Impact of TP53 gene variants on prognosis and survival of childhood acute lymphoblastic leukemia.

The tumor suppressor protein 53 (TP53) gene is one of the most studied genes in cancer. Although TP53 variants are rare events in acute leukemia, recent observations showed that relapse samples might harbor TP53 variants. Here, we aimed to determine TP53 variants (hotspot region, exon 4-11) in childhood acute lymphoblastic leukemia (B and T-ALL) patients (n = 94) including diagnostic-relapse pairs (n = 15) by amplicon sequencing and evaluate the clinical impact of these variants. In total, nine different (E298*, R283C, R273H, L252F, C229F, I195T, E286G, c.955_956insC, and c.920-1G > C) variants were identified in 17 (18%) childhood ALL patients. c.(920-1G> C) splice site variant and c.(955_956insC) insertion were reported for the first time. In diagnose-relapse pair samples, we identified acquired and/or loss of TP53 variants in the samples at the time of relapse. TP53 variants were found to be more common in T-ALL (37%) than in B-ALL patients (9%). Pathogenic TP53 variants were associated with a shorter overall survival time (p = 0.001).TP53 variants were found to be associated with inferior outcomes in our cohort and can be an independent risk factor for poor prognosis in childhood acute leukemia patients. Identification of low-frequent variants with next-generation sequencing approaches enables better knowledge of the clonal dynamics of ALL.

Sleep-related Breathing Disorders in Children with Asthma: Impact on Asthma Control.

OBJECTIVE: To investigate the frequency of sleep-related breathing disorder and the relationship between asthma control and sleep-related breathing disorder in children with persistent asthma. STUDY DESIGN: Comparative cross-sectional study. PLACE AND DURATION OF STUDY: University of Health Sciences, Hamidiye Etfal Training and Research Hospital, Istanbul/Turkey, from January 2019 to June 2019. METHODOLOGY: Children aged 4-11 years with persistent asthma were included. At enrollment, socio-demographic and asthmatic characteristics were investigated, and pediatric sleep questionnaire and childhood asthma control tests were administered. RESULTS: Out of 120 patients, 75 (62.5%) were males and 45 (37%) females. According to GINA guidelines, asthma was well controlled in 23.3% children, partially controlled in 50.8% children and uncontrolled in 25.8% children. The frequency of habitual snoring was reported as 20.8% and the frequency of sleep-related breathing disorder was 29.2%. The prevalence of sleep-related breathing disorders was significantly higher in the uncontrolled asthma group (p <0.001). Significant-independent efficacy of physician-diagnosed allergic rhinitis, habitual snoring, and low asthma control test scores was observed in predicting sleep-related breathing disorders in multivariate logistic regression model (p <0.001). CONCLUSION: Uncontrolled asthma is associated with sleep-related disordered breathing. The authors suggest that allergic rhinitis, habitual snoring, and low asthma control test scores are important risk factors for sleep-related breathing disorders in children with persistent asthma. KEY WORDS: Asthma, Asthma control test, Allergic rhinitis, Habitual snoring, Pediatric sleep questionnaire, Sleep-related breathing disorder.

Prognostic evidence of LEF1 isoforms in childhood acute lymphoblastic leukemia.

INTRODUCTION: The lymphoid enhancer factor 1 (LEF1) is a DNA-binding transcription factor that functions in the Wnt signaling pathway. Increased LEF1 activity is associated with progression of several types of cancer including leukemia. Here, we investigated LEF1 isoform expression and genomic variations in acute lymphoblastic leukemia (ALL). METHODS: LEF1 isoform expression was evaluated by quantitative real-time PCR in 87 newly diagnosed childhood ALL patients and controls. Moreover, Western blot analysis was performed for detection of LEF1 expression and the hotspot region of LEF1 was screened by deep sequencing. RESULTS: The LEF1 mRNA expression of B cell ALL patients was higher than the controls (LEF1-total P = .011, LEF1-long P = .026). Moreover, B-ALL samples showing higher total LEF1 expression had significantly shorter relapse-free survival (P = .008) and overall survival (P = .011). Although full-length LEF1 expression was similar to the controls in T-ALL, 50% (n = 15) of the ALL patients had increased full-length LEF1 protein expression. Imbalance between short- and full-length LEF1 isoforms may lead to cell survival in ALL. Beside the LEF1 activation, LEF1 gene variations were rarely observed in our cohort. CONCLUSION: The results indicate that the Wnt pathway may have a pathogenic function in a group of ALL patients and high LEF1-total expression might be a marker for shorter relapse-free survival time in B cell ALL.

Deferasirox in children with transfusion-dependent thalassemia or sickle cell anemia: A large cohort real-life experience from Turkey (REACH-THEM).

OBJECTIVES: To evaluate the long-term efficacy and safety of deferasirox therapy in a large observational cohort of children with transfusion-dependent thalassemia (TDT) and sickle cell anemia (SCA) in Turkey. METHODS: This was a multicenter, prospective cohort study including TDT and SCA patients aged 2-18 years with iron overload (≥100 mL/kg of pRBC or a serum ferritin [SF] level >1000 µg/L) receiving deferasirox. Patients were followed for up to 3 years according to standard practice. RESULTS: A total of 439 patients were evaluated (415 [94.5%] TDT, 143 [32.6%] between 2 and 6 years). Serum ferritin levels consistently and significantly decreased across 3 years of deferasirox therapy from a median of 1775.5 to 1250.5 µg/L (P < 0.001). Serum ferritin decreases were noted in TDT (1804.9 to 1241 µg/L), SCA (1655.5 to 1260 µg/L), and across age groups of 2-6 years (1971.5 to 1499 µg/L), 7-12 years (1688.5 to 1159.8 µg/L), and 13-18 years (1496.5 to 1107 µg/L). Serum ferritin decreases were also noted for all deferasirox dose groups but only significant in patients with doses ≥30 mg/kg/d (n = 120, -579.6 median reduction, P < 0.001). Only 9 (2%) patients had adverse events suspected to be related to deferasirox. Serum creatinine slightly increased but remained within the normal range. CONCLUSIONS: Deferasirox has long-term efficacy and safety in children with TDT and SCA, although higher doses (≥30 mg/kg/d) may be required to achieve iron balance.

Both Granulocytic and Non-Granulocytic Blood Cells Are Affected in Patients with Severe Congenital Neutropenia and Their Non-Neutropenic Family Members: An Evaluation of Morphology, Function, and Cell Death

Objective: To examine granulocytic and non-granulocytic cells in children with severe congenital neutropenia (SCN) and their non-neutropenic parents. Materials and Methods: Fifteen patients with SCN and 21 non-neutropenic parents were evaluated for a) CD95, CD95 ligand, annexin V, propidium iodide, cell cycle, and lymphocyte subsets by flow cytometry; b) rapid cell senescence (of leukocytes) by senescence-associated ß-galactosidase stain; c) aggregation tests by aggregometer; d) in vitro bleeding time by PFA-100 instrument; e) mepacrine-labeled dense granule number of thrombocytes by fluorescence microscope; and f) hematomorphology by light and electron microscope. HAX1, ELANE, G6PC3, CSF3R, and JAGN1 mutations associated with SCN were studied in patients and several parents. Results: Significant increase in apoptosis and secondary necrosis in monocytes, lymphocytes, and granulocytes of the patients and parents was detected, irrespective of the mutation type. CD95 and CD95 ligand results implied that apoptosis was non-CD95-mediated. Leukocytes of 25%, 12.5%, and 0% of patients, parents, and controls showed rapid cell senescence. The cell cycle analysis testable in four cases showed G1 arrest and apoptosis in lymphocytes of three. The patients had HAX1 (n=6), ELANE (n=2), G6PC3 (n=2), and unidentified (n=5) mutations. The CD3, CD4, and NK lymphocytes were below normal levels in 16.6%, 8.3%, and 36.4% of the patients and in 0%, 0%, and 15.4% of the parents (controls: 0%, 0%, 5.6%). The thrombocytes aggregated at low rates, dense granule number/thrombocyte ratio was low, and in vitro bleeding time was prolonged in 37.5%-66.6% of patients and 33.3%-63.2% of parents (vs. 0% in controls). Under electron and/or light microscope, the neutrophils, monocytes, lymphocytes, and thrombocytes in the peripheral blood of both patients and parents were dysplastic and the bone marrow of patients revealed increased phagocytic activity, dysmegakaryopoiesis, and necrotic and apoptotic cells. Ultrastructurally, thrombocyte adhesion, aggregation, and release were inadequate. Conclusion: In cases of SCN, patients' pluripotent hematopoietic stem cells and their non-neutropenic parents are both affected irrespective of the genetic defect.

A Possible Role for WNT5A Hypermethylation in Pediatric Acute Lymphoblastic Leukemia.

OBJECTIVE: WNT5A is one of the most studied noncanonical WNT ligands and is shown to be deregulated in different tumor types. Our aim was to clarify whether hypermethylation might be the cause of low WNT5A mRNA levels and whether we could restore this downregulation by reversing the event. MATERIALS AND METHODS: The expression of WNT5A mRNA was studied in a large acute lymphoblastic leukemia (ALL) patient group (n=86) by quantitative real-time PCR. The methylation status was detected by methylation-specific PCR (MSPCR) and bisulphate sequencing. In order to determine whether methylation has a direct effect on WNT5A expression, disease-representative cell lines were treated by 5'-aza-20-deoxycytidine. RESULTS: Here we designed a validation experiment of the WNT5A gene, which was previously examined and found to be differentially expressed by microarray study in 31 T-cell ALL patients. The expression levels were confirmed by quantitative real-time PCR and the expression levels were significantly lower in T-cell ALL patients than in control thymic subsets (p=0.007). MSPCR revealed that 86% of the patients were hypermethylated in the WNT5A promoter region. Jurkat and RPMI cell lines were treated with 5'-aza-20-deoxycytidine and WNT5A mRNA expression was restored after treatment. CONCLUSION: According to our results, WNT5A hypermethylation does occur in ALL patients and it has a direct effect on mRNA expression. Our findings show that epigenetic changes of WNT signaling can play a role in ALL pathogenesis and reversing methylation might be useful as a possible treatment of leukemia.

Biochemical, radiologic, ultrastructural, and genetic evaluation of iron overload in acute leukemia and iron-chelation therapy.

Iron overload in hereditary hemochromatosis and hematologic malignancy has unfavorable effects on morbidity. Herein, 53 children (age 108.4±58.3 mo, 25 girls and 28 boys) with acute myeloblastic and lymphoblastic leukemia, who received 4 different chemotherapy protocols, were evaluated for iron overload throughout chemotherapy. Iron overload arose: (1) before chemotherapy, which was dependent on neither chemotherapy nor packed red blood cell transfusions and (2) after chemotherapy, which was dependent on the duration and nature of chemotherapy and partially on transfusion of packed red blood cells. Iron overload was documented in 75% of patients with a ferritin level >1000 ng/mL, by liver and heart magnetic resonance imaging, and they were administered iron-chelation therapy with success. Three of 10 radiologically iron-overloaded patients were heterozygous for H63D mutation. Aminolevulinic acid and porphobilinogen levels were normal. Light microscopic examination of the bone marrow revealed increased iron granules in erythroblasts, platelets, and megakaryocytes, iron-laden macrophages, free iron in the matrix, dyshematopoiesis, and apoptotic cells. Electron microscopic examination revealed iron-laden secondary lysosomes and autolysosomes in normoblasts and iron-laden primary granules in promyelocytes, irrelevant to the ferritin level, implying autophagia due to chemotherapy as a source of the excess iron. We think that iron overload, which is an important complication of acute leukemia, should be evaluated separately from "transfusion overload," and the management principles specific to leukemia should be implemented.

Comparison of piperacillin tazobactam and cefoperazone sulbactam monotherapy in treatment of febrile neutropenia.

BACKGROUND: Monotherapy has tended to replace the combination therapy in emprical treatment of febrile neutropenia. There is no reported trial which compares the efficacy of cefoperazone-sulbactam (CS) and piperacillin-tazobactam (PIP/TAZO) monotherapies in the treatment of febrile neutropenia. In this prospective randomized study, we aimed to compare the safety and efficacy of CS versus PIP/TAZO as empirical monotherapies in febrile neutropenic children with cancer. PROCEDURE: The study included febrile, neutropenic children hospitalized at our center for cancer. They were randomly selected to receive CS 100 mg/kg/day or PIP/TAZO 360 mg/kg/day. Duration of fever and neutropenia, absolute neutrophil count, modification, and success rate were compared between the two groups. Resolution of fever without antibiotic change was defined as success and resolution of fever with antibiotic change or death of a patient was defined as failure. Modification was defined as changing the empirical antimicrobial agent during a febrile episode. RESULTS: One hundred and two febrile neutropenic episodes were documented in 55 patients with a median age of 4 years. In 50 episodes CS and in 52 episodes PIP/TAZO was used. Duration of fever and neutropenia, neutrophil count, age, sex, and primary disease were not different between two groups. Success rates in the CS and PIP/TAZO groups were respectively 56 and 62% (P > 0.05). Modification rate between two groups showed no significant difference (P > 0.05). No serious adverse effect occurred in either of the groups. CONCLUSION: CS and PIP/TAZO monotherapy are both safe and effective in the initial treatment of febrile neutropenia in children with cancer.

Immunosuppressive treatment in children with acquired aplastic anemia.

OBJECTIVE: Immunosuppressive treatment (IST) is an alternative for children with acquired aplastic anemia (AA) that do not have HLA-matched donors. The objective of this study was to evaluate the outcome of IST in children with acquired AA. MATERIAL AND METHODS: The study included 18 pediatric acquired AA patients that were retrospectively evaluated. The patients either did not have an HLA-matched related donor or were unable to undergo transplantation within 6 months despite having an HLA-matched donor. RESULTS: In all, 6 of the patients were characterized as very severe AA, 6 as severe AA, and 6 as moderate AA. Mean duration of follow-up was 44.5 months. In total, 9 patients that could not be treated with equine anti-thymocyte globulin (hATG) following diagnosis received high-dose methylprednisolone treatment. Among the 6 very severe AA patients, 2 achieved complete remission (22%); the other 16 patients received hATG+cyclosporine and short-term methylprednisolone. In total, 4 of the patients died during the first month of treatment. Of the remaining 12 patients, 3 responded to the treatment (25%). Of the 9 patients that did not respond after 3 months of treatment, 7 received a second course of immunosuppressive treatment with rabbit ATG (rATG)+cyclosporine and short-term methylprednisolone; 2 of the 7 patients responded (22%), but 5 did not respond to any treatment. Median survival among the patients was as 64 ± 8 months CONCLUSION: Combination IST with ATG+cyclosporine and low-dose methylprednisolone was an effective treatment in the pediatric acquired AA patients with non-identical HLA donors. In the patients that couldn't be treated with ATG high-dose methylprednisolone treatment was safe and effective.

Analysis of Chromosomal Aberrations and FLT3 gene Mutations in Childhood Acute Myelogenous Leukemia Patients.

OBJECTIVE: To identify the well-known common translocations and FLT3 mutations in childhood acute myelogenousleukemia (AML) patients in Turkey. MATERIAL AND METHODS: The study included 50 newly diagnosed patients in which t(15;17), t(8;21), and inv(16)chromosomal translocations were identified using real-time PCR and FLT3 gene mutations were identified via direct PCR amplification PCR-RE analysis. RESULTS: In all, t(15;17) chromosomal aberrations were observed in 4 patients (8.0%), t(8;21) chromosomal aberrationswere observed in 12 patients (24.0%), inv(16) chromosomal aberrations were observed in 3 patients (6.0%), and FLT3-ITD mutations were observed in 2 patients (4.0%); FLT3-D835 point mutation heterozygosity was observed in only 1patient (2.0%) patient. CONCLUSION: Despite of the known literature, a patient with FLT3-ITD and FLT3-D835 double mutation shows a bettersurvival and this might be due to the complementation effect of the t(15;17) translocation. The reportedmutation ratein this article (4%) of FLT3 gene seems to be one of the first results for Turkish population.

Assessment of hepatitis B immunization status after antineoplastic therapy in children with cancer.

BACKGROUND AND OBJECTIVES: Hepatitis B is a disease that is preventable with vaccination. Antibody levels after vaccination may be affected by suppression of the immune system due to cancer therapy. Children with cancer have a high risk of hepatitis B virus (HBV) infection. We aimed to assess the pretreatment immunization status against HBV infection and the rate of continuity of immunization after therapy in children with cancer. DESIGN AND SETTING: Retrospective case review of patients treated from 2004 to 2008. PATIENTS AND METHODS: We reviewed the medical records of patients treated in the departments of pediatric hematology and oncology and collected data on immunization history and hepatitis B serology. Anti-HBs antibody titers were compared before and after treatment. RESULTS: This study included 159 (99 males, 60 females) children who had a serologic examination. Antineoplastic therapy had been given for acute leukemia (n=66), non-Hodgkin lymphoma (n=27), Hodgkin lymphoma (n=20), and solid tumors (n=46). Fifty-one patients had not been immunized against HBV prior to the therapy; HBV serology was negative in 49 of these patients and HBsAg was positive in 2 patients. Anti-HBs antibody positivity was present in 99 of 108 patients with an immunization history, whereas no vaccination response was present in 9 patients. The titer of anti-HBs antibody was decreased below the protection level in 33 (33%) patients with positive anti-HBs antibody, whereas the protection level was found to be maintained in 66 (67%) patients. The most significant decrease (63.6%) was observed in leukemia patients. Posttreatment HBsAg and HBV DNA positivity was detected in two of the patients with negative pretreatment serology, whereas no HBV infection developed in the group with positive anti-HBs antibody. CONCLUSIONS: This study demonstrated the importance of routine childhood vaccination in reducing the risk of HBV infection in patients with cancer.

Acute liver failure, autoimmune hepatitis, and leptospirosis: a case report.

The etiology of acute liver failure varies widely in children, but the most common causes are viral hepatitis, drugs, and toxins. We report herein a case of autoimmune hepatitis and acute liver failure caused by leptospirosis, which is involved rarely in etiology.

Brucellosis presenting with pancytopenia due to hemophagocytic syndrome.

Reactive hemophagocytic syndrome is clinically characterized by fever, hepatosplenomegaly, pancytopenia, and coagulopathy, and is histologically characterized by excessive proliferation and activation of histiocytes or macrophages. It can occur with systemic infections, immunodeficiency, or underlying malignancy. Brucellosis is one of the rare causes of hemophagocytosis. Herein we report an 11-year-old male with pancytopenia due to hemophagocytosis during the course of brucellosis that responded favorably to therapy. Although rare, hemophagocytosis should be considered as a possible cause of pancytopenia in patients with brucellosis, especially in regions where brucellosis is frequently encountered.

The role of Treg cells and FoxP3 expression in immunity of ß-thalassemia major AND ß-thalassemia trait patients.

There is increased susceptibility to infections in ß-thalassemia. Changes in T- and B-lymphocyte subsets and functions, defective chemotaxis, and phagocytosis of neutrophils and macrophages have been described in these patients. Regulatory T cells (Treg cells) play a crucial role in the maintenance of immunological self-tolerance. The FOXP3 gene is specifically expressed on Treg cells. Increased antigenic stimuli due to repeated blood transfusions might change the Treg cells and FOXP3 percentage in ß-thalassemia. Immune functions of peripheral blood lymphocytes, percentage of Treg cells (defined as CD4(+)CD25(+)FoxP3(+)) were evaluated in 30 ß-thalassemia major, 30 ß-thalassemia trait, and 20 healthy children. Percentage of CD4(+)CD45RA(+) cells were increased in ß-thalassemia trait compared to both ß-thalassemia major and controls, whereas percentage of CD4(+)CD45RO(+) cells were higher in ß-thalassemia major and trait patient compared to controls. Percentages of CD4(+)CD25(bright) and CD4(+)CD25(+)FoxP3(+) Treg cells were increased only in ß-thalassemia major patients compared to controls (P = .001 and P = .0001, respectively). T lymphocytes express activated phenotype both in ß-thalassemia major and trait patients. However, only in ß-thalassemia major patients who were exposed to chronic antigenic stimulus as a result of repeated blood transfusions was an increase observed in Treg cells, which might suppress immune activation status.

Imipenem-cilastatin versus piperacillin-tazobactam as monotherapy in febrile neutropenia.

BACKGROUND: In view of the recent trend toward monotherapy in the treatment of febrile neutropenia, we evaluated the clinical efficacy and safety of imipenem-cilastatin versus piperacillin-tazobactam as an empiric therapy for febrile neutropenia in children with malignant diseases. METHODS: Febrile neutropenic patients received either imipenem-cilastatin or piperacillin-tazobactam randomly. Improvement without any changes in the initial antibiotic treatment was defined as "success" and improvement with modification of the initial treatment and death was defined as "failure". RESULTS: Over 12 months, 99 febrile neutropenic episodes were treated with monotherapy in 63 patients with a median age of 5 years. At admission, median absolute neutrophil count was 50/mm(3) and in 67% of episodes, neutrophil count was under 100/mm(3). Median duration of neutropenia was 5 days. In 22% of episodes, neutropenia persisted for more than 10 days. Piperacillin-tazobactam was used in 52 episodes and imipenem-cilastatin was used in 47 episodes. There was no difference between groups in terms of age, sex, primary diseases, neutrophil count or duration of neutropenia. In the whole group, the success rate was 67% and the failure rate was 33%, whereas in the piperacillin-tazobactam group, the rates were 71% and 29%; and in the imipenem-cilastatin group they were 62% and 38%, respectively (P > 0.05). There were no deaths. No major adverse effects were seen in either group. CONCLUSIONS: Although failure was slightly higher in the imipenem-cilastatin group, this was statistically insignificant. Both of these antibiotics can be used safely for initial empirical monotherapy of febrile neutropenia.

Comparison of idiopathic thrombocytopenic purpura in children between 3 months and 2 years versus 2-5 years.

It has been reported that infantile idiopathic thrombocytopenic purpura (ITP) has different clinical features than ITP seen in older ages and classification of bleeding sites and grading of bleeding severity can be used in determining the risk of bleeding. In this study, patients with ITP were divided into two groups according to age (<2 years and 2-5 years). The clinical features, laboratory findings, treatment modalities, rate of response and chronicity, bleeding sites, grades of bleeding were compared between each group. No significant differences were established.

Nutritional vitamin B12 deficiency in hospitalized young children.

The authors sought to determine prevalence, social, economic, and dietary patterns of young children (n = 20) identified as having vitamin B12 deficiency anemia after admission to their hospital in the last 3 years. The diagnosis of vitamin B12 deficiency was based on symptoms and clinical findings, findings on peripheral blood films and bone marrow aspirates, and serum levels of vitamin B12. The children had been exclusively breast-fed without any animal food supplementation. Serum vitamin B12 levels were also measured in the sera of mothers and found to be low. The authors concluded that vitamin B12 deficiency might be an important health problem among children of mothers who do not consume animal foods adequately.

Neutrophil hypersegmentation and thrombocytosis in children with iron deficiency anemia.

Neutrophil hypersegmentation is an expected peripheral blood smear finding in megaloblastic anemias. But some clinical reports suggest that neutrophil hypersegmentation may also occur in patients with iron deficiency anemia. In this study we searched the presence of neutrophil hypersegmentation and thrombocytosis in patients with iron deficiency anemia but who had normal serum vitamin B12 and folic acid levels. The study comprised 102 patients with iron deficiency anemia and 21 age-matched healthy controls. All routine tests for iron deficiency anemia were done, serum folate and cobalamin levels were measured, and platelets were counted in all patients and controls. Peripheral blood smears were examined for neutrophil hypersegmentation. Hypersegmentation was found in 30.4% of anemic patients and in 9.5% of controls (p < 0.05). The number of platelets was also significantly higher in anemic children (p < 0.05). These results show that neutrophil hypersegmentation may also be seen in patients with iron deficiency anemia, and thrombocytosis is a common laboratory finding in this disorder.

Antiplatelet antibodies and their correlation with clinical findings in childhood immune thrombocytopenic purpura.

The demonstration of antiplatelet antibodies (PAIgG, PAIgM) and decreased detection of platelet surface antigens (CD41, CD61, CD42b) in children with immune thrombocytopenic purpura (ITP) have a diagnostic role. This study was conducted to determine whether these parameters differed in acute and chronic ITP. Chronic ITP was defined as thrombocytopenia persisting for more than 6 months from the onset of illness. A total of 80 subjects were divided into three groups: group 1 included 39 patients with acute ITP; group 2 included 31 patients with chronic ITP, and group 3 included 10 healthy children. At diagnosis, blood samples were obtained for platelet count, mean platelet volume, plateletcrit and platelet distribution width along with platelet surface antigens and antiplatelet immunoglobulins. We found that platelet surface antigens were significantly decreased in both acute and chronic ITP when compared to the control group (p = 0.001). In contrast, PAIgG was increased in acute and chronic ITP patients compared to the control group. PAIgM was significantly higher in acute ITP. We conclude that decreased platelet surface antigens and increased antiplatelet antibodies are observed in both acute and chronic ITP. In patients with chronic progress, a relatively lower level of PAIgM can be identified.

Severe iron-deficiency anemia among hospitalized young children in an urban hospital.

The aim of this study was to investigate the prevalence and some characteristics of young children with severe iron-deficiency anemia hospitalized in an urban hospital. All of the young children (aged 7-24 months) hospitalized in a city hospital during the last 3 years were searched for iron-deficiency anemia and those with severe anemia were retrospectively evaluated. During this period, 3117 young children were hospitalized and 61.6% of them had a hemoglobin value of less than 11 g/dL and 52 children (2.7%) had severe iron-deficiency anemia (hemoglobin < 6 g/dL). It was concluded that iron-deficiency anemia is still an important health problem among young children in our society.