Ali Bay

Dr. Sami Ulus Children's Hospital, Engüri, Ankara, Turkey

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Publications (4)3.65 Total impact

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    ABSTRACT: Background: Hepcidin, a key regulator of iron homeostasis, increases when inflammation and some infections occur. It plays a critical role in macrophage iron retention, which underlies inflammation/infection caused anemia. It is known that Helicobacter pylori (HP) may lead to iron deficiency (ID) due to occult blood loss or reduced iron absorption. This study investigates the role of prohepcidin, hepcidin's precursor, in ID and ID anemia (IDA) with a concurrent HP infection. Methods: In this prospectively designed study, 15 patients with IDA and a concurrent HP infection (group 1), 11 patients with an ID and a concurrent HP infection (group 2), and 18 patients with HP infection (group 3) were observed. All groups received only HP eradication therapy. Twenty-five age- and sex-matched children without ID/IDA and HP infection were included in the study as the control group. In all groups and control group, measurements were taken for pre- and posttreatment hemoglobin, serum prohepcidin, serum ferritin, serum iron (SI), transferrin saturation, erythrocyte sedimentation rate, fibrinogen, and C-reactive protein levels. Results: The pretreatment prohepcidin levels were significantly higher only in group 1 compared to the control group (P < .05). In group 1, a significant increase in hemoglobin and SI levels and a significant reduction in prohepcidin levels were additionally observed following HP eradication treatment (P < .05). However, in groups 2 and 3, significant differences in hemoglobin, iron, and prohepcidin levels between pre- and posttreatment were not observed. Conclusion: Elevated serum prohepcidin might indicate the role of inflammation in the etiology of anemia concurrent with HP.
    Pediatric Hematology and Oncology 04/2013; · 0.90 Impact Factor
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    ABSTRACT: To review our experience with typhlitis among children treated for acute leukemia. The medical records of children with acute leukemia and typhlitis between 2006 and 2009 were reviewed for demographics and symptoms, and for microbiological and imaging findings. In the 75 children with acute leukemia--54 with acute lymphoblastic leukemia (ALL) and 21 with acute myeloid leukemia (AML)--there were 10 episodes of typhlitis (4.5%) that developed during 221 periods of severe neutropenia. The cumulative risk of typhlitis was 7.4% in patients with ALL and 28.5% in patients with AML. Frequent symptoms were: abdominal pain and tenderness (100% each); fever and nausea (90% each); emesis (80%); diarrhea (50%), and hypotension, peritonitis and abdominal distension (10% each). The median duration of symptoms was 6 days (range: 2-11 days), and that of neutropenia 14 days (range: 3-25 days). All patients were treated medically and none surgically. Two patients died because of typhlitis and sepsis. In our study, the rate of typhlitis among leukemic children was 4.5%; however, the mortality rate was 20%. Thus, rapid identification and timely, aggressive medical intervention are necessary to reduce the morbidity and mortality from typhlitis.
    Medical Principles and Practice 01/2012; 21(1):36-9. · 0.96 Impact Factor
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    ABSTRACT: Ankaferd blood stopper (ABS) is a standardized medicinal plant extract that stimulates the formation of an encapsulated protein network that provides focal points for erythrocyte aggregation. It has a therapeutic potential to be used for the management of external hemorrhage. Here, the authors report an infant bleeding from peptic ulcer was stopped successfully by gastroscopic application of ABS and other cases that used topical ABS for mucosal bleedings are also presented.
    Pediatric Hematology and Oncology 11/2010; 27(8):592-6. · 0.90 Impact Factor
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    ABSTRACT: The presence of central cyanosis that is unrelated to cardiopulmonary causes alerts clinicians to a possible diagnosis of methemoglobinemia. Congenital methemoglobinemia due to deficiency of nicotinamide-adenine dinucleotide (NADH)-cytochrome b5 reductase (cb(5)r) is an autosomal recessive disorder characterized by life long cyanosis. Here we report a six-year old boy who presented with central cyanosis and upon examination revealed a methemoglobin level of 19.0%. Sequencing the CYB5R3 gene identified a homozygous T-->C transition at base c.653, which changed codon 218 from leucine to proline (L218P) in cb(5)r protein. Treatment with ascorbic acid relieved the cyanosis and returned methemoglobin levels to normal.
    Pediatric Hematology and Oncology 01/2009; 26(5):381-5. · 0.90 Impact Factor