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Biomedical subjects

E Montserrat

Publications and source records attributed to E Montserrat.

At least 127 records · Page 7Linked to original sources
PubMed1998

[Contribution of magnetic resonance to the differential diagnosis of a collapsed vertebra in a patient with multiple myeloma].

The only safe method to determine whether or not patients diagnosed of smoldering myeloma will progress to symptomatic multiple myeloma (MM) is periodic follow-up. In the last years, several studies have emphasized the efficacy of magnetic resonance imaging (MRI) to detect bone marrow involvement in these patients. However, the detection of a focal spinal lesion in elderly patients raises a diagnostic problem, sometimes difficult to solve, between a benign or malignant origin. We present the case of an elderly women with marked osteoporosis and smoldering myeloma who suddenly complained of pain in dorsal spine. MRI showed focal lesions in two dorsal vertebra consistent with myeloma involvement. However, there were no other signs of progression, the lesions were considered secondary to osteoporosis and calcitonin was administered. This resulted in the disappearance of the pain and the MRI abnormalities, which confirmed its benign etiology. The role and limitations of MRI to detect bone marrow involvement by MM in the evaluation of these patients is reviewed.

Aged↗
PubMed1998

High frequency of donor chimerism after allogeneic transplantation of CD34+-selected peripheral blood cells.

Ex vivo T cell depletion of allogeneic grafts is associated with a high (up to 80%) rate of mixed chimerism (MC) posttransplantation. The number of transplanted progenitor cells is an important factor in achieving complete donor chimerism in the T cell depletion setting. Use of granulocyte colony-stimulating factor (G-CSF) peripheral blood allografts allows the administration of large numbers of CD34+ cells. We studied the chimeric status of 13 patients who received allogeneic CD34+-selected peripheral blood progenitor cell transplants (allo-PBPCTs/CD34+) from HLA-identical sibling donors. Patients were conditioned with cyclophosphamide (120 mg/kg) and total-body irradiation (13 Gy in four fractions). Apheresis products were T cell-depleted by the immunoadsorption avidin-biotin method. The median number of CD34+ and CD3+ cells infused was 2.8x10(6)/kg (range 1.9-8.6x10(6)/kg) and 0.4x10(6)/kg (range 0.3-1x10(6)/kg), respectively. Molecular analysis of the engraftment was performed using polymerase chain reaction (PCR) amplification of highly polymorphic short tandem repeat (PCR-STR) sequences in peripheral blood samples. MC was detected in two (15%) of 13 patients. These two patients relapsed at 8 and 10 months after transplant, respectively. The remaining 11 patients showed complete donor chimerism and were in clinical remission after a maximum follow-up period of 24 months (range 6-24 months). These results were compared with those obtained in 10 patients who were treated with T cell-depleted bone marrow transplantation by means of elutriation and who received the same conditioning treatment and similar amounts of CD3+ cells (median 0.45x10(6)/kg; not significant) but a lower number of CD34+ cells (median 0.8x10(6)/kg; p = 0.001). MC was documented in six of 10 patients (60%), which was significantly higher than in the allo-PBPCT/CD34+ group (p = 0.04). We conclude that a high frequency of complete donor chimerism is achieved in patients receiving allo-PBPCT/CD34+ and that this is most likely due to the high number of progenitor cells administered.

Adult↗
PubMed1998

Transient pancytopenia after non-A non-B non-C acute hepatitis preceding acute lymphoblastic leukemia.

Transient pancytopenia preceding childhood acute lymphoblastic leukemia (ALL) is an unfrequent but well-known event. The association of this preleukemic syndrome with hepatitis is extremely rare, with only two such cases having been published in the literature. We report the case of a 16-year-old boy who was diagnosed with B-cell type ALL that was preceded by transient pancytopenia with absent hemopoietic cells in the bone marrow following a seronegative hepatitis episode. The clinical, morphologic and immunophenotypic features of this patient are described and the literature on this preleukemic syndrome reviewed, with special emphasis being made on its differential diagnosis with hepatitis-associated aplastic anemia.

Adolescent↗
PubMed1998

[Primary MALT-type lymphoma of the breast].

A 47 year old woman with a MALT lymphoma affecting the breast exclusively is reported. Complete response was achieved after CHOP chemotherapy but three years later a relapse was observed. Second-line chemotherapy (CNOP) and local radiotherapy were administered, and a second remission was obtained lasting for 1 year at last follow-up. A bibliographic search of MALT lymphomas of the breast showed that most such cases correspond to localized forms (stage I-II) and that from the radiologic point of view nodular lesions are almost the rule, although in the present case diffuse involvement was observed. MALT lymphomas of the breast tend to remain localized, and to relapse locally, and these facts appear as independent of the treatment applied (surgery, radiotherapy, chemotherapy or any combination).

Antineoplastic Combined Chemotherapy Protocols↗
PubMed1998

K-ras gene mutations in the diagnosis of fine-needle aspirates of pancreatic masses: prospective study using two techniques with different detection limits.

Detection of K-ras mutations may be useful in the evaluation of pancreatic cancer. The aim of this study was to assess, in a prospective design, the diagnostic utility of K-ras mutation analysis in 62 consecutive fine-needle aspirates of pancreatic masses, using two PCR-based techniques-standard and enriched-with detection limits of a mutant allele in the presence of 10(2) or 10(3) wild-type alleles, respectively. Cytology alone offered a diagnostic sensitivity of 75%. The enriched higher sensitivity detection technique, in combination with cytology, offered a diagnostic sensitivity of 91% without false positives. The molecular analysis would have contributed to diagnosis in an additional 14 cases of pancreatic cancer. The standard technique contributed to diagnosis in an additional 9 cases. These results strongly support the use of the enriched method of detecting K-ras mutations as a complement to cytology in the evaluation of pancreatic masses.

Aged↗
PubMed1997

[Idiopathic myelofibrosis: initial features, evolutive patterns and survival in a series of 106 patients].

BACKGROUND: Idiopathic myelofibrosis (IM) is an infrequent myeloproliferative disorder with few large series published in the medical literature. Information on the characteristics of more recently diagnosed patients with IM is scarce. PATIENTS AND METHODS: The initial features, evolutive patterns and survival from 106 patients diagnosed with IM in a single institution between 1975 and 1996 were analyzed. RESULTS: Median age of the series was 64 years (range: 17-89); there were 61 males and 55 females. One third of the patients were asymptomatic at IM diagnosis. The most common presenting symptoms were related to hypermetabolism, anemia and splenomegaly. A palpable spleen was noted in 85% of patients, and 66% had hepatomegaly. Anemia was the most frequent hematologic abnormality (50% of cases). Bone marrow biopsy showed cellular phase IM in 50 patients, IM without osteosclerosis in 39, and osteosclerotic IM in the remaining 17. Evolution into acute leukemia was seen in 14 patients (actuarial probability at 7 years: 20%, 95% CI: 0-40%), 8 patients developed portal hypertension, 5 liver failure without portal hypertension and 14 heart failure. With 62 patients having died, the series' median survival was 59 months (95% CI: 41-75). CONCLUSION: IM is usually diagnosed in the old age. From the histologic point of view, a predominance of the cellular phase is observed at disease presentation. In recent years an increased proportion of patients asymptomatic at diagnosis is observed.

Adolescent↗
PubMed1997

[Second allogeneic progenitor cell transplantation for leukemia relapse: results in 10 patients].

BACKGROUND: Leukemia relapse is an important cause of treatment failure after allogeneic progenitor cells transplantation. A minority of patients achieve a long-term disease free survival with a second transplant, but the majority die of toxicity or relapse. We report our experience with second allogeneic transplant for leukemia relapse. PATIENTS AND METHODS: Ten patients were treated with a second transplant. Their diagnosis were chronic myelogenous leukemia (n = 5) and acute leukemia (n = 5). The interval between transplants ranged from 4 to 59 months (median 26 months). Conditioning regimens were busulfan alone (n = 1), associated to cyclophosphamide (n = 6) or to cyclophosphamide plus etoposide (n = 3). Acute graft-versus-host disease (GVHD) prophylaxis consisted of cyclosporin (CSA) (n = 4), CSA plus methotrexate (n = 4), CSA plus prednisolone (n = 1), or CSA, methotrexate plus partial T cell depletion (n = 1). RESULTS: All patients engrafted after second transplant. Seven developed acute GVHD. Four out of the nine patients at risk (44%) developed chronic GVHD. Three had clinical criteria of hepatic veno-occlusive disease. Three patients died in complete remission due to treatment-related toxicity: pulmonary invasive aspergillosis during an acute GVHD, interstitial pneumonitis plus chronic GVHD, and, hepatic veno-occlusive disease, respectively. Two patients relapsed 4 and 5 months after second transplant. Five remained alive in complete remission after a median follow-up of 27 months. In all of them acute or chronic GVHD incidence and severity after second transplant was higher than after the first transplant. All surviving patients were transplanted more than 12 months after the first transplant. CONCLUSIONS: A proportion of patients that relapse after an allogeneic progenitor cells transplant may benefit from second transplant; especially, young patients having a good performance status, and with a long interval between transplants.

Adult↗
PubMed1997

Rapid engraftment without significant graft-versus-host disease after allogeneic transplantation of CD34+ selected cells from peripheral blood.

We have prospectively evaluated the feasibility and results of the biotin-avidin immunoadsorption method (Ceprate SC system) for a phase I/II study of T-cell depletion of granulocyte colony-stimulating factor (G-CSF) mobilized peripheral blood progenitor cells (PBPC) for allogeneic transplantation. Twenty consecutive patients, median age, 40 years (21 to 54) and diagnoses of chronic myeloid leukemia in chronic phase (n = 5), acute myeloblastic leukemia (n = 7), acute lymphoblastic leukemia (n = 2), chronic myelomonocytic leukemia (n = 1), refractory anemia with excess of blasts in transformation (n = 3), histiocytosis X (n = 1), and chronic lymphocytic leukemia (n = 1), were conditioned with cyclophosphamide (120 mg/kg) and total body irradiation (13 Gy; 4 fractions). HLA identical sibling donors received G-CSF at 10 microg/kg/d subcutaneously (SC); on days 5 and 6 (19 cases) and days 5 to 8 (1 case) donors underwent 10 L leukapheresis. PBPC were purified by positive selection of CD34+ cells using immunoadsorption biotin-avidin method (Ceprate SC) and were infused in the patients as the sole source of progenitor cells. No growth factors were administered posttransplant. The median recovery of CD34+ cells after the procedure was of 65%. The median number of CD34+ cells infused in the patients was 2.9 (range, 1.5 to 8.6) x 10(6)/kg. The median number of CD3+ cells administered was 0.42 x 10(6)/kg (range, 0.1 to 2). All patients engrafted. Neutrophil counts >500 and >1,000/microL were achieved at a median of 14 days (range, 10 to 18) and 15 days (range, 11 to 27), respectively. Likewise, platelet counts >20,000 and >50,000/microL were observed at a median of 10 days (range, 6 to 23) and 17 days (range, 12 to 130), respectively. Graft-versus-host disease (GVHD) prophylaxis consisted of cyclosporine plus methylprednisolone. No patient developed either grade II to IV acute or extensive chronic GVHD. After a median follow-up of 7.5 months (range, 2 to 22) three patients have relapsed, and one of them is again in hematologic and cytogenetic remission after infusion of the donor lymphocytes. Two patients died in remission: one on day +109 of pulmonary aspergillosis and the other on day +251 of metastasic relapse of a previous breast cancer. Sixteen of the 20 patients are alive in remission after a median follow-up of 7.5 months (range, 2 to 22). In conclusion, despite the small number of patients and limited follow-up, it appears that this method allows a high CD34+ cell recovery from G-CSF mobilized PBPC and is associated with rapid engraftment without significant GVHD, and with low transplant related mortality.

Adolescent↗
PubMed1997

[Hemopoietic progenitor cell transplantation: 20 years' experience at the Hematology School "Farreras-Valentí"/Clinical Hospital of Barcelona].

BACKGROUND: Hemopoietic progenitor cell transplantation (HPCT) is acquiring an increasing role in the therapy for a variety of disorders. In this study, main characteristics and results of HPCT along 20 years are analyzed from the experience of Postgraduate School of Hematology "Farreras-Valentí" at the Hospital Clínic in Barcelona. PATIENTS AND METHODS: Six-hundred ninety-five patients transplanted between June 1976 and January 1996 were analyzed. Median age (range) were 33 (4-63) years. The following aspects were considered: donor type, source or progenitor cells, type of disease and disease-stage at transplantation, transplant related mortality and survival. RESULTS: A total of 714 HPCT were performed (448 allogeneic, 13 isogeneic, 253 autogeneic). Allogeneic HPCT were from an HLA-identical sibling in 408 cases, from other familial donors in 10, and from non-familial donors in 30. Most HPCT from non-familial donors (93%) were performed during the last five years of the study (1991-1995). The source of hemopoietic progenitor cells was bone marrow in 625 instances (88%), peripheral blood in 88 (12%), and fetal liver in one. During more than 15 years, the only source of progenitors was the bone marrow; in contrast, in the last 3 years (1993-1995) transplants using peripheral blood were predominant. Main indications for HPCT were the following: acute leukemias (n = 387) (54%), chronic leukemias (n = 134) (19%), severe aplastic anemia (n = 58) (8%), lymphomas (n = 80) (11%), multiple myeloma (n = 39) (5%) and myelodysplastic syndromes (n = 14) (2%). In patients with hematological malignancies (n = 656), HPCT was performed in first complete remission or in first chronic phase in 321 instances (49%), in subsequent remissions in 144 (22%), and in more advanced stages in the remaining 191 (29%). In the more recent years, a progressive decrease in the number of HPCT for acute leukemia or aplastic anemia was observed, contrasting with an increase in transplants for lymphoma, multiple myeloma and myelodysplastic syndromes. Of note, a significant decrease in transplant related mortality was evident along the years, both after autogeneic HPCT (21% during 1985-1992 and 6% thereafter) (p = 0.001) and after allogeneic transplantation (54%, 44%, and 20% during the periods 1976-1984, 1985-1992 and 1993-1995, respectively) (p = 0.004). The fact translated into an increase in the actuarial probability of survival after allogeneic HPCT (25%, 33% and 58% in the three mentioned periods, respectively) (p = 0.0003), and after autogeneic HPCT (33% in the interim 1985-1992, and 55% in the period 1993-1995) (p = 0.001). CONCLUSIONS: During the last 20 years, HPCT has significantly evolved in aspects such as type of donor, source of progenitor cells and indications. Remarkably, a progressive decrease in transplant related mortality has been observed translating into a improvement in survival after the procedure.

Actuarial Analysis↗
PubMed1997

Deletions and loss of expression of p16INK4a and p21Waf1 genes are associated with aggressive variants of mantle cell lymphomas.

Mantle cell lymphoma (MCL) is molecularly characterized by bcl-1 rearrangement and cyclin D1 gene overexpression. Some aggressive variants of MCL have been described with blastic or large cell morphology, higher proliferative activity, and shorter survival. The cyclin-dependent kinase inhibitors (CDKIs) p21Waf1 and p16INK4a have been suggested as candidates for tumor-suppressor genes. To determine the role of p21Waf1 and p16INK4a gene alterations in MCLs, we examined the expression, deletions, and mutations of these genes in a series of 24 MCLs, 18 typical, and 6 aggressive variants. Loss of expression and/or deletions of p21Waf1 and p16INK4a genes were detected in 4 (67%) aggressive MCLs but in none of the typical variants. Two aggressive MCLs showed a loss of p16INK4a expression. These cases showed homozygous deletions of p16INK4a gene by Southern blot analysis. An additional aggressive MCL in which expression could not be examined showed a hemizygous 9p12 deletion. Loss of p21Waf1 expression at both protein and mRNA levels was detected in an additional aggressive MCL. No p21Waf1 gene deletions or mutations were found in this case. The p21Waf1 expression in MCLs was independent of p53 mutations. The two cases with p53 mutations showed p21Waf1 and p16INK4a expression whereas the 4 aggressive MCLs with p16INK4a and p21Waf1 gene alterations had a wild-type p53. p21Waf1 and p16INK4a were expressed at mRNA and protein levels in all typical MCLs examined. No gene deletions or point mutations were found in typical variants. Two typical MCLs showed an anomalous single-stranded conformation polymorphism corresponding to the known polymorphisms at codon 148 of p16INK4a gene and codon 31 of p21Waf1 gene. These findings indicate that p21Waf1 and p16INK4a alterations are rare in typical MCLs but the loss of p21Waf1 and p16INK4a expression, and deletions of p16INK4a gene are associated with aggressive variants of MCLs, and they occur in a subset of tumors with a wild-type p53 gene.

Blotting, Southern↗
PubMed1997

Abdominal ultrasound findings of disseminated tuberculosis in AIDS.

The sonographic findings of 76 patients with tuberculosis and HIV infection are described. These findings were compared with a control group of 76 HIV-positive patients without associated pathology. Those patients with tuberculosis and positive HIV titers commonly (p = 0.05) showed retroperitoneal and mesenteric adenopathies with node diameters greater than 1.5 cm (n = 27), and multiple, splenic, hypoechoic nodules between 0.5 cm and 1 cm (n = 11). Additional findings include hepatic hyperechoic nodules (n = 1) and retroperitoneal abscess (n = 1). The combination of ultrasound features can help in the diagnosis of abdominal tuberculosis in HIV-positive patients with non-specific clinical infections.

AIDS-Related Opportunistic Infections↗
PubMed1997

New therapeutic issues in CLL.

The treatment armamentarium for CLL has dramatically increased in the last few years. New cytotoxic agents such as the purine analogues produce a high number of responses which in some cases can be molecular. The synergism between purine analogues and other drugs (e.g., cyclophosphamide, platinum, ara-C) has opened the door to the use of purine analogues in combination chemotherapy regimens. In addition, exciting developments are being made in the field of biotherapy, particularly vaccines and monoclonal antibodies. Whereas the use of vaccines is still in its infancy, monoclonal antibodies (e.g., CAMPATH 1H) have already been proved to be highly effective in CLL treatment with response rates similar to those obtained with purine analogues. Finally, transplants of hemopoietic precursors are increasingly performed in young patients with high-risk CLL. The role of transplants in CLL, however, is still unknown and prospective, controlled studies are required to determine its potential role in the management of patients with CLL.

Humans↗
PubMed1997

Chronic lymphocytic leukemia: a changing natural history?

There are some data suggesting that the natural history of chronic lymphocytic leukemia (CLL) may be changing, but a systematic analysis of this topic is lacking. To address this issue, we examined two cohorts of CLL patients in whom the diagnosis was established in 1960-1979 (group I) and in 1980-1989 (group II), respectively. Striking differences were observed between both cohorts. The diagnosis in the second group was established at higher age (65.8 vs 61.3 years; P = 0.0001), both in males (63.8 vs 59.1 years; P = 0.004) and females (68.3 vs 64.2 years; P = 0.01); the proportion of patients in whom the diagnosis was established in low-risk clinical stage (Binet's A) was significantly higher in group II (65.7% vs 42.6%; P < 0.001), and the survival was more than double in group II (median of 11.1 vs 5.3 years; P < 0.0001). Moreover, the impact of the disease on life expectancy was much lower in the more recent cohort. These differences may be due, at least in part, to changes in the natural history of the disease.

Age Factors↗
PubMed1997

Identification of 'short-lived' and 'long-lived' patients at presentation of idiopathic myelofibrosis.

To contribute to a better knowledge of the prognosis of idiopathic myelofibrosis (IM), the prognostic value of the presenting features in 106 patients diagnosed with IM at a single institution during a 21-year period was retrospectively analysed. Median survival was 59.4 months (95% CI 40.7-75.4). Using univariate analysis, age > 64 years, constitutional symptoms (fever, night sweats, weight loss), Hb < 10 g/dl, circulating blasts (> or= 1%), and serum LDH > 3 times upper normal level were associated with a significantly shorter survival; male sex, platelet count < 100 x 10(9)/l, blood percentage of immature granulocytes (excluding blasts), low cholesterol levels and advanced marrow histological stage had borderline significance. Using multivariate study, only age > 64 years, constitutional symptoms, Hb < 10 g/dl, and circulating blasts retained their prognostic relevance. The latter three variables confirmed their predictive value in patients above and below the series median age, and were able to identify two groups of patients: a low-risk group of 67 patients with none or one bad prognostic factor, in whom IM had an indolent course (median survival 98.8 months, 95% CI 68.7-127.6), and a high-risk group, including 39 patients with two or three factors, with a more aggressive disease (median survival 20.6 months, 95% CI 10-28.2). Finally, the application of two recently proposed scoring systems (in which three prognostic groups are considered) was unable to separate intermediate- from high-risk patients.

Adolescent↗
PubMed1997

Successful autografting in chronic myelogenous leukaemia using Philadelphia negative blood progenitor cells mobilized with rHuG-CSF alone in a patient responding to alpha-interferon.

Several non-randomized studies suggest a possible survival advantage for chronic myelogenous leukaemia (CML) patients treated with an autologous stem-cell transplantation. Due to the possible contribution of residual leukaemic cells present in the inoculum in post-transplant relapse, several methods are being evaluated to eliminate neoplastic cells or to select 'normal' (Ph1 negative) progenitor cells for autografting. Recently, several studies have shown that Ph1 negative blood progenitor cells can be mobilized by rHuG-CSF alone in patients who have a cytogenetic response to alpha-interferon (IFN). We describe the first case, as far as we are aware, of a CML patient responding to IFN autografted by using blood progenitor cells collected by rHuG-CSF alone.

Adolescent↗
PubMed1997

Chronic lymphoproliferative disorders.

Chronic lymphoproliferative disorders are a heterogeneous group of diseases with a highly variable clinical course. In the past few years, important progress has been made in the classification, biology, and therapy of some of these disorders of which B-cell chronic lymphocytic leukemia is not only the most frequent but also the model for their study. Regarding classification, entities that may be confounded with chronic lymphocytic leukemia have been identified (eg, splenic lymphoma with villous lymphocytes, mantle-cell lymphoma in leukemic phase); these diseases should be known and clearly separated from chronic lymphocytic leukemia because their prognosis and treatment is different from that of chronic lymphocytic leukemia. On the other hand, the molecular basis of some of these diseases (eg, the overexpression of the Prad1/CCND1 gene in mantle-cell lymphomas, the relationship between bcl-2 and bax expression in chronic lymphocytic leukemia homeostasis, the role of p53 tumor suppressor gene mutations in chronic lymphocytic leukemia progression) are increasingly well known. Cytokines (eg, tumor necrosis factor-alpha or IL-2, IL-4, and IL-13) also contribute to the pathogenesis of lymphoproliferative disorders by either promoting cell growth or inhibiting apoptosis. In addition, new treatment possibilities (eg, purine analogues, hemopoietic progenitors transplants) are changing the treatment objectives in some of these diseases. Thus, symptoms' palliation is no longer the only realistic aim in the management of patients with chronic lymphoproliferative disorders, but sustained complete remissions and even cures can be achieved.

Antineoplastic Agents↗