The Population Reference Intakes are higher than the US Recommended Dietary Allowances, with the exception of pregnancy. Iron malabsorption
Iron from food is absorbed into the bloodstream in the small intestine, primarily in the duodenum. Iron malabsorption is a less common cause of iron-deficiency anemia, but many gastrointestinal disorders can reduce the bodys ability to absorb iron. There are different mechanisms that may be present. In celiac disease, abnormal changes in the structure of the duodenum can decrease iron absorption. Abnormalities or surgical removal of the stomach can also lead to malabsorption by altering the acidic environment needed for iron to be converted into its absorbable form. If there is insufficient production of hydrochloric acid in the stomach, hypochlorhydria/achlorhydria can occur (often due to chronic H. pylori infections or long-term proton-pump inhibitor therapy), inhibiting the conversion of ferric iron to the absorbable ferrous iron.Bariatric surgery is associated with an increased risk of iron deficiency anemia due to malabsorption of iron. During a Roux-en-Y anastamosis, which is commonly performed for weight management and diabetes control, the stomach is made into a small pouch and this is connected directly to the small intestines further downstream (bypassing the duodenum as a site of digestion). About 17-45% of people develop iron deficiency after a Roux-en-Y gastric bypass. Pregnant women
Without iron supplementation, iron-deficiency anemia occurs in many pregnant women because their iron stores need to serve their own increased blood volume, as well as be a source of hemoglobin for the growing baby and for placental development.
The disease is common in farmers and those exposed to soil and animals, suggesting that the infection is acquired from these sources.Individuals who are most susceptible to the disease are those with decreased ability to perform intracellular degradation of ingested pathogens or particles, particularly within macrophages. Several studies indicate that defective T-lymphocyte (particularly TH1 population) function may be an important predisposing factor for the disease. In particular, circulating cells which are CD11b (also known as integrin alpha) expressive are reduced in susceptible individuals. CD11b has a vital role in activation of macrophages to destroy intracellularly ingested T. whipplei bacteria. Diagnosis
Common clinical signs and symptoms of Whipples disease include diarrhea, steatorrhea, abdominal pain, weight loss, migratory arthropathy, fever, and neurological symptoms. Weight loss and diarrhea are the most common symptoms that lead to identification of the process, but may be preceded by chronic, unexplained, relapsing episodes of nondestructive seronegative arthritis, often of large joints.Endoscopy of the duodenum and jejunum can reveal pale yellow shaggy mucosa with erythematous eroded patches in patients with classic intestinal Whipples disease, and small bowel X-rays may show some thickened folds. Other pathological findings may include enlarged mesenteric lymph nodes, hypercellularity of lamina propria with "foamy macrophages", and a concurrent decreased number of lymphocytes and plasma cells, per high power field view of the biopsy.Diagnosis is made by biopsy, usually by duodenal endoscopy, which reveals PAS-positive macrophages in the lamina propria containing nonacid-fast, Gram-positive bacilli.