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Query: UMLS:C0162316 (iron deficiency anemia)
 3,806 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This paper critically reviews the current literature on extragastric diseases associated with Helicobacter pylori infection, with an emphasis on methodologic issues that complicate interpretation of study findings. This review reveals common study limitations and overall uncertainty that H. pylori infection plays a role in extragastric diseases, although such a role has not been clearly ruled out for specific diseases of relevance. Evidence suggests that anti-H. pylori therapy may lead to improvement of a few extragastric diseases, in particular, idiopathic thrombocytopenic purpura, iron deficiency anemia, and chronic idiopathic urticaria, but the data from randomized controlled trials are insufficient to confirm this beneficial effect; if the benefit of anti-H. pylori therapy for specific diseases is real, it is not clear if it results from removing H. pylori-specific injurious effects, eliminating some other infectious pathogen, or reducing the total infectious burden.
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PMID:Extragastric diseases associated with Helicobacter pylori infection. 1710 83

The significance of hyperplastic polyps of the gastric antrum in anemic patients with suspected gastrointestinal bleeding has not been determined. The aim of this study is to evaluate the prevalence and prognosis of such polyps in this patient group. Clinical records of patients referred to our endoscopy lab from November 1999 to February 2003 for the evaluation of iron deficiency anemia or suspected gastrointestinal bleeding were reviewed. There were 987 patients. Fourteen patients (1.4%) had hyperplastic polyps in the gastric antrum. Five of the patients reported melena, but the rest were asymptomatic. Multiple antral polyps were present in seven cases. The largest polyp measured 5.0 cm. Helicobacter pylori infection was present in one patient. All patients were anemic and nine had documented iron deficiency. No follow-up information was available in four patients. Hyperplastic polyps of the gastric antrum are a rare but significant cause of gastrointestinal blood loss in older patients. Removal of the polyps using endoscopic or surgical methods may be required for resolution of the blood loss along with iron supplementation. Gastroenterologists should be aware that hyperplastic polyps of the gastric antrum might result in gastrointestinal blood loss and iron deficiency anemia.
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PMID:Hyperplastic polyps of the gastric antrum in patients with gastrointestinal blood loss. 1715 10

Two hundred and thirty-eight subjects of both sexes, age range 7.5 months-16 years, with iron deficiency (ID), were included in a retrospective review of ID causes, to determine the best treatment. Inadequate iron intake was the cause of ID or iron deficiency anemia (IDA) in 59 subjects from the first months of life to adolescence. Blood loss linked to cow's milk intolerance was the cause of ID or IDA in 37 younger children. Meckel's diverticulum (MD) (6 cases), reflux esophagitis (RE) (10 cases), some drugs such as acetyl salicylic acid (11 cases) induced bleeding with ID or IDA in children and adolescents. In pubertal females with ID or IDA, polymenorrhea was observed in 16 cases. Coelic disease (CD) (37 cases), Helicobacter pylori infection (HPI) (39 cases), association of HPI and CD (8 cases), enteromonas infection (15 cases), determining particularly malabsorption, were causes of ID or IDA in patients of a wide age range, unresponsive to iron therapy. Our findings show that iron replacement therapy was not always required and should not be prescribed until the diagnosis is certain.
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PMID:Iron deficiency in childhood and adolescence: retrospective review. 1732 59

Autoimmune atrophic gastritis is encountered in 20-27% of patients with obscure, or refractory iron deficiency anemia and is 4 to 6 times more common than celiac disease causing unexplained iron deficiency. The unique clinical features of iron deficiency anemia associated with achlorhydria and mucosal atrophy sparing the gastric antrum have all been accurately described by Faber and others over 100 years ago, including its refractoriness to oral iron treatment, female predominance, relatively young age, increased prevalence of thyroid disease and tendency to progress to pernicious anemia. A significant new development is the relation between autoimmune gastritis and Helicobacter pylori infection. H. pylori per se impairs gastric acid secretion and it is quite likely that a proportion of patients described originally as achylia gastrica represented H. pylori and not autoimmune gastritis. The demonstration of H. pylori antibodies in atrophic gastritis directed against epitopes on gastric mucosal cells implies an autoimmune mechanism triggered by H. pylori and directed against gastric parietal cells by antigenic mimicry of H+K+-ATPase, the most common autoantigen in pernicious anemia. These findings introduce a new element into the 100-year-old saga of achylia gastrica and open new options for its prevention and management.
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PMID:The anemia of achylia gastrica revisited. 1749 46

Proper management of Helicobacter pylori infection in clinical practice--when supported by evidence-based data--is expected to produce substantial cost-efficacy advantages. This consideration has prompted the Cervia Working Group to organise a meeting of experts to update the National Guidelines on the diagnosis and treatment of H. pylori infection in Italy. Recommendations in the new European Guidelines were considered in the National setting, here in the light of factors such as the incidence of gastric cancer and gastric lymphoma, the accessibility to different diagnostic tools, the prevalence of bacterial resistance against antibiotics, and the availability of different drugs. The main revisions in respect to the previous guidelines include H. pylori eradication in non-ulcer dyspepsia patients and in non-steroidal, anti-inflammatory drug users, as well as in patients with idiopathic thrombocytopenic purpura and iron deficiency anaemia. The stool antigen test is now accepted as a valid test for confirmation of H. pylori eradication following therapy. New therapeutic approaches have been recommended for both first- (sequential therapy) and second-line (levofloxacin-based) treatment in our country.
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PMID:"Cervia II Working Group Report 2006": guidelines on diagnosis and treatment of Helicobacter pylori infection in Italy. 1760 19

The approach to the treatment of Helicobacter pylori infection has changed during the last years. In fact, during the last decade, the success rate of usual eradication regimens, based on a proton pump inhibitor plus clarithromycin associated with amoxicillin or metronidazole, declined from over 90% to about 80%, a critical threshold under which the eradication rate is considered unsatisfactory, according to current guidelines. This finding is mainly due to the raising prevalence of clarithromycin resistance, which is in turn linked to the widespread use of this antibiotic for respiratory tract infections. Therefore, obtaining a personal history negative for a previous use of macrolides is now mandatory, before administering clarithromycin-based antibiotic therapy. Should history data be uncertain, local resistance rates (if available) may be considered, with levels higher than 20% precluding the use of clarithromycin. In this case, alternative antibiotic combinations, previously used in the rare instances of failure of clarithromycin-based therapy, should be used. We examined also the possible additional beneficial effect of some novel non antibiotic agents such as lactoferrin, probiotics and natural substances. Other advances in the treatment of the infection are represented by the discovery that some extragastric disorders such as unexplained iron deficiency anemia and idiopathic thrombocytopenic purpura, may be causally linked to Helicobacter pylori, and that eradication therapy may lead to their regression in many cases. Finally, some "gray areas" (nonulcer dyspepsia, concomitant use of nonsteroidal anti-inflammatory drugs) which are the subject of debate as far the indication to treatment is concerned, have been discussed.
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PMID:Recent Advances in the Treatment of Helicobacter pylori Infection. 1822 Nov 77

Knowledge about Helicobacter pylori infection in children continues to advance. While its prevalence appears to be falling in developed countries, it remains a major problem in developing nations. Its transmission pathway remains highly controversial. It has not yet been definitively elucidated, although the oral-oral route seems most probable. Infection is most often intrafamilial. Risk factors for infection are associated with low socioeconomic level, including overcrowding, unhygienic conditions, sharing beds in childhood, low maternal educational level. Infection in children differs from that in adults in three respects: symptoms, endoscopic appearance of the gastric mucosa, and histologic appearance of lesions. No study has established a clear association between recurrent abdominal pain and H. pylori infection. Nonetheless, in proven infections, recurrent abdominal pain is the most common marker. More recently, an association has been reported between H. pylori infection and iron deficiency anemia. The endoscopic aspect most suggestive of H. pylori infection in children is micronodular gastritis, but it is not specific to H. pylori infection. In children as in adults, H. pylori infection is always associated with histologic gastritis. Many questions about H. pylori remain unanswered, and numerous studies are still needed.
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PMID:[Helicobacter pylori infection in children]. 1825 52

The pathogenesis of Brunner gland hamartoma of the duodenum is unknown. This case report describes the chronology of the development of Brunner gland hamartoma from Brunner gland hyperplasia over a 12-year interval. The study subject, a 64-year-old man with chronic iron deficiency anemia, underwent serial upper endoscopies during this period. Repeated endoscopies demonstrated the evolution of Brunner gland hyperplasia, as manifest endoscopically by a submucosal mass, to a pedunculated polyp with histologic features of Brunner gland hamartoma. The duodenal polypoid mass was removed by snare polypectomy. The patient also had a chronic Helicobacter pylori infection of the stomach. This report details the time-dependent evolution of Brunner gland hyperplasia to hamartoma in association with chronic gastric H. pylori infection.
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PMID:Evolution of Brunner gland hamartoma associated with Helicobacter pylori infection. 1847 38

The causes of iron deficiency vary significantly during different stages of life, and according to gender and socioeconomic circumstances. Although dietary iron is important, iron deficiency anemia (IDA) is mostly attributed to blood loss and may be the presenting clinical feature of occult bleeding from the gastrointestinal (GI) tract heralding underlying malignancy. Conventional GI diagnostic workup fails to establish the cause of iron deficiency in about one third of patients. However, abnormal iron absorption caused by hereditary iron-refractory iron deficiency anemia (IRIDA) or acquired disease is increasingly recognized as an important cause of unexplained iron deficiency. The recent availability of convenient, non-invasive screening methods to identify celiac disease, autoimmune atrophic gastritis and Helicobacter pylori infection has greatly facilitated the recognition of patients with these entities. Cure of previously refractory IDA by H pylori eradication provides strong evidence supporting a cause-and-effect relation. The intriguing recent observations of H pylori antibodies directed against epitopes on gastric mucosal cells in atrophic gastritis imply an autoimmune mechanism triggered by H pylori and directed against gastric parietal cells by means of antigenic mimicry. Improved understanding of the role of abnormal iron absorption in IDA has important implications for current concepts related to the pathogenesis and management of IDA.
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PMID:Pathogenesis and management of iron deficiency anemia: emerging role of celiac disease, helicobacter pylori, and autoimmune gastritis. 1978 2

The role of Helicobacter pylori infection in the development of iron deficiency anaemia has been the focus of attention over the past decade. However, confirmation of a relationship has not confirmed the pathophysiological mechanisms involved in the phenomenon. The aim of the present work is to study the levels of fasting gastric acidity (free and total) as well as the level of tumour necrosis factor-alpha (TNF alpha) in male refractory iron deficiency anaemia patients seropositive for H. pylori infection versus those who are seronegative. Thirty adult patients with iron deficiency anaemia and gastroduodenitis were subdivided into two groups of matched age and haemoglobin value. Group 1 was H. pylori-seropositive for infection and these patients did not receive prior treatment for eradication of H. pylori infection. Group 2 comprised patients seronegative for H. pylori infection (control group). Patients with active bleeding or previous medical problems were excluded from the study. All patients and controls were subjected to the following at presentation: history taking and thorough clinical examination, complete blood picture, reticulocytes (%), assessment of serum iron, total iron binding capacity, serum ferritin, IgG anti-Helicobacter antibody and TNF alpha, stool for occult blood and measurement of gastric acidity (total and free). Upper endoscopy was performed and multiple biopsies were taken and tested for expression of cytotoxin-associated gene A (cagA) by the polymerase chain reaction (PCR). Results showed significantly higher values of free and total gastric acidity as well as TNF alpha levels in Group 1 compared to controls (Group 2). Among those in Group 1, higher TNF alpha levels were seen in seven H. pylori cagA-positive patients than in eight cagA-negative patients. Haemoglobin values were inversely correlated with TNF alpha levels. Thus, elevated serum TNF alpha in the H. pylori-seropositive group may be one of the underlying pathophysiological mechanism for iron deficiency anaemia observed in these patients.
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PMID:Role of Helicobacter pylori in refractory iron deficiency anaemia. 1983 23


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