Systematic review with meta-analysis: the worldwide prevalence of Helicobacter pylori infection.

BACKGROUND: The epidemiology of Helicobacter pylori infection is poorly understood. AIM: To establish the reported regional and national prevalence of H. pylori infection, stratified by age and gender. METHODS: All relevant English publications from 2000 to 2017 cited by PubMed and Scopus were retrieved using comprehensive combinations of keywords. The overall prevalence of H. pylori was estimated using both random effect and fixed effect meta-analyses, and presented as prevalence rate (% and 95% CI). The analyses were extended by separation into gender and age groups. RESULTS: A total of 14 056 records were obtained initially. After applying exclusion criteria in several steps, 183 studies were selected. Analysis of 410 879 participants from 73 countries in six continents revealed an overall prevalence of 44.3% (95% CI: 40.9-47.7) worldwide. This rate ranged from 50.8% (95% CI: 46.8-54.7) in developing countries compared with 34.7% (95% CI: 30.2-39.3) in developed countries. The global H. pylori infection rate was 42.7% (95% CI: 39-46.5) in females compared to 46.3% (95% CI: 42.1-50.5) in males. The prevalence in adults (≥18 years) was significantly higher than in children (48.6% [95% CI: 43.8-53.5] vs 32.6% [95% CI: 28.4-36.8], respectively). There was a statistically nonsignificant decrease in the prevalence in 2009-2016 compared with the 2000-2009 period. CONCLUSIONS: The observed differences between countries appear to be due to economic and social conditions. H. pylori infection can be a benchmark for the socioeconomic and health status of a country. Further studies are suggested to investigate the natural history of the acquisition of H. pylori infection from childhood into adult life.

High remission rate in acute myeloblastic leukemia in children treated with high-dose methylprednisolone.

Since the differentiating effect of high-dose methylprednisolone (HDMP) on myeloid leukemic cells has been shown in one of our patients with acute myeloblastic leukemia (AML-M4), 27 previously untreated children with AML were given HDMP (20-30 mg/kg per day) combined with cytosine arabinoside (Ara-C; 3 mg/kg) for the first 2 weeks of induction therapy. Marked clinical improvement was observed in all patients with the exception of one who died within 24 hours of the treatment. Enlarged liver and spleen (greater than 5 cm) became nonpalpable in 3 (37%) out of 8 and 5 (100%) out of 5 patients, respectively, and bone marrow blasts decreased below 5% in 7 patients (27%) within 2 wk of HDMP and Ara-C treatment. Adriamycin (1 mg/kg) was added 2 wk after initiation of induction therapy. Twenty-two (84.6%) of the 26 patients achieved complete remission, 3 (11.5%) had partial remission and no response was obtained in one. Treatment was well tolerated. The addition of HDMP as a differentiating and/or cytolytic agent to conventional anti-leukemic chemotherapy increased the complete remission rate and prolonged the duration of remission of our AML patients.

High-dose methylprednisolone for remission induction in children with acute nonlymphoblastic leukemia.

The effectiveness of high-dose intravenous methylprednisolone (HIVMP) in inducing an initial remission was examined in a child with acute nonlymphoblastic leukemia (ANLL). Dramatic clinical and hematological improvement with 7% marrow blasts was obtained in 3 weeks with HIVMP treatment without giving any other antileukemic drugs. Based on the results of this preliminary observation we suggest that high-dose methylprednisolone (20-30 mg/kg) might be a useful approach when applied as an initial short treatment in childhood ANLL.

Poor prognosis in children with acute nonlymphoblastic leukemia in Turkey.

Two hundred fourteen children with acute nonlymphoblastic leukemia (ANLL) were diagnosed between July 1975 to January 1987 in our center. Only 106 (50%) of the children could be treated. An initial hematologic remission was attained in 61 (58%) with a median duration of hematologic remission of 7.5 months and median survival of 12 months. Five patients who completed 36 months of therapy are still in initial remission, less than or equal to 84 months. Exophthalmos at presentation, which is clearly related to shorter duration of remission, was observed in 11% of these children. In two cases, it was the first sign of leukemia, 6 and 7 months prior to obvious bone marrow involvement. Twenty percent of the 61 patients who achieved remission discontinued their chemotherapy during the course of treatment while they were in remission, which indicates a different problem in the treatment of these patients in Turkey. Despite administration of similar treatment protocols, the prognosis of our patients was worse than the results observed in developed countries. We conclude that poor socioeconomic and nutritional conditions should also be considered among the high-risk factors for children with ANLL, as experienced in our patients with acute lymphoblastic leukemia (ALL).

Acute leukemia in two patients with hemophilia.

A 10-year-old classic hemophiliac and 1.5-year-old child with hemophilia B who developed acute lymphocytic and acute myelomonocytic leukemia respectively are presented. No changes in coagulation status of the patients were observed. It is suggested that hemophiliacs should be regarded as "population at risk" for the development of leukemia.

Platelet aggregation in neonates with hyperbilirubinaemia.

In 19 jaundiced newborns who had no evidence of kernicterus the effect of bilirubin on adenosine-5'-diphosphate (ADP), epinephrine and collagen-induced platelet aggregation was studied. Compared to 20 normal adult controls, no significant difference was found for ADP and collagen-induced platelet aggregation in jaundiced infants. However, with epinephrine, significantly decreased aggregation was observed, but this was also the case for non-jaundiced infants. This suggests that the reduced response to epinephrine in hyperbilirubinaemic infants is related to age rather than to bilirubin. Increased bilirubin is therefore not responsible for any increased bleeding tendency due to impaired platelet function.