Malabsorption

Gastrointestinal manifestations Depending on the nature of the disease process causing malabsorption and its extent, gastrointestinal symptoms may range from severe to subtle or may even be totally absent. Diarrhea, weight loss, flatulence, abdominal bloating, abdominal cramps, and pain may be present. Although diarrhea is a common complaint, the character and frequency of stools may vary considerably ranging from over 10 watery stools per day to less than one voluminous putty-like stool, the latter causing some patients to complain of constipation. On the other hand, stool mass is invariably increased in patients with steatorrhea and generalized malabsorption above the normal with 150–200 g/day. Not only do unabsorbed nutrients contribute to stool mass but mucosal fluid and electrolyte secretion is also increased in diseases associated with mucosal inflammation such as coeliac disease. In addition, unabsorbed fatty acids, converted to hydroxy-fatty acids by colonic flora, as well as unabsorbed bile acids both impair absorption and induce secretion of water and electrolytes by the colon adding to stool mass. Weight loss is common among patients with significant intestinal malabsorption but must be evaluated in the context of caloric intake. Some patients compensate for fecal wastage of unabsorbed nutrients by significantly increasing their oral intake. Eliciting a careful dietary history from patients with suspected malabsorption is therefore crucial. Excessive flatus and abdominal bloating may reflect excessive gas production due to fermentation of unabsorbed carbohydrate, especially among patients with a primary or secondary disaccharidase deficiency, such as lactose intolerance or sucrose intolerance. Malabsorption of dietary nutrients and excessive fluid secretion by inflamed small intestine also contribute to abdominal distention and bloating. Prevalence, severity, and character of abdominal pain vary considerably among the various disease processes associated with intestinal malabsorption. For example, pain is common in patients with chronic pancreatitis or pancreatic cancer and Crohn's disease, but it is absent in many patients with coeliac disease or postgastrectomy malabsorption. Presentation Symptoms can manifest in a variety of ways and features might give a clue to the underlying condition. Symptoms can be intestinal or extra-intestinal - the former predominates in severe malabsorption. • Diarrhoea, often steatorrhoea, is the most common feature. Watery, diurnal and nocturnal, bulky, frequent stools are the clinical hallmark of overt malabsorption. It is due to impaired water, carbohydrate and electrolyte absorption or irritation from unabsorbed fatty acid. The latter also results in bloating, flatulence and abdominal discomfort. Cramping pain usually suggests obstructive intestinal segment e.g. in Crohn's disease, especially if it persists after defecation. • Growth retardation, failure to thrive, delayed puberty in children • Swelling or oedema from loss of protein • Anaemias, commonly from vitamin B12, folic acid and iron deficiency presenting as fatigue and weakness, and the first of which can give rise to neuropsychiatric symptoms such as abnormal sensations, difficulty walking, and decreased mental abilities. • Muscle cramp from decreased vitamin D, calcium absorption. Also lead to osteomalacia and osteoporosis • Bleeding tendencies from vitamin K and other coagulation factor deficiencies. ==Causes==

The main purpose of the gastrointestinal tract is to digest and absorb nutrients (fat, carbohydrate, protein, micronutrients (vitamins and trace minerals), water, and electrolytes. Digestion involves both mechanical and enzymatic breakdown of food. Mechanical processes include chewing, gastric churning, and the to-and-fro mixing in the small intestine. Enzymatic hydrolysis is initiated by intraluminal processes requiring gastric, pancreatic, and biliary secretions. The final products of digestion are absorbed through the intestinal epithelial cells. Malabsorption constitutes the pathological interference with the normal physiological sequence of digestion (intraluminal process), absorption (mucosal process) and transport (postmucosal events) of nutrients. Intestinal malabsorption can be due to: • Congenital or acquired reduction in absorptive surface • Defects of ion transport • Defects of specific hydrolysis • Impaired enterohepatic circulation • Mucosal damage (enteropathy) • Pancreatic insufficiency ==Diagnosis==

There is no single, specific test for malabsorption. As for most medical conditions, investigation is guided by symptoms and signs. A range of different conditions can produce malabsorption and it is necessary to look for each of these specifically. Many tests have been advocated, and some, such as tests for pancreatic function are complex, vary between centers and have not been widely adopted. However, better tests have become available with greater ease of use, better sensitivity and specificity for the causative conditions. Tests are also needed to detect the systemic effects of deficiency of the malabsorbed nutrients (such as anaemia with vitamin B12 malabsorption). Classification Some prefer to classify malabsorption clinically into three basic categories: • selective, as seen in lactose malabsorption. • partial, as observed in abetalipoproteinaemia. • total, as in exceptional cases of coeliac disease. Blood tests • Routine blood tests may reveal anaemia, high CRP or low albumin; which shows a high correlation for the presence of an organic disease. In this setting, microcytic anaemia usually implies iron deficiency and macrocytosis can be caused by impaired folic acid or B12 absorption or both. Low cholesterol or triglyceride may give a clue toward fat malabsorption. • Serological studies. Specific tests are carried out to determine the underlying cause.IgA Anti-transglutaminase antibodies or IgA Anti-endomysial antibodies for Coeliac disease (gluten sensitive enteropathy). Stool studies • Microscopy is particularly useful in diarrhoea, may show protozoa like Giardia, ova, cyst and other infective agents. • Fecal fat study to diagnose steatorrhoea is rarely performed nowadays. • Low fecal pancreatic elastase is indicative of pancreatic insufficiency. Chymotrypsin and pancreolauryl can be assessed as well Radiological studies • Barium follow through is useful in delineating small intestinal anatomy. Barium enema may be undertaken to see colonic or ileal lesions. • CT abdomen is useful in ruling out structural abnormality, done in pancreatic protocol when visualising pancreas. • Magnetic resonance cholangiopancreatography (MRCP) to complement or as an alternative to ERCP. Interventional studies showing coeliac disease manifested by blunting of villi, crypt hyperplasia, and lymphocyte infiltration of crypts. • OGD to detect duodenal pathology and obtain D2 biopsy (for coeliac disease, tropical sprue, Whipple's disease, abetalipoproteinaemia etc.) • Enteroscopy for enteropathy and jejunal aspirate and culture for bacterial overgrowth • Capsule Endoscopy is able to visualise the whole small intestine and is occasionally useful. • Colonoscopy is necessary in colonic and ileal disease. • ERCP will show pancreatic and biliary structural abnormalities. Other investigations • 75SeHCAT test to diagnose bile acid malabsorption in ileal disease or primary bile acid diarrhea. • Glucose hydrogen breath test for bacterial overgrowth • Lactose hydrogen breath test for lactose intolerance • Sugar probes or 51Cr-EDTA to determine intestinal permeability. Obsolete tests no longer used clinically • D-xylose absorption test for mucosal disease or bacterial overgrowth. Normal in pancreatic insufficiency. • Bile salt breath test (14C-glycocholate) to determine bile salt malabsorption. • Schilling test to establish cause of B12 deficiency. ==Management==

Treatment is directed largely towards management of underlying cause: • Replacement of nutrients, electrolytes and fluid may be necessary. In severe deficiency, hospital admission may be required for nutritional support and detailed advice from dietitians. Use of enteral nutrition by naso-gastric or other feeding tubes may be able to provide sufficient nutritional supplementation. Tube placement may also be done by percutaneous endoscopic gastrostomy, or surgical jejunostomy. In patients whose intestinal absorptive surface is severely limited from disease or surgery, long term total parenteral nutrition may be needed. • Pancreatic enzymes are supplemented orally in pancreatic insufficiency. • Dietary modification is important in some conditions: • Gluten-free diet in coeliac disease. • Lactose avoidance in lactose intolerance. • Antibiotic therapy to treat Small Bowel Bacterial overgrowth. • Cholestyramine or other bile acid sequestrants will help with reducing diarrhoea in bile acid malabsorption. ==See also==