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Biomedical subjects

F Avcu

Publications and source records attributed to F Avcu.

At least 19 recordsLinked to original sources
PubMed2006

Differentiating effect of thalidomide and FGM-CS combination on HL-60 acute promyelocytic leukemia cells.

AIM: To investigate whether granulocyte-macrophage colony-stimulating factor (GM-CSF) with or without thalidomide can induce apoptosis and differentiation of HL-60 acute promyelocytic leukemia cell line in vitro. METHODS: Effect of GM-CSF and thalidomide on proliferation of HL-60 cells was evaluated by MTT assay, cell cycle analysis was performed by propidium iodide staining approach and flow cytometry, and apoptosis rate was analyzed using FITC-conjugated annexin-V and FACScan flow cytometry. RESULTS: The study revealed that thalidomide alone at high concentrations inhibited HL-60 cell growth and induced apoptosis. Three days treatment of low-dose thalidomide in combination with GM-CSF induced marked terminal differentiation of HL-60 cells, as it was assessed by increased expression of differentiation antigens on cell surface. CONCLUSION: Treatment of HL-60 cells by low concentration of thalidomide combined with GM-CSF induced terminal differentiation of HL60 cells in vitro, which may be advantageous for the elaboration of novel therapeutic regimens in patients with differentiation-inducible leukemias.

Antigens, Differentiation↗
PubMed2001

Successful treatment of severe aplastic anemia associated with human parvovirus B19 and Epstein-Barr virus in a healthy subject with allo-BMT.

Several reports have noted pancytopenia associated with Human parvovirus B19 (PVB19) or Ebstein-Barr virus (EBV) infections in patients who have no history of immunodeficiency. To our knowledge, we report the first case of severe aplastic anemia associated with both EBV and PVB19 infections in a previously healthy 22-year-old man. He was admitted to our hematology service due to anemia and thrombocytopenia. He had no symptoms or signs of infections of these viruses. His bone marrow biopsy revealed a hypocellular marrow. Specific IgM and IgG antibodies to EBV and PVB19 were elevated. EBV and PVB19 virus genomes were detected by PCR in the bone marrow nucleated cells and the peripheral blood lymphocytes. Two months after treatment with prednisone, acyclovir, and intravenous immune globulin (IVIg), the genomes of both these viruses disappeared. However, his transfusion requirement for platelet suspensions and packed red blood cells persisted. The patient underwent allogeneic bone marrow transplant (allo-BMT) and has had an enduring complete hematological response for 8 months.

Adult↗
PubMed2001

Leptin does not play a major role in platelet aggregation in obesity and leptin deficiency.

OBJECTIVE: A recent study suggested that high concentrations of leptin enhance platelet aggregations. Therefore, the aim of this study was to investigate whether platelet aggregation is altered in patients with leptin gene mutations compared with obese subjects or controls. RESEARCH METHODS AND PROCEDURES: Four men (one homozygous man and his three heterozygous brothers) carrying a leptin gene mutation; 20 age-matched, healthy, unrelated men; and 18 age-matched obese men were enrolled in the study. Adenosine diphosphate (ADP)-, collagen-, and epinephrine-induced platelet aggregation were evaluated in all individuals. RESULTS: Our results show that patients with the leptin gene mutation (both the homozygous and heterozygous patients) had significantly higher ADP-induced (78.3 +/- 3.4% vs. 57.9 +/- 9.3%, p = 0.001), collagen-induced (78.1 +/- 2.9% vs. 56.7 +/- 9.3%, p = 0.007), and epinephrine-induced (76.5 +/- 9.2% vs. 59.5 +/- 7.70%, p = 0.003) platelet aggregation compared with controls. However, ADP-, collagen-, or epinephrine-induced platelet aggregations were similar to those in obese patients. Platelet aggregation responses to a combination of pretreatment with leptin at concentrations of 20, 50, 100, or 500 ng/mL for 5 minutes and ADP at concentrations of 2 micromol/liter also were evaluated. However, we did not find significant increases in platelet aggregation even at high concentrations of leptin (100 or 500 ng/mL) in leptin-deficient patients, obese subjects, or controls. DISCUSSION: Our data show that similar to findings in obese humans, homozygous or heterozygous leptin deficiency is associated with increased platelet aggregation compared with controls, and that higher concentrations of leptin do not increase platelet aggregation.

Adenosine Diphosphate↗
PubMed2001

The relationship between gastric-oral Helicobacter pylori and oral hygiene in patients with vitamin B12-deficiency anemia.

OBJECTIVE: The aim of this study was to determine whether a relationship exists between gastric and oral Helicobacter pylori and oral hygiene in patients with vitamin B12 deficiency. STUDY DESIGN: One hundred eight patients with vitamin B12 deficiency who were H pylori -positive in their gastric mucosa were enrolled in the study. These patients were divided into 3 groups determined by Oral Hygiene Index (OHI) scores of good, fair, or poor. H pylori was detected in the dental plaque with camphylobacter-like organism test gels. All patients were treated with a combination regimen to eradicate H pylori. RESULTS: H pylori positivity in dental plaque was correlated with OHI scores; the positivity was 28.5%, 90.2%, or 100% in patients with good, fair, or poor OHI scores, respectively. The eradication of H pylori was associated with recovery from anemia and increased serum vitamin B12 level (P <.0001 and P <.0001). The patients with poor OHI scores had the most frequent gastric recurrence of H pylori (58.3%) compared with those with fair OHI scores (41.2%) and good OHI scores (4.8%). CONCLUSIONS: H pylori seems to be an etiologic factor in vitamin B12 deficiency, since anemia was cured and the level of vitamin B12 in the serum increased as a result of its eradication. However, eradication of H pylori from gastric mucosa alone is not enough to prevent gastric recurrence of the bacteria. Proper oral hygiene must be established to eliminate H pylori in dental plaque. Therefore, we suggest that control of H pylori in dental plaque is necessary to control recurrence of H pylori.

Adult↗
PubMed2001

Erythema annulare centrifugum as the presenting sign of CD 30 positive anaplastic large cell lymphoma--association with disease activity.

Erythema annulare centrifugum is a figurate erythema that has been associated with many different entities. A case of erythema annulare centrifugum related to non-Hodgkin's lymphoma in a 38-year-old woman is described in this case report. Response of the lymphoma to a combination chemotherapy was accompanied by disappearance of skin lesions. When therapy was discontinued, both disorders recurred, and both responded to reinstitution of a different chemotherapy regimen. To our knowledge, this case is the first reported association of erythema annulare centrifugum and non-Hodgkin's lymphoma in the medical literature.

Adult↗
PubMed2000

The role of prothrombotic mutations in patients with Buerger's disease.

Thromboangiitis obliterans (TAO), or Buerger's disease, is a segmental occlusive inflammatory disorder of the arteries and veins, and etiopathogenesis is still obscure. In the present study we investigated the prevalence of prothrombin 20210 G-->A, factor V 1691 G-->A (Factor V Leiden), and factor V 4070 A-->G (His 1299 Arg) mutations, found to be associated with increased risk for vascular thrombosis, in 36 patients with TAO. We performed a case-control study of these mutations. The odds ratio for prothrombin 20210 A allele compared with G allele was 7.98 (95% confidence intervals 2. 45-25.93). Only this prothrombotic genetic factor was associated with the risk of TAO (p=0.032). In conclusion, carrying the prothrombin 20210 G-->A may be an important prothrombotic risk factor of TAO. This genetic predisposition must be screened in these patients routinely, and clinical importance must be supported by further investigations.

Adolescent↗
PubMed2000

Helicobacter pylori--is it a novel causative agent in Vitamin B12 deficiency?

BACKGROUND: Evidence for vitamin B12 deficiency usually involves combinations of low serum vitamin B12 levels, clinical and metabolic abnormalities, and therapeutic response. Identification of the underlying cause is important in the diagnosis of vitamin B12 deficiency that is usually attributed to malabsorption. Helicobacter pylori is one of the most common causes of peptic ulcer disease worldwide and a major cause of chronic superficial gastritis leading to atrophy of gastric glands. It is suggested that there may be a casual relationship between H. pylori and food-cobalamin malabsorption. OBJECTIVES: To evaluate the H. pylori incidence in patients with vitamin B12 deficiency prospectively and to assess whether treatment for H pylori infection could correct this deficiency over time. PATIENTS AND METHODS: We performed a prospective cohort study involving 138 patients who had anemia and vitamin B12 deficiency. An upper gastrointestinal endoscopy was performed to assess the severity of atrophic gastritis and biopsy specimens for Campylobacter-like organisms tests and histological examination for H pylori were obtained at the time of diagnosis. The diagnosis of H. pylori prompted a combination treatment. RESULTS: Helicobacter pylori was detected in 77 (56%) of 138 patients with vitamin B12 deficiency and eradication of H pylori infection successfully improved anemia and serum vitamin B12 levels in 31 (40 %) of 77 infected patients. CONCLUSIONS: Helicobacter pylori seems to be a causative agent in the development of adult vitamin B12 deficiency. Eradication of H. pylori infection alone may correct vitamin B12 levels and improve anemia in this subgroup of patients.

Adult↗
PubMed2000

Effect of plasminogen activator inhibitor-1 4G/5G polymorphism in Turkish deep vein thrombotic patients with and without FV1691 G-A.

A decreased fibrinolytic activity due to increased levels of plasminogen activator inhibitor-1 has been shown in deep vein thrombosis patients. Elevated plasma plasminogen activator inhibitor-1 levels are associated with the 4G allele of a 4G/5G polymorphism located in the promoter region of the plasminogen activator inhibitor-1 gene. Because there is no existing data in the Turkish population, we aimed to study these mutations in patients with deep vein thrombosis (n = 136) and normal controls (n = 113), consecutively selected among unrelated healthy subjects without personal and familial history of atherothrombosis from Ankara, Turkey. DNA was extracted by conventional methods, and polymerase chain reaction of the plasminogen activator inhibitor-1 4G/5G polymorphism was performed according to a previously described method. Genotype distributions of FV 1691G-A and plasminogen activator inhibitor-1 4G/5G are as follows: plasminogen activator inhibitor-1 4G (patients) 0.562, plasminogen activator inhibitor-1 4G (controls) 0.50 (p = 0.6); FV1691A (patients) 0.147, FV1691A (controls) 0.035 (p = 0.005). Our data indicated that plasminogen activator inhibitor-1 4G/5G does not have an effect on the thrombotic risk. Carrying the 4G allele either in heterozygous or homozygous state increases the risk in the presence of FV1691A (odds ratio: 9.8 and 6.9, confidence interval 95% 2.9-32.7 and 1.3-35.8). FV1691A is an independent risk factor for thrombosis (odds ratio: 5.5, confidence interval: 95% 2.5-12.1). We concluded that coexistence of FV1691A and plasminogen activator inhibitor-1 4G allele leads to an increased risk for thrombosis leading a further evidence to another prothrombotic factor that may be necessary for the development of a manifest thrombotic event.

Adult↗
PubMed2000

Effect of methylenetetrahydrofolate reductase 677 C-T, 1298 A-C, and 1317 T-C on factor V 1691 mutation in Turkish deep vein thrombosis patients.

Possible effect of three common mutations in (MTHFR 677 C-T; 1317 T-C; 1298 C-A) and FV 1691 G-A mutation was studied in Turkish patients with thrombosis and compared with normal controls. The case-control study included 68 patients with the diagnosis of deep vein thrombosis and 66 controls, consecutively selected among subjects without personal and familial history of atherothrombosis. Patients with deep vein thrombosis were selected if Doppler ultrasonography was positive. Only, the comparison of factor V 1691 G-A mutation revealed statistically significant difference in control (6.06%) and deep vein thrombosis (23.5%) group. Risk assessment of double prothrombotic gene alterations revealed only FV 1691 G-A mutation as an independent risk factor for thrombosis (odds ratio 4.7 [1.5-15.0]), but our data suggested that MTHFR 677 has effect on its own (odds ratio 1.97 [0.6-2.7]) but may have synergy with FV 1691 G-A (odds ratio 8.12 [2.0-25.3]). However, MTHFR 1298 A-C and 1317 T-C does not have any effect; furthermore, being heterozygote at two different loci or homozygosity at least in a locus for 677 and 1298 revealed a significant increase (odds ratio 9 and 24 [1.3-59.3 and 2.3-240.3]) between these two groups.

Case-Control Studies↗
PubMed2000

Chronic myelomonocytic leukemia developed 2 years after the onset of immune thrombocytopenic purpura like syndrome.

An 80-year old man was diagnosed as having immune thrombocytopenic purpura based on epistaxis, purpura and by the platelet count 8 x 10(9)/l. Prednisolone and gamma globulin were administered and the platelet count had been kept around 50 x 10(9)/l during his follow up. Two years from the onset of immune thrombocytopenic purpura he was admitted because of leukocytosis (79 x 10(9)/l with 79% monocytes), anemia and thrombocytopenia. Hypercellular bone marrow with dysplasia of three lineages was observed. In the bone marrow cytogenic analysis, a -6, clonal cytogenic abnormality was observed. 45XY, der(6), t(6;6)(q16;q23). He was diagnosed as having chronic myelomonocytic leukemia. This is a difficult case in which it was diagnosed as refractory thrombocytopenia as a subgroup of myelodysplastic syndrome, rather than immune thrombocytopenic purpura. which might have preceded the development of chronic myelomonocytic leukemia.

Aged↗
PubMed2000

Prothrombin gene 20210 G-->A and Factor V Arg 506 to Gln mutation in a patient with Buerger's disease--a case report.

Thromboangiitis obliterans, or Buerger's disease, is a segmental occlusive inflammatory disorder of the arteries and veins most commonly affecting the lower extremities of young male cigarette smokers. The etiopathogenesis of the thromboangiitis obliterans is still obscure. The authors have identified heterozygosity for the recently described prothrombin gene 20210 G-->A variation and Factor V Arg 506 to Gln (Factor V Leiden) mutation in a patient with Buerger's disease. Both mutations confer a high risk of thrombosis. This coincidental observation may serve as further evidence that a thrombotic mechanism is involved in Buerger's disease.

Adult↗
PubMed1998

Search for genetic factors favoring thrombosis in Turkish population.

Common mutations in three genes (MTHFR 677 C-T; MS 2756 A-G; CBS Exon 8,844 ins 68) in homocysteine metabolism have been shown to cause increased plasma homocysteine levels thus causing a predisposition to thrombosis. FV 1691 G-A mutation, which is very common in the Turkish population, was also studied. As there is no existing data in the Turkish population, we aimed to study these mutations in patients with thrombosis and normal controls. The case-control study included 52 patients with the diagnosis of deep vein thrombosis (DVT) and 106 controls, consecutively selected among subjects without personal and family history of atherothrombosis. Patients with DVT were selected if Doppler ultrasonography was positive. The comparison of FV 1691 G-A mutation revealed statistically significant difference in control and DVT group. Risk assessment of double prothrombotic gene alterations indicated only FV 1691 G-A mutation as an independent risk factor for thrombosis, but our data suggested that MTHFR 677 has little effect on its own but may have synergy with FV 1691 G-A. Other possible risk genotypes at the homocysteine pathway did not have a significant effect on thrombosis. Furthermore, being heterozygote at two different loci or homozygosity at least in one locus also did not reveal a significant difference between these two groups in our population.

Case-Control Studies↗
PubMed1997

Molecular analysis of the Turkish form of deletion-inversion (delta beta)(0) thalassaemia.

Two unrelated (delta beta)(0)-thalassaemia patients from Southern Turkey are presented. DNA studies indicated that both of them are homozygous for the Turkish type of (delta beta)(0)-thalassaemia characterized by one large deletion of 11.5 kb including the delta and beta globin genes at the 5' end and one small deletion of 1.6 kb at the 3' end, which are separated by an inverted 7.6 kb long DNA segment that includes L1 repetitive sequence. In the present study a PCR-based method was performed to produce a unique deletion-specific product and subjected to sequence analysis for the determination of the breakpoint. DNA polymorphisms in the beta-globin gene cluster of deletion-inversion type of (delta beta)(0)-thalassaemia, IVS-I-6 and beta-39 globin genes were examined. Analysis of sequence variations in regulatory regions including the 5' hypersensitive site-2 of the locus control region (LCR), the delta, (G)gamma and (A)gamma 5' flanking regions and the second intervening sequence (IVS-II) of (A)gamma and (G)gamma genes indicated the presence of close similarities between the chromosome carrying the Turkish form of deletion-inversion (delta beta)(0)-thalassaemia and the chromosome associated with beta-39 nonsense mutation in haplotype II. These two chromosomes are characterized by the presence of a 4 base pair deletion in the (A)gamma(T) globin gene promoter. A C --> T alteration at position -199 5' to the delta gene was also found to be associated with the Turkish type of (delta beta)(0)-thalassaemia and beta-39 chromosome.

Adult↗