their subsets obtained in the stage of the disease when the total leukocyte count was below 20 x 10(9)/L, were markedly decreased in all three types of leukaemias. The most significant decrease of relative count of T cells and their subpopulations was obtained in CLL patients. Analysis of T cells subsets and their ratio in CLL patient in the stage of disease when the total leukocyte count as higher than 20 x 10(9)/L, demonstrated the most pronounced decrease of total T lymphocytes and CD4+ cells. The relative count of the "active" (A-RFC)T cells and CD8+ cells did not change, and was the same as in the patients suffering from CLL with a lower leukocyte count.
It was recently proposed that prolonged hypoxia produces hypomegakaryocytic thrombocytopenia by reducing the pool of committed megakaryocyte progenitor cells at the expense of a greatly expanded erythroid progenitor pool. In order to test this hypothesis we have studied the relationship between megakaryocytopoiesis, erythropoiesis, and granulopoiesis at the level of progenitor cells (megakaryocyte colony-forming unit, CFU-Mk; erythroid CFU, CFU-E; erythroid burst-forming units; BFU-E; and granulocyte-macrophage CFU, CFU-GM) in the marrow of rats exposed for 4 weeks to normobaric hypoxia. We have found that hypomegakaryocytic thrombocytopenia was accompanied by decreased CFU-Mk, increased CFU-E, and a normal number of BFU-E and CFU-GM. These results support the hypothesis that prolonged hypoxia reduces the precursor cell commitment to differentiate into the megakaryocyte series by enhancing demand for differentiation into the erythroid cell line. However, the underlying mechanism needs further investigation.
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A patient with Ph1(Philadelphia chromosome) positive chronic granulocytic leukemia and extramedullary blast transformation (crisis) in lymph nodes of neck and axillae which appeared after 4-year of treatment with busulfan is presented. Biopsy of lymph node and histopathological examination showed lymphoblastic infiltration. The patient was treated with radiotherapy and chemotherapy with protocol COP. He survived 7 months and expired due to renal insufficiency.