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D Tomin

Publications and source records attributed to D Tomin.

11 recordsLinked to original sources
PubMed2002

[Late results of splenectomy in patients with chronic immune thrombocytopenic purpura].

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.

Adolescent↗
PubMed2002

[Cesarean section combined with splenectomy in severely resistant immune thrombocytopenia].

Immune thrombocytopenic purpura (ITP) associated with pregnancy often involves considerable risk both for mother and child, and usually worsens in the third trimester of gestation. Pregnancy and delivery are especially difficult in patients with severe ITP (platelet count below 20 x 10(9)/L), who are resistant to prednisone and high dose intravenous immunoglobulin (IVIgG). In those cases we applied cesarean section (CS), to prevent intracranial haemorrhage due to fetal/neonatal ITP, and splenectomy at the same time as an effective therapeutic strategy for ITP. We present 5 patients (4 with chronic ITP and 1 with ITP associated with HIV infection), aged 21-35 years, with severe ITP (platelet count 2-10 x 109/L), resistant to prednisone (1-2 mg/kg), and 2/3 were resistant to IVIgG (0.4 g/kg x 5 d). Four patients with severe resistant ITP were supported with 1-2 doses of platelets from cell separator before CS and 1-3 dose during splenectomy. One patient increased platelet count to 55 x 109/L after treatment with IVIgG and splenectomy following CS were done without platelet transfusion. Splenectomy was performed immediately after CS in all patients, and two of them were hysterectomised (one with HIV infection). After splenectomy, platelet count was normalised in all patients, and they had no haemorrhage, wound haematoma formation or any adverse events. But ITP relapsed in 2/5 patients after 1-2 months. Two newborns had severe thrombocytopenia, which solved spontaneously after 3 days in one or after treatment with IVIgG in other. We propose that splenectomy following cesarean section should be considered as approach for delivery and treatment option for mothers with severe resistant ITP.

Adult↗
PubMed2000

Pregnancy after treatment of secondary acute promyelocytic leukemia following Hodgkin's disease: a case report.

The authors report a case of therapy-related acute promyelocytic leukemia (t-APL), with typical cytogenetic translocation t(15;17), which appeared following chemotherapy (ABVD), and radiotherapy for Hodgkin's disease (IIB). After treatment with all-trans retinoic acid (Vesanoid(R) 45 mg/m2 daily) complete remission of t-APL was achieved. Then only one course of chemotherapy '3+7' (doxorubicin 45 mg/m2 1-3 d, cytosar 200 mg/m2 1-7d) was applied and the patient interrupted further treatment in July 1994. Four years later she had a normal pregnancy and delivered a healthy female infant in December 1998.

Adolescent↗
PubMed1989

Chronic myeloid leukemia associated with pure red cell aplasia and terminating in promyelocytic transformation.

After intermittent treatment with busulphan over a 7-year period for chronic myeloid leukemia (CML) in chronic phase, a 39-year-old female developed leukocytosis in association with pure red cell aplasia (PRCA). Bone marrow examination confirmed erythroid aplasia, and culture revealed a total absence of erythroid progenitor cells. The patient then was treated with azathioprine, corticosteroids, cyclophosphamide, plasma exchange, and cyclosporin A, but she remained erythroblastopenic and transfusion dependent for more than a year, at which time a promyelocytic transformation supervened. The authors propose that this sequence of events, hitherto unreported, is a manifestation of the multistep progression of CML.

Adult↗
PubMedDate not supplied

[T-cell-rich B-cell lymphoma].

The authors present three patients, one female and two males, with special forms of non-Hodgkin's lymphoma, the so called T-cell rich B-cell lymphoma (TCRBCL). This is a relatively new entity which has not yet been described in our literature. The first diagnosis in our female patient was Hodgkin's disease. However, the revision of old and new lymph node samples and use of immunohistochemical analysis helped the establishing of diagnosis--TCRBCL. In the other two patients the diagnosis of TCRBCL was established on the basis of immunohistochemical analysis of the lymph node which indicated the dominating T-lymphocytes, positive to pan-T antigen (CD45 RO+), with considerably lower count of B-lymphocyte elements positive to CD20+. The female patient survived 33 months from the time of diagnosis. The other two patients experienced complete remission lasting 10 and 12 months after the end of therapy.

Adult↗
PubMedDate not supplied

[Neuroleukemia in adults].

Involvement of CNS with leukemic cells is well recognized complication of acute lymphatic leukemia (ALL) in childhood, but with recent improvements in systemic treatment and longer survival the incidence of this complication has increased in adults. Neurological symptomatology in patients with CNS leukemia is due to meningeal infiltration, but sometimes also to diffuse and nodular cerebral infiltration. Between January 1991 and December 1994, 36 patients suffering of acute leukemia, 28 with ALL, and 8 with acute myeloid leukemia (AML) were demonstrated to have neuroleukemia by the following criteria: (1) the presence at lumbar puncture (LP) pleocytosis and blast cells on CSF sediment (without positive bacteriologic and fungal cultures), and (2) the presence of neurological symptoms and signs. All 36 patients had 46 episodes of CNS involvement. All patients had neurological examinations during every episode, and according to the neurological abnormalities were classified into four categories. LP was performed in all, and CSF sediments obtained by sedimentation in Sayk's chambers, were routinely stained by MGG and cytochemical stains to detection of leukemic cells (Fig. 1). EEG was done during 21 episodes, CT scan during 15. We divided patients into four groups according to the most prominent neurological symptoms and signs. First was the group included 23 episodes (50%), (18 ALL, 5 AML), where symptoms and signs of meningeal irritation predominated, mimicking the clinical picture of meningitis. This meningeal syndrome can sometimes produce differential diagnostic problems with CNS infections, when CSF examination is of primary importance. Second was the group of 9 patients (6 ALL and 3 AML) with 10 episodes (21.74%) where cranial nerve symptoms and signs-predominated, or were exclusively present. Most frequently affected were bulbomotors, facials and opticus. Third group consisted of 8 ALL patients (8 episodes, 17.39%) with dominant spinal root symptomatology, caused by pathological infiltration of either spinal roots or meninges surrounding them. This group includes also one patient with mononeuritis multiplex and the other with painful polyneuropathy. All patients in this group had pain on straight leg raising, but we stress here that all patients from other groups had positive Lazarevitsh's sign, too. So, it can be a good differential diagnostic parameter for distinguishing toxic medicamentous polyneuropathy from leukemic poliradiculoneuropathy. Fourth group included 5 patients (5 episodes, 10.87%). 4 ALL and 1 AML, where cerebral symptoms, such as seizures, hemiparesis and psychoorganic syndromes were prominent. CSF was obtained during all episodes by lumbar puncture. The protein concentration ranged from 21-3180 mg/dl, and was above normal (45 mg/dl) during 28 episodes. Mild hypoglycoracchia was present during 16 episodes. Cell count ranged from 11-4816 cells/cm3, malignant cells were identified during all episodes with same morphological and cytochemical characteristics of identified type of leukaemia. It has been established that the most valuable diagnostic procedure in CNS leukemia is CSF examination, and detection of blasts is sufficient for diagnosis. All other procedures like EEG, myelography and CT have only supplemental diagnostic significance. Finally, in this study we showed that neurological symptomatology in patients with acute leukemia is not dependent of the type of leukemia, moreover different types of AL can have same neurological manifestations. As others, we sometimes used the term CNS leukemia in this paper, although it is clear that meninges and peripheral nervous system are most often involved. This is the reason why we suggest that neuroleukemia, or NS leukemia should be used as more appropriate expressions.

Acute Disease↗
PubMedDate not supplied

[Results of treatment of patients with advanced multiple myeloma with the vincristine-adriamycin-dexamethasone protocol].

UNLABELLED: A very few treatment regimens have shown a benefit in patients with multiple myeloma resistant to conventional melphalan/prednosone therapy or similar combinations. The first "biologically designed" protocol for the treatment of advanced, refractory myeloma was a combination of vincristine, doxorubicin and intermittent high-dose dexamethasone, so called VAD regimen. This report summarizes our experience in VAD regimen in the treatment of advanced, refractory myeloma patients, initially treated with melphalan-based chemotherapy. METHODS: Between July 1989 and July 1995, 27 patients with high-tumour-mass stage (Durie Salmon staging system) of the disease were treated with VAD combination. Clinical characteristics of patients are shown in Table 1. There were 17 pts who never responded (9 pts) of who progressed during induction therapy (8 pts). The second group of 10 pts responded to induction therapy and relapsed. Five pts (four with progressive and one with resistant myeloma) were treated with VAD therapy particularly due to significant extramedullary infiltrates. All pts in this study were initially treated with VMCP induction therapy. Seven of them were additionally treated with ABP combination, and this subgroup of pts was characterized as "resistant to melphalan and doxorubicin". The VAD regimen consisted of four-day continuous infusions of vincristine (0.4 mg per day) and doxorubicin (9 mg/m2 per day) in addition to dexamethasone in a dose of 40 mg for four days, beginning od days 1.9 and 17 of each cycle. The response was defined as a reduction of serum myeloma-protein concentration exceeding 75 per cent, with disappearance of Bence-Jones protein excretion. RESULTS: "Good" response to VAD regimen was achieved in 12 of 27 pts (44 per cent), mainly after three cycles of chemotherapy (Table 2). The tumour reduction occurred rapidly (Table 3), without significant myelosuppression. Response-rate was significantly higher in relapsing myeloma pts than in pts with progressive or resistant disease (chi 2 = 4.2; p < 0.05). Neither previous treatment (Table 2) nor the type or paraprotein concentration, degree of marrow infiltration and cytologic type of plasma cells affected the response to VAD. Among 15 pts with "bad" response to VAD, seven died during first four months of treatment. All pts with significant extramedullary infiltrates failed to respond to VAD (chi 2 = 4.91; p < 0.05). Median survival of all pts was 16 months. In responsive pts remissions were of good quality and survival was significantly longer that that in whom treatment failed (Figure 1, left). In responsive pts the median duration of "plateau-phase" was 11 months (Figure 1, right). In three pts who relapsed after the treatment, reinstitution of VAD regimen restored the "plateau-phase". The most important complications of treatment with VAD combination were infections (8 pts) but, fortunately, serious forms (i.e. pneumonia) were observed only in two pts. DISCUSSION: The antitumour effect of VAD regimen originates from a combined effect of doxorubicin and vincristine continuous infusions and intermittent pulses of high-dose corticosteroids. The rationale for protracted administration of vincristine and doxorubicin was based on long generation time and low growth fraction of plasma cells in most patients, while the use of high-dose dexamethasone was based on well-known dose-depend antimyeloma effect of corticosteroids. Using this chemotherapy schedule, significant prolongation of survival was achieved in our responding patients comparing to patients with VAD-resistant myeloma. The major toxic effect of treatment was infection, which was attributed in part to intensive steroid program. Relapse of the disease could be expected about one year after completion of VAD therapy. Nevertheless, the second "plateau-phase" can be obtained upon reinitiation of VAD (ABSTRACT TRUNCATED).

Adult↗