Is the Association Between <i>Helicobacter pylori</i> Infection and Anemia Age Dependent?

Muhsen, Khitam; Barak, Mira; Henig, Clara; Alpert, Gershon; Ornoy, Asher; Cohen, Dani

doi:10.1111/j.1523-5378.2010.00793.x

Cited by 41 publications

(44 citation statements)

References 28 publications

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“…In adult T1DM patients, autoimmune gastritis is characterized by gastric atrophy, APCA autoantibodies, achlorydria and hypergastrinemia, iron deficiency anemia, and B 12 deficiency [27], and may predispose to gastric carcinoid tumors [27]. Interestingly, iron deficiency anemia is a common and initial manifestation of autoimmune gastritis [28], but may also result from H. pylori infection [29], as corroborated in 2 of our patients. One of our APCA-positive patients had hypergastrinemia without concomitant H. pylori infection.…”

Section: Discussionmentioning

confidence: 72%

“…As gastric autoimmunity is usually asymptomatic [29], it has been suggested that patients with APCA positivity should be annually investigated with gastrin, ferritin, vitamin B 12 and complete blood count [26]. Should elevated APCA levels and hypergastrinemia be detected, gastroscopy with multiple biopsies should be performed [26].…”

Section: Discussionmentioning

confidence: 99%

“…Moreover, all T1DM children and adolescents should be screened for APCA status at diagnosis and, in case they are APCA negative, every 4 years, or at any other time if there are clinical indications, as gastric autoimmunity can occur at any age [26,29]. In particular, APCA negative patients with thyroid autoimmunity and/or the persistence of anti-GAD should be investigated every 2 years for APCA status, as they are at increased risk to develop gastric autoimmunity [26,29]. …”

Section: Discussionmentioning

confidence: 99%

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Gastric Autoimmunity in Children and Adolescents with Type 1 Diabetes: A Prospective Study

Kakleas

Kostaki²,

Critselis³

et al. 2012

Horm Res Paediatr

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Background/Aims: Type 1 diabetes (T1DM) is associated with gastric autoimmunity, which is characterized by the presence of parietal cell antibodies (APCA). We investigated gastric autoimmunity prevalence in T1DM children, its manifestations, determinants and association with thyroid gland (anti-Tg, anti-TPO) and pancreatic β-cell autoimmunity (anti-GAD) at baseline and 4 years later. Methods: The initial cohort (D1) included 97 children with T1DM. At follow-up after 4 years (D2), 84.5% of participants were evaluated. We assessed APCA, anti-Tg, anti-TPO, and anti-GAD presence, as well as symptoms of gastritis. APCA-positive patients were evaluated with gastrin, B₁₂, ferritin levels and were submitted to gastroscopy. Results: Thyroid antibody positivity was increased among the APCA-positive patients. Four years later, among initially APCA-positive patients, 2/6 became APCA negative, while 4/6 developed high titers of APCA. On gastroscopy, 2 patients had chronic hypertrophic gastritis and one Helicobacter pylori gastritis. Conclusions: Gastric autoimmunity was associated with thyroid autoimmunity and anti-GAD persistence. After 4 years, the majority of APCA-positive patients developed high titers of APCA and mild symptoms of gastritis. Thus, patients with T1DM, and in particular those with thyroid and/or pancreatic autoimmunity, should have periodic autoantibody screening for the early diagnosis and follow-up of gastric autoimmunity.

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Section: Discussionmentioning

confidence: 72%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Gastric Autoimmunity in Children and Adolescents with Type 1 Diabetes: A Prospective Study

Kakleas

Kostaki²,

Critselis³

et al. 2012

Horm Res Paediatr

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“…In addition, Helicobacter pylori has been implicated in several earlier studies as a cause of IDA refractory to oral iron treatment, with a favorable response to H pylori eradication [4,5].…”

Section: Introductionmentioning

confidence: 98%

Response to parenteral iron therapy distinguish unexplained refractory iron deficiency anemia from iron‐refractory iron deficiency anemia

Akın

Sarbay

Güler

et al. 2016

Int J Lab Hematology

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Six weeks after the start of treatment, ferritin, MCV, MCH and Hb values were in normal range in 10 patients. The increase in Hb, MCH, MCV, and ferritin values ranged 2.6-3.5 g/dL, 1.7-4.2 pg, 2-9 fL, and 13-25 ng/mL, respectively. In five patients, Hb, MCH, and MCV mean (range) values [11.2 g/dL (11-12.2), 24.5 pg (24-25.6), and 67 fL (65-70)] were nearly normal but ferritin mean (range) values [9.8 ng/mL (8-11)] were below normal. Six weeks after the start of treatment, Hb, MCH, MCV and ferritin values of patients with IRIDA were increased. The increase in Hb, MCH, MCV, and ferritin values ranged 0.8-2.7 g/dL, 1.7-4.2 pg, 2-9 fL, and 13-25 ng/mL, respectively. IRIDA is only partially responsive to parenteral iron supplementation. In conclusion, this study demonstrated that the response to intravenous iron therapy for the URIDA cases improved blood parameters more effectively than hereditary IRIDA. Response to parenteral iron therapy would be helpful to distinguish unexplained refractory IDA from hereditary IRIDA for clinicians who do not have access to hepcidin or TMPRS6 mutation analysis.

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“…Major population surveys conducted over diverse geographic areas [16][17][18][19][20][21][22][23] indicate that H pylori positivity is associated with an increased prevalence of iron deficiency, and meta-analysis of 19 observational epidemiologic studies and 6 interventional trials revealed an increased risk for IDA with a pooled odds ratio (OR) of 2.8 among H pylori-infected subjects. 24 Meta-analysis of 16 randomized trials involving 956 patients with documented H pylori infection and IDA showed that the increments from baseline to end point in Hb, serum iron, and serum ferritin were significantly higher with anti-H pylori treatment plus oral iron compared with oral iron alone.…”

Section: H Pylori Gastritismentioning

confidence: 99%

How I treat unexplained refractory iron deficiency anemia

Hershko

Camaschella

2014

Blood

140

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Endoscopic gastrointestinal workup fails to establish the cause of iron deficiency anemia (IDA) in a substantial proportion of patients. In patients referred for hematologic evaluation with unexplained or refractory IDA, screening for celiac disease, autoimmune gastritis, Helicobacter pylori, and hereditary forms of IDA is recommended. About 4% to 6% of patients with obscure refractory IDA have celiac disease, and autoimmune gastritis is encountered in 20% to 27% of patients. Stratification by age cohorts in autoimmune gastritis implies a disease presenting as IDA many years before the establishment of clinical cobalamin deficiency. Over 50% of patients with unexplained refractory IDA have active H pylori infection and, after excluding all other causes of IDA, 64% to 75% of such patients are permanently cured by H pylori eradication. In young patients with a history suggestive of hereditary iron deficiency with serum ferritin higher than expected for IDA, mutations involving iron trafficking and regulation should be considered. Recognition of the respective roles of H pylori, autoimmune gastritis, celiac disease, and genetic defects in the pathogenesis of iron deficiency should have a strong impact on the current diagnostic workup and management of unexplained, or refractory, IDA.

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Is the Association Between Helicobacter pylori Infection and Anemia Age Dependent?

Abstract: H. pylori infection is associated with higher prevalence of anemia in school-age children independently of socioeconomic variables. Such association was not observed in infants. These findings are of clinical and public health importance.

Cited by 41 publications

References 28 publications

Gastric Autoimmunity in Children and Adolescents with Type 1 Diabetes: A Prospective Study

Gastric Autoimmunity in Children and Adolescents with Type 1 Diabetes: A Prospective Study

Response to parenteral iron therapy distinguish unexplained refractory iron deficiency anemia from iron‐refractory iron deficiency anemia

How I treat unexplained refractory iron deficiency anemia

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