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Query: UMLS:C0240066 (iron deficiency)
 7,156 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Almost all segments of the gastrointestinal tract have been used as urinary tract substitutes. The specific nutritional and gastrointestinal complications depend on the particular portion of bowel that is removed from the alimentary tract. The use of stomach theoretically may predispose the patient to hypergastrinemia and peptic ulcer disease, hypocalcemia, and iron deficiency or megaloblastic anemia. Resection of a large amount of jejunum causes malabsorption. Limited use of colon segments usually is well tolerated, but loss of large parts of the colon directly decreases available absorptive area, resulting in diarrhea. Resection of the ileum and ileocecal valve can lead to several disease states. One is mixed secretory-osmotic diarrhea. Decreased ileal reabsorption of bile salts results in fat malabsorption and steatorrhea. The presentation of increased amounts of bile salts and fatty acids to the colon decreases water absorption and stimulates active chloride and water secretion, producing a cholera-like high-volume secretory diarrhea. The loss of the ileocecal valve and ileum segment accelerates intestinal transit time, which does not allow for complete digestion and absorption of food. Water and electrolytes remain associated with undigested food particles and may overwhelm the absorptive capacity of the colon, resulting in an osmotic diarrhea. A second problem is vitamin B12 deficiency. Surgical reduction of sites in the terminal ileum for active and exclusive uptake of vitamin B12 might lead to hypovitaminosis. If this is unrecognized, patients may develop irreversible neurologic injury. A third problem is cholelithiasis. Derangements in bile salt metabolism can occur when as little as 10 cm of ileum is resected, and the propensity to form gallstones is increased. Pigment gallstones appear to be the predominant stone associated with ileal resections. The fourth possible problem is urolithiasis, the etiology of which is multifactorial in patients with ileal resections. With decreased availability of bile salts, fat malabsorption occurs. Fatty acids bind with calcium and magnesium to form soaps, resulting in increased levels of free oxalate available for absorption. Moreover, fatty acids directly increase colonic permeability to oxalate.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Nutritional and gastrointestinal complications of the use of bowel segments in the lower urinary tract. 194 6

An 11-year-old boy with eosinophilic gastroenteritis treated by an elimination diet alone presented with a perforated gastroduodenal ulcer subsequent to blunt trauma to the abdomen. Peripheral eosinophilia, chronic iron deficiency, chronic hypoalbuminemia and severe failure to thrive had been present since age 2 years. Immunological work-up revealed food allergies, documented by skin tests. A review of the literature since 1966 revealed only six other cases of perforation of the gastrointestinal tract, one of whom was also a child.
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PMID:Perforated duodenal ulcer in a pediatric patient with eosinophilic gastroenteritis. 916 27

In institutionalized adults with intellectual disability (ID), Helicobacter pylori infection occurs at approximately twice the rate it appears in the general population, and it may be responsible for the twofold higher rates of peptic ulcer disease and gastric cancer in this population. Medical, behavioural and additional environmental factors, as well as level of ID, may be related to the risk of infection with H. pylori. One hundred and sixty-eight adults with ID who were currently, had previously been or had never been institutionalized underwent a biopsychosocial evaluation. This included assessment of: level of ID using the Adaptive Behaviour Scale (ABS) Part I; levels of maladaptive behaviour using the ABS Part II; demographic, medical and environmental factors; as well as H. pylori tests using serology and faecal antigen. The overall rates of past or current infection with H. pylori in institutionalized and previously institutionalized participants were about twice that of the overall group of never-institutionalized participants, i.e. 87% and 79% compared to 44%, respectively (P < 0.001). The rates of H. pylori infection appeared to increase with age in the never-institutionalized group, but were consistently high across all ages in the other groups. The rate of infection was higher in those institutionalized for more than 5 years (95% versus 76%, P=0.02), in those with flatmates with excessive oral secretions (65% versus 21%, P < 0.001) or faecal incontinence (67% versus 27%, P < 0.001), and in those with more chronic illness and medications. All mean domain scores of the ABS Part I (Intellectual Disability) were significantly lower (indicating more severe ID) in the group currently infected with H. pylori compared to their non-infected counterparts. The majority of mean domain scores of the ABS Part II (Behaviour) were also worse, with half of these score differences reaching statistical significance in the currently infected group. The presence of alarm symptoms (e.g. vomiting, weight loss, haematemesis and melena), iron deficiency and body mass index were not significantly different in currently infected subjects. Adults with ID appear to be particularly at risk of infection with H. pylori. Environmental associations with infection include past or current institutionalization, a longer period of institutionalization, living with flatmates with excessive oral secretions and faecal incontinence. Medical associations include chronic disease and more medications, but not alarm symptoms or body mass index. Demographic associations may include increasing age in never-institutionalized adults, but no age effect in currently or previously institutionalized individuals. Psychosocial associations include more severe ID and maladaptive behaviour with current infection.
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PMID:Environmental, medical, behavioural and disability factors associated with Helicobacter pylori infection in adults with intellectual disability. 1185 56

Using data from the current National Health and Nutrition Examination Survey (1999-2000), the authors assessed whether Helicobacter pylori infection is associated with iron deficiency and iron-deficiency anemia (IDA) in the United States. Iron deficiency was defined as at least two abnormal results out of three biomarkers of iron stores. IDA was defined as a low hemoglobin level in the presence of iron deficiency. H. pylori infection was measured by serology. Complex survey estimators were used in the analysis. For 7,462 survey participants aged >or=3 years, H. pylori infection was associated with decreased serum ferritin levels (percent change = -13.9%, 95% confidence interval (CI): -19.5, -8.0) but not with levels of free erythrocyte protoporphyrin, transferrin saturation, or hemoglobin (percent change = 1.5%, -2.8%, and -1.1%, respectively). Multinomial logistic regression analyses indicated that H. pylori infection was associated with the prevalence of IDA (prevalence odds ratio (POR) = 2.6, 95% CI: 1.5, 4.6) and, to a lesser degree, other types of anemia (POR = 1.3, 95% CI: 1.0, 1.7). H. pylori infection was associated with a 40% increase in the prevalence of iron deficiency (POR = 1.4, 95% CI: 0.9, 2.0) after controlling for relevant covariates. In the United States, H. pylori infection was associated with iron deficiency/IDA regardless of the presence or absence of peptic ulcer disease.
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PMID:Iron deficiency and Helicobacter pylori infection in the United States. 1630 9

Helicobacter pylori (H.pylori), a bacterial pathogen, is a causative agent of gastritis and peptic ulcer disease and is a strong risk factor for development of gastric cancer. Environmental conditions, such as poor dietary iron resulting in iron deficiency anemia (IDA), enhance H.pylori virulence and increases risk for gastric cancer. IDA affects billions of people worldwide, and there is considerable overlap between regions of high IDA and high H.pylori prevalence. The primary aims of our study were to evaluate the effect of H.pylori infection on behavior, iron metabolism, red blood cell indices, and behavioral outcomes following comorbid H. pylori infection and dietary iron deficiency in a mouse model. C57BL/6 female mice (n = 40) were used; half were placed on a moderately iron deficient (ID) diet immediately post-weaning, and the other half were maintained on an iron replete (IR) diet. Half were dosed with H.pylori SS1 at 5 weeks of age, and the remaining mice were sham-dosed. There were 4 study groups: a control group (-Hp, IR diet) as well as 3 experimental groups (-Hp, ID diet; +Hp, IR diet; +Hp,ID diet). All mice were tested in an open field apparatus at 8 weeks postinfection. Independent of dietary iron status, H.pylori -infected mice performed fewer exploratory behaviors in the open field chamber than uninfected mice (p<0.001). Hippocampal gene expression of myelination markers and dopamine receptor 1 was significantly downregulated in mice on an ID diet (both p<0.05), independent of infection status. At 12 months postinfection, hematocrit (Hct) and hemoglobin (Hgb) concentration were significantly lower in +Hp, ID diet mice compared to all other study groups. H.pylori infection caused IDA in mice maintained on a marginal iron diet. The mouse model developed in this study is a useful model to study the neurologic, behavioral, and hematologic impact of the common human co-morbidity of H. pylori infection and IDA.
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PMID:Helicobacter pylori infection and low dietary iron alter behavior, induce iron deficiency anemia, and modulate hippocampal gene expression in female C57BL/6 mice. 2835 10

Proton pump inhibitors (PPIs) are the most effective and preferred class of drugs used to treat peptic ulcer disease, gastroesophageal reflux disease, and other diseases associated with increased production of gastric acid. PPIs in general have an excellent long-term safety profile and are well-tolerated. However, studies have shown some adverse reactions (e.g., osteoporosis, Clostridium difficile-associated diarrhea, Vitamin B12 and iron deficiency, and acute interstitial nephritis) on long-term PPI use. Thrombocytopenia attributed to use of PPIs has been described in a few case reports and a retrospective study. In this case report, we describe a case of PPI-induced thrombocytopenia. In our patient, thrombocytopenia immediately developed after the initiation of PPI on two separate occasions and resolved after its discontinuation. The strong association found in our case implies the potential role of PPI in causing this rare but serious adverse reaction. Based on this case report and the observation from other studies, a PPI-induced adverse event should be considered as a possible etiology for new-onset idiopathic thrombocytopenia.
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PMID:Adverse Effects of Proton Pump Inhibitors on Platelet Count: A Case Report and Review of the Literature. 2985 91