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PubMed1989

Impaired in-vitro proliferation of hemopoietic precursors in HIV-1-infected subjects.

Patients with acquired immunodeficiency syndrome (AIDS) and persistent lymphadenopathy syndrome (LAS) display significant hematological abnormalities of one or more cell lineages. In order to understand the pathophysiologic mechanisms leading to these abnormalities we studied the proliferation capacity of pluripotent and committed hemopoietic precursors using in-vitro colony assays. Anemia, leukopenia and thrombopenia were relatively frequent findings in HIV-infected subjects irrespectively of the patients' clinical status. The colony growth capacity of AIDS patients' GM-CFU and BFU-E was significantly decreased whereas no GEMM-CFU colonies could be obtained. There was no correlation between the number of BFU-E and GM-CFU colony number and the hemoglobin or the absolute number of polynuclear cells, respectively. The plating efficiency of both committed and pluripotent hematopoietic precursors from HIV infected patients could not be enhanced when additional exogenous recombinant GM-CSF, human interleukin 3 or erythropoietin were added in contrast to normal patients' cells. In addition, the impaired colony growth of these precursors could not be restored after adherent or T-cell depletion or the addition of normal allogenic irradiated adherent or/and T cells. Since this colony growth abnormality was also detected in HIV seropositive asymptomatic subjects our findings strongly suggest that the in-vitro growth of hematopoietic precursors is affected early after HIV-1 infection.

Acquired Immunodeficiency Syndrome↗
PubMed1986

Translocation t(3;20) associated with thrombocythemia in Ph-positive CML.

A patient with Philadelphia (Ph) chromosome positive chronic myelocytic leukemia is described who also developed an abnormality of chromosome #3, i.e., t(3;20)(p21;p13), in blast crisis. This abnormality may be connected with the advent thrombocythemia. The disease was a thrombopenia in the initial phase.

Adult↗
PubMed1992

New case of t(3;17)(q26;q22) as an additional change in a Philadelphia-positive chronic myelogenous leukemia in acceleration.

A new case of t(3;17)(q26;q22) was observed in a Philadelphia-positive (Ph+) chronic myelogenous leukemia in acceleration 1 month before occurrence of the blastic phase. Abnormal megakaryocytopoiesis and thrombopenia were noted, but blast cells did not express platelet markers. The same translocation was previously reported in three myeloproliferative disorders in acceleration or in the process of becoming acute. Translocations or inversions of chromosome 3 with breakpoint involving the band 3q26 were specifically associated with megakaryoblastic acute phase or abnormal megakaryocytopoiesis. This report confirms that the t(3;17)(q26;q22) is a specific nonrandom chromosomal abnormality associated with the acute nonlymphoblastic phase of myeloproliferative disorders and megakaryocytopoiesis dysfunction.

Bone Marrow↗
PubMed1995

[Transient dysfibrinogenemia and thrombocytopenia associated with recurrent acute pancreatitis in the course of isotretinoin therapy].

A 17 year-old young man developed two episodes of acute pancreatitis, separated by a 2 year interval and associated with isotretinoin therapy. In 1989, vesicular sludge without lithiasis was evidenced and in 1991, gall bladder stones were found by cholecystectomy. Concomitantly, transient dysfibrinogenemia and thrombopenia were present. It is interesting to note that far away from the use of isotretinoin, the patient suffered from another episode of acute pancreatitis without any coagulation disorder. The involvement of Roaccutane in cellular differentiation is discussed as well as its causal association with acquired dysfibrinogenemia and transient thrombocytopenia.

Acute Disease↗
PubMed1996

[Thrombotic microangiopathies in HIV infection: 4 cases].

Thrombotic microangiopathy (TMA) has been rarely described in HIV-infected patients. We report four cases of TMA during HIV infection and we analyse clinical, biological, etiologic, therapeutic and evolutive aspects of these four cases. Initial symptomatology is non specific and diagnosis is often delayed. Peripheric thrombopenia with haemolytic anemia and renal failure must be suggestive of the diagnosis. TMA can be present at any stage of HIV infection. Physiopathological mechanism of TMA during HIV infection remains unclear. These cases lead to suspect the role of opportunistic infections, neoplasia or HIV directly by endothelial injury or indirectly by cytokines secretion. Therapy of TMA is not different from non-HIV patients. Improvement with treatment must be obtained but long-term prognosis remains poor in account of HIV infection.

Adult↗
PubMed1983

A phase I clinical tolerance study of rDNA alpha 2 human interferon in patients with non-reticuloendothelial system malignancies.

Twenty-seven patients with non-reticuloendothelial malignancies were treated with a single intramuscular injection of recombinant leukocyte alpha 2 interferon (rIFN) to assess clinical tolerance and define a maximum tolerated dose. A single patient in each of six increasing dosage groups (0.3 X 10(6) IU, 1 X 10(6) IU, 3 X 10(6) IU, 10 X 10(6) IU, 30 X 10(6) IU, 100 X 10(6) IU) received a low dose (0.01 X 10(6) IU) and served as a control for subjective and objective toxicity measurements. Severe fatigue proved dose-limiting at 100 X 10(6) IU, and all dosages above 3.0 X 10(6) IU produced one or more signs or symptoms, which typically resembled a 'flu-like' syndrome. Objective toxicity was mild to moderate (leukopenia, thrombopenia) and no toxicities were found not already known from work with interferon obtained directly from leukocytes. Evidence of an antitumor effect was apparent in 3/19 evaluable patients.

Adult↗
PubMed1990

Intraperitoneal human recombinant interferon alpha-2b in minimal residual ovarian cancer.

Twenty evaluable patients with minimal residual ovarian cancer at second look laparotomy were treated with human recombinant interferon alpha-2b (IFN) intraperitoneally. The dose administered was 50 x 10(6) units once weekly for 8 weeks. Seventeen patients were evaluated by a relaparotomy: five had a pathological complete remission, four a partial response, six patients disease stabilization and two patients had progression. Three patients, two stable and one with clinical progression, had no laparotomy. Nine of the 11 patients with residual tumor smaller than 5 mm had a response, while no response was found in six patients with residuals over 5 mm. The median duration of CR is 11+ months (6-13+ months) after evaluation. For toxicity, 156 treatment cycles could be studied. Fever was seen in 80% of all cycles within 24 h following administration of IFN, in 58 cycles (37%) over 38 degrees C and in 65 cycles (43%) over 39 degrees C. Abdominal pain was slight in 32% and moderate in 3% of all cycles. The peripheral blood leukocyte counts dropped after 52% of all cycles, in 27% below 4.0, in 22% below 3.0, and in one patient below 2.0 x 10(9)/l. IFN dosage was not reduced for leukopenia, but in one patient reduction was necessary for thrombopenia, resulting from insufficient marrow reserve after a previous autologous bone marrow transfusion. Pharmacokinetic studies showed i.p. IFN levels 50-100 times the blood levels. Blood levels were still elevated 2 days after i.p. infusion, but normalized within 1 week on repeated administration. At the second instillation, lower peak serum levels were reached. In conclusion, high doses of i.p. IFN appear to be active in patients with minimal residual disease, with ongoing response in CR patients. Apart from general malaise on the day of treatment, toxicity was acceptable. IFN may be active in patients with minimal residual ovarian cancer through local as well as systemic effects.

Adult↗
PubMed1992

Myopathology and a mitochondrial DNA deletion in the Pearson marrow and pancreas syndrome.

A patient with the Pearson marrow and pancreas syndrome is presented. She showed an anaemia with neutropenia and thrombopenia, failure to thrive, diarrhoea, disturbed glucose homeostasis and lactic acidosis. An exocrine pancreatic insufficiency was lacking. The disease followed a fatal course. Biochemical investigations of skeletal muscle revealed a disturbed mitochondrial energy metabolism, while many ultrastructural abnormal features were observed in the muscle tissue. Molecular genetic studies showed a de novo deletion in the mitochondrial DNA (mtDNA), different in size from the already published deletions and flanked by two 4 bp direct repeats, interspaced by 4-5 non-repeated nucleotides. mtDNA from 12 other tissues showed the same deletion in different percentages. No obvious relation between these percentages and tissue dysfunction was found. In spite of an open reading frame of 74 codons, only little transcription product of the genomic region resulting from the deletion was found.

B-Lymphocytes↗
PubMed1993

In vitro study of pesticide hematotoxicity in human and rat progenitors.

Some pesticides are hematotoxic and cause aplastic anemia, agranulocytosis, neutropenia, and thrombopenia. In order to evaluate hematopoietic progenitor cultures in the exploration of pesticide hematotoxicity, human and rat colony-forming unit-granulocyte and macrophage (CFU-GM) were cultured in the presence of different concentrations of pesticides, known to be either hematotoxic or innocuous for blood cells. The results were compared to the control culture of the same sample. Four insecticides (lindane, azinphos, mevinphos, parathion methyl), three herbicides, (2,4,5, T, bromacil, MCPA), and two fungicides (fosethyl-aluminum, DNOC) were tested and exhibited the following data: 1) Pesticides, known to be hematotoxic, inhibited the development of progenitors. Different phenomena were observed and suggested different mechanisms: cell destruction, block in mitosis, decrease or delay in mitosis. 2) Difference in sensitivity to molecules between human and rat progenitors was observed. Human progenitors were more sensitive to pesticides, except for 2,4,5 T.

Animals↗
PubMed2005

Food-cobalamin malabsorption in elderly patients: clinical manifestations and treatment.

PURPOSE: Approximately 15% of people aged more than 60 years old have a cobalamin (vitamin B12) deficiency, mainly in relation with food-cobalamin malabsorption (FCM). To date, no study has documented this disorder in the elderly. There is also little information on clinical consequences. SUBJECTS AND METHODS: We studied 92 elderly patients with well-established FCM who were extracted from an observational cohort study (1995-2004) of 172 consecutive elderly patients with documented cobalamin deficiency. RESULTS: The median patient age was 76 +/- 8 years; 60 patients were women. The most common clinical manifestations were neurologic or psychologic: mild sensory polyneuropathy (44.6%), confusion or impaired mental functioning (22.8%), and physical asthenia (20.7%). Hematologic abnormalities were reported in at least one third of the patients: anemia (21%), leukopenia (10.9%), thrombopenia (8.7%), and pancytopenia (6.5%). All patients had low serum vitamin B12 levels (<200 pg/mL), with a mean value (+/- standard deviation) of 131 +/- 38 pg/mL and total serum homocysteine level of 22.1 +/- 9.3 micromol/L. The mean hemoglobin level was 10.9 +/- 2.5 g/dL and the mean erythrocyte cell volume 95.7 +/- 12.7 fL. Correction of the serum vitamin B12 levels and hematologic abnormalities was achieved equally well in patients treated with either intramuscular or oral crystalline cyanocobalamin. CONCLUSIONS: This study suggests that in elderly patients, FCM may be associated with significant neurologic, psychologic, and hematologic abnormalities, which seem to respond equally well to either oral or parenteral vitamin B12 therapy.

Aged↗
PubMedDate not supplied

[Thrombosis of a cardiopulmonary bypass circuit despite recommended hypocoagulation with danaparoid during the acute phase of type II heparin-induced thrombocytopenia].

A 36-year-old patient was admitted to our hospital with ischaemic stroke. The initial assessment allowed the diagnosis of an antiphospholipid syndrome (APS) and an intracardiac mass suggestive of a heart tumour. The patient was treated with unfractionated heparin. Type II heparin-induced thrombopenia (HIT) was diagnosed on the 18th day of therapy. Given the risk of stroke recurrence it was decided to remove the cardiac tumour surgically. Cardiopulmonary bypass (CPB) was performed using danaparoid in a state of deep hypothermia, in accordance with the well-established protocol in use in our department. As the CPB and surgical procedure came to an end a massive thrombus began forming in the circuit, requiring immediate displacement of the CPB cannulae. The anti-Xa activity level obtained had been considered effective at an estimated 1.20 IU/ml, although, the level recommended by Magnani is between 1.50 and 2.0 IU/ml. There was no clinical consequence and postoperative recovery was uneventful. The discrepancy between the satisfactory level of anti-Xa activity and the thrombus formation in the CPB circuit raises the issue of the diversity of published anticoagulation protocols, the difficulty to extrapolate within a surgical team, the need for intensive laboratory monitoring within a narrow therapeutic range, as well as the patient profiles variability with concurrent disorders complicating their clinical management.

Adult↗
PubMed2006

[Hemangioma: complications].

Hemangioma (HMG) is a benign tumour of the child generally evolving to spontaneous regression. Sometimes this evolution can become complicated in a more or less serious way according to its localization or of its importance. If local complications are, in the most of cases, without gravity, complications of a general nature like thrombopenia or cardiac failure may compromise the vital prognosis. There are in addition serious forms where, according to its localization or its importance, the HMG can compromise the aesthetic, or functional even vital outcome.

Cardiac Output, Low↗
PubMed2003

[Bernard-Soulier syndrome revealed by major neonatal thrombocytopenia].

Bernard-Soulier syndrome (BSS) is a congenital autosomal recessive bleeding disorder characterised by giant platelets, the lack of thrombocytopenia or a moderate one, prolongation of skin bleeding time, and absent platelet aggregation in response to ristocetin. We report a case of BSS revealed by major neonatal thrombocytopenia. A newborn was admitted for thrombocytopenic purpura initially believed to be due to a maternal auto-immune thrombocytopenia. Because of the persistence of the thrombopenia till the age of 7 months despite therapy by corticosteroids and immunoglobulins, and because of the detection of anti-1b antiplatelets antibodies after transfusion, BSS diagnosis was evoked. In such a situation of major thrombocytopenia, the main therapeutic measure is prevention. Therapy by DDAVP may be used after the age of 3 years in situations of high haemorrhagic risk. This case report underlines the importance of a precise diagnosis in front of a maternal thrombocytopenia and the possibility of antenatal diagnosis of BSS.

Bernard-Soulier Syndrome↗
PubMed2006

[Perinatal consequences of maternal connective tissue diseases: a prospective study of 73 cases].

AIM: To describe a group of newborns born from mothers with connective tissue diseases, to determine their perinatal characteristics and the neonatal morbidity, and to assess the possible role of drugs received by mothers on the obstetrical and neonatal morbidity. PATIENTS AND METHODS: During a 34-month period, newborns born from mothers with connective tissue diseases and followed in a single center were prospectively included in the study. In all cases, maternal treatments (i.e. hydroxychloroquine and/or prednisone) were continued during pregnancy. RESULTS: Among the 73 included infants, 18 (25%) were born before 37 weeks of gestation and 3 (4%) were small for gestational age. A neonatal lupus syndrome with facial rash and thrombopenia was observed in 1 case. No neonatal congenital heart block was observed and maternal treatment did not significantly influence the mean PR or QT intervals. Four infants had minor congenital abnormalities and 3 had feto-maternal infection. CONCLUSION: These data show that perinatal morbidity is lower than that previously published. We postulate that a strict follow-up during pregnancy may have played a significant positive role in these results.

Adult↗
PubMed2005

A randomised phase II trial of weekly high-dose 5-fluorouracil with and without folinic acid and cisplatin in patients with advanced biliary tract carcinoma: results of the 40955 EORTC trial.

UNLABELLED: Previous small phase II trials have demonstrated that the combination of 5-fluorouracil (5FU) and cisplatin(CDDP) could have clinical activity in metastatic biliary tract cancer. This randomised phase II trial was designed to assess the activity and safety of a high-dose infusional weekly 5FU alone (HDFU) and the combination of 5FU, folinic acid (FA) and CDDP. Patients were included if they had histologically proven locally advanced or metastatic biliary tract carcinoma, World Health Organisation (WHO) performance status < or = 2, bilirubin <2 x upper normal limit, adequate haematological and renal functions and had not received prior chemotherapy, even in the adjuvant setting. TREATMENTS: Arm A (HDFU) consisted of cycles of 5FU 3 g/m(2) intravenously (i.v.), 24 h infusion, weekly, for 6 weeks, followed by 1 week rest, every 7 weeks; Arm B (5FU+FA+CDDP) consisted of cycles of 5FU 2.0 g/m(2) i.v. with folinic acid 500 mg/m(2), 2 h-infusion, weekly, for 6 weeks, followed by 1 week rest plus cisplatin 50 mg/m(2), once every two weeks, for 6 weeks, followed by 1 week rest, every 7 weeks. From February 1997 to June 1999, 58 patients were randomised (29 in each arm). Patients had a median age of 58 years in Arm A and 62 years in Arm B, locally advanced disease was present in 21% of the patients in Arm A and 11% in Arm B. WHO performance status of 0/1/2 was noted in 48%/45%/7% of the patients in Arm A and 54%/43%/4% in Arm B. In both arms, the most common metastatic sites were the liver and peritoneum. Twenty-eight patients were eligible in each arm and one patient did not start the allocated therapy in Arm B. The median number of cycles was 2 [range 1-12] in Arm A and 2 [range 1-6] in Arm B. Responses for the eligible patients who started their allocated therapy were as follows: Complete Response (CR) 0% in Arm A, 4% in Arm B, Partial Response (PR) 7% in Arm A, 15% in Arm B resulting in an overall response rate [95% CI] of 7.1% in Arm A [0.9-23.5%] and 19% [6.3-38.1%] in Arm B. Disease stabilisation was observed in 46% in Arm A and 44% in Arm B. National Cancer Institute of Canada (NCIC) grade 3-4 adverse events (% of patients in Arm A/Arm B) were neutropenia 4%/26%, thrombopenia 0%/7%, stomatitis 0%/4%, vomiting 7%/14%, diarrhoea 0%/11% and neurotoxicity 4%/0%. There was one early toxic death in Arm B. The median overall survival (OS) [95% CI] was in Arm A/Arm B: 5.0 [4.0-7.4] months/8.0 [5.8-11.8] months and the median progression-free survival (PFS) was 3.3 [1.7-4.7] months/3.3 [2.3-6.7] months. Cisplatin in combination with 5FU+FA showed a higher activity than HDFU, but was more toxic. These results are not sufficient to start a phase III trial. However, our group is planning a phase III trial comparing 5FU+folinic acid versus the same schedule+oxaliplatin a platinum analogue.

Antineoplastic Combined Chemotherapy Protocols↗
PubMed2005

Allergic-type reactions to oxaliplatin: retrospective analysis of 42 patients.

Oxaliplatin is a platinum salt that is particularly effective in treating gastrointestinal tumours. Its increased use has resulted in emergence of allergic reactions, including anaphylactic shock. Allergic reactions to oxaliplatin documented over the last 5 years have been analysed using predefined criteria. The 42 analysed patients had cancer and received a FOLFOX regimen in first line or beyond. Two types of allergy were observed: a type I immediate allergic reaction in 39 patients in whom the most frequent signs were respiratory (50%) and cutaneous (40%); anaphylactic shock that occurred in three patients; type II allergy (immunological thrombopenia) was observed in three patients. All the toxicities were reversible on symptomatic treatment. No predictive factor was evidenced. Anaphylactic shock, is rare but serious, and must be considered in the event of any severe blood pressure decrease. For the non-life-threatening reactions, prolonging infusion duration, "Stop and Go" regimen seem to be effective means of preventing recurrence.

Adult↗
PubMed2005

Myelodysplastic/myeloproliferative disease with erythropoietic hyperplasia (erythroid preleukemia) and the unique translocation (8;9)(p23;p24): first description of a case.

We report on a patient fulfilling the diagnostic criteria of unclassifiable myelodysplastic/myeloproliferative diseases with prominent erythropoietic hyperplasia/dysplasia (erythroid preleukemia) and the unique translocation (8;9)(p23;p24). The patient presented with B-symptoms, erythroblastemia, thrombopenia, marked eosinophilia, presence of myeloid precursors in the peripheral blood, and decreased erythropoietin level. Nodular peritrabecular polymorphous blasts, dysplastic megakaryocytes, and a diffuse argyrophilic fibrosis were detected in the trephine bone marrow biopsy. Immunohistochemically, the blasts stained positively for glycophorin C and hemoglobin A; the proliferation fraction was nearly 90% in the Ki-67 stain. Expression of the phosphorylated Janus kinase 2 was detected in almost all megakaryocytes and in isolated erythroblast islets, suggesting a probable activation of Janus kinase 2, the jak-2 gene being mapped on 9p24. Ten months after initial diagnosis, the disease progressed to frank acute erythroid leukemia. We report for the first time a myelodysplastic/myeloproliferative disease (erythroid preleukemia) accompanied by the specific chromosomal aberration t(8;9)(p23;p24), distinct histopathology, and clinical and laboratory symptoms, and progress to acute erythroid leukemia.

Biopsy↗
PubMed2005

Clinical and laboratory features of murine typhus in central Tunisia: a report of seven cases.

INTRODUCTION: Murine or endemic typhus, caused by Rickettsia typhi, has been reported in all continents. In the 1970s, no cases of murine typhus were diagnosed in Tunisia. METHODS: The clinico-epidemiological characteristics of seven cases of murine typhus diagnosed at our hospitals since 1993 are reported. Diagnosis was confirmed by indirect fluorescence assay detecting specific R. typhi antibodies. RESULTS: Murine typhus occurred in all ages from 18-80 years during the hot season in rural areas. Clinical features were: sudden onset of fever and absence of eschar in all cases, with maculo-papular rash (five cases), prostration (four cases), meningism (three cases) and pneumonia (four cases). Frequent laboratory findings were moderate thrombopenia (four cases) and elevated transaminases (four cases). Before the results of serology, clinical diagnoses were Mediterranean Spotted Fever (four cases), Q fever (one case), pneumonia (one case), and lymphocytic meningitis (one case). Serology confirmed all diagnoses with cross-reactivity with Rickettsia conorii. CONCLUSION: Murine typhus exists in Tunisia and its prevalence is underestimated. Further, more specific studies are needed to evaluate the true prevalence.

Adolescent↗