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Malabsorption in children

MALABSORPTION IN CHILDREN SIMPLIFIED
REFERENCES :
NELSON 20th edition
RIYAZ ahmed - pediatric gastroentrerology

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Malabsorption in children

  1. 1. CHETHAN CHANNEGOWDA 20-06-2018
  2. 2. ▪Include numerous clinical entities that result in - 1]Chronic Diarrhea 2]Abdominal distension 3]Failure to thrive
  3. 3. • Maldigestion: Defective intraluminal hydrolysis of nutrients. Impaired breakdown of nutrients Carb → mono , di , oligosaccharides Protein → amino acids , oligopeptides Fat → fatty acids , monoglycerides
  4. 4. ▪Malabsorption: Defective mucosal uptake and transport of digested nutrients , vit , minerals . Mechanisms of malabsorption ▪The integrated processes of digestion and absorption can be described in three phases: ❖ Luminal Phase ❖ Mucosal phase ❖ Postabsorbtive /Removal phase ▪Disturbances of the absorptive process can take place in any of these three phases
  5. 5. ▪Luminal phase Dietary fats, proteins and carbohydrates are hydrolyzed and solubilized, largely by pancreatic and biliary secretions. Pancreatic insufficiencies cystic fibrosis ,chronic pancreatitis Bile salt insufficiency obstructive jaundice bacterial overgrowth Rapid transit of food through gut Gastroenterostomy -partial gastrectomy Increased bile salt loss in faeces CROHNS , ileal resection Lack of intrinsic factor Pernicious anemia Reduced gastric acid Atrophic gastritis
  6. 6. ▪MUCOSAL PHASE : final hydrolysis , uptake , processing and Packaging Epithelial transport defect →inflammation, infections Brush border defect→ cong/acq disacharidase deficiency Defect in epithelial transport -coeliac disease -tropical sprue -lymphoma
  7. 7. ▪ During the removal phase, the absorbed nutrients enter the vascular or lymphatic circulation. ▪ Enterocyte processing – Abetalipoproteinemia ▪ Lymphatic obstruction - Intestinal lymphangectasia Abdominal lymphoma
  8. 8. - Progressive weight loss - Failure to thrive - Chronic diarrhea - Abdominal distension - - Steatorrhea - Edema - Weakness, Malaise, Fatigue - Abd pain - Excessive flatus - Symptoms reflecting specific deficiencies, such as bleeding tendency, muscle cramps, tetany, bone pains and paresthesias
  9. 9. ASC WITH GENERALISED MUCOSAL DEFECT BASED ON PREDOMINANT NUTRIENT MALABSORBED
  10. 10. MUCOSAL DISORDERS ▪ CELIAC DIESEASE – GLUTEN SENSITIVE ENTEROPATHY ▪ Cow’s milk and other protein-sensitive enteropathies ▪ Eosinophilic enteropathy PROTEIN-LOSING ENTEROPATHY ▪ Lymphangiectasia (congenital and acquired) ▪ bowel mucosal inflammationCrohn disease ▪ Microvillous inclusion disease ▪ Immunodeficiency disorders ▪ Autoimmune enteropathy - IPEX ▪ Short bowel syndrome ▪ Blind loop syndrome ▪ Radiation enteritis ▪ Protein–energy malnutrition ▪ Crohn disease
  11. 11. CARBOHYDRATE MALABSORPTION ▪ Lactose malabsorption ▪ Congenital lactase deficiency ▪ Congenital sucrase-isomaltase deficiency ▪ Glucose galactose malabsorption FAT MALABSORPTION Secondary exocrine pancreatic insufficiency Bile acid synthetic defects Bile acid malabsorption (terminal ileal disease) Cholestatic liver disease Chronic pancreatitis Abetalipoproteinemia Lymphangiectasia Cystic fibrosis Lipase/colipase deficiency Protein–calorie malnutrition
  12. 12. ▪ PROTEIN/AMINO ACID MALABSORPTION ▪ Enterokinase deficiency ▪ Hartnup disease (defect in free neutral amino acids) ▪ Blue diaper syndrome (isolated tryptophan malabsorption ) ▪ Lowe syndrome (lysine and arginine malabsorption) ▪ MINERAL ANDVITAMIN MALABSORPTION ▪ Acrodermatitis enteropathica ▪ Vitamin B12 malabsorption ▪ Autoimmune pernicious anemia ▪ Congenital chloride diarrhea ▪ Congenital sodium absorption defect ▪ Folate malabsorption ▪ Vitamin D dependent rickets
  13. 13. DRUG INDUCED ▪ Sulfasalazine: folic acid malabsorption ▪ Cholestyramine: calcium and fat malabsorption ▪ Anticonvulsant drugs such as phenytoin (causing vitamin D deficiency and folic acid and calcium malabsorption) ▪ Gastric acid suppression: vitamin B12 ▪ Methotrexate: mucosal injury ▪ Laxatives Endocrine and metabolic disorders - Hyperthyroidism - Adrenal insufficiency - Diabetes mellitus - Hypoparathyroidism - Carcinoid syndrome
  14. 14. - Infections: Giardiasis, Strongyloidiasis,Tuberculosis - Celiac sprue (Gluten sensitivity) - Lactose intolerance - Tropical sprue - Chronic pancreatitis - Lymphoma, Immunoproliferative small intestinal disease (IPSID)
  15. 15. ▪ Immune-mediated systemic disorder elicited by GLUTEN and related PROLAMINES in genetically susceptible individuals ▪ Characterised by : onset 9 – 18 months , F3 : M1 ➢Malabsorption ➢Histological abnormalities of small bowel mucosa ➢Improvement in gluten free diet (clinical + histological ) ➢Relapse on gluten ➢Strong asc with HLA – DQ2 , DQ8 haplotype
  16. 16. TRIGGERS RICE , CORN , OATs - SAFE ▪ WHEAT → GLUTEN ▪ RYE → SECALIN ▪ BARLEY→ HORDEIN GLIADINS ▪ Single polypeptides – 30 – 75k mw ▪ Glutamine n proline rich ▪ Alfa , Beta , Gamma , Omega subtypes . GLIADINS GLUTENINS ALBUMIN S GLOBULINS
  17. 17. ▪ Inflammatory process – T cell mediated → disruption of structure / function of mucosal lining → malabsorption ▪ IL-15 activation by gluten peptides , triggers killing of enterocytes by lymphocytes - Blunting of villi - Crypt hypertrophy - Lymphocytic infiltration image!!!!!! N / celiac
  18. 18. Peripheral edema Clubbing Smooth tongue Long eye lashes Delayed dentition
  19. 19. ▪ Gold std – ESPGHAN CRITERIA (European society of pediatric gastroent , hepatology and nutrition) ✓Flat mucosa of GIT ✓Unequivocal clinical response to gluten free diet ▪ Histological evaluation based on MARSH CRITERIA ▪ IMAGES 2
  20. 20. ▪ IgA ab to Tissue TRANSGLUTAMINASE (tTG) : Sn , Sp 90-100 % , ELISA, ideal ▪ IgA ANTIENDOMYSIAL ANTIBODY – expensive D/D – Villous changes in developing country cow milk protein intolerance , tropical sprue , sev PEM , persistent GI infection So always confirm by SEROLOGY +BIOPSY . ENDOSCOPY Scalloping of small bowel loops Cracked mud appearance of mucosa
  21. 21. ▪ COMPLICATIONS Celiac crisis – severe dehydration , acidosis , shock Malignancy - lymphoma , adenocarcinoma Refractory sprue Ulceration / stricture
  22. 22. ▪ Lifelong strict adherence to GLUTEN FREE DIET (GFD) ▪ CODEX Alimentarius guidelines suggests - <20ppm ▪ Refractory – AZATHIOPRINE ▪ Family role – special recipes from locally available brown rice , corn , dal , millets , ragi , soy flour ,milk products meat products , fruits , vegetables , pulses . Sensitize parents for growth charts , monitoring .
  23. 23. ▪ Chronic systemic infection acquired in endemic tropical areas with abnormal small bowel structure / function . ▪ West indies , cuba , India , sri lanka etc ▪ Aetiology : persistent infection of small bowel by Klebsiella pneumoniae E coli Enterobacter cloacae ▪ Starts as an acute episode of diarrhea → takes longer to subside → excess flatus , abd cramps → followed by anorexia , weakness , FTT
  24. 24. ▪ BLOOD : LOW levels of B12 , A , E , D , K , folate , calcium ▪ D – XYLOSE test is positive ▪ Stearorrhea in 90% ▪ H2 breath test – POSITIVE (d/t bacterial overgrowth) ▪ Barium meal – thickened small bowel ▪ Biopsy – thick basement membrane , triglyceride accumulation near to surface epithelium [celiac – lipid droplets in enterocyte] ▪ injury to entire small bowel (not proximal as in celiac sprue) ▪ No changes with GLUTEN FREE DIET ▪ Rx – TETRACYCLINE / CO – TRIMOXAZOLE for 3 - 6months ▪ Deficiency correction – B12 , folic acid
  25. 25. D-XYLOSE TEST - Pentose sugar , passive diffusion in jejunum. - Not metabolized in body - Depends on → mucosal integrity , absence of diarrhea - Independent of bile salts , pancreatic enzyme, disaccharidases - 8hr fast → give 5g D-Xylose → measure serum levels @ 1hr urine levels @ 5 hr Useful In Celiac ds Tropical sprue Whipple’s Crohns
  26. 26. Measure blood level (> 20 mg/dl) Measure fraction of ingested dose excreted in urine (>22%) d-xylose consumed 50% excreted50% absorbed in gut 25% hepatic metabolism25% released into general circulation 25% excreted via kidney measure blood level (>20 mg/dL) measure fraction of ingested dose excreted (>22%) Fate of d-xylose in the body < 20mg/dl in blood < 16 % excretion in urine In abnormal intestinal absorption
  27. 27. ▪ Loss of >50% of the small bowel, with or without a portion of large intestine ▪ At birth – 200- 250 cm Adult – 300 – 800cm ▪ Generalised / specific nutrient malabsorption depending on bowel region
  28. 28. INTESTINAL ADAPTATION - Harmonal : inc gastrin , enteroglucagon - Nutrients : essential fatty acids , glutamine → stimulate mucosal hyperplasia - Growth factors : transforming growth factors (TGF) regulates proliferation n turnover
  29. 29. ▪ Initial → focus on fluid replenishment and correct electrolytes ▪ After stabilization – BOWEL REHABILITATION ▪ Continuous small volume enteral feeds , hydrolysed protein + mct oil For gut stimulation and mucosal growth , inc pancreaticobiliary flow ▪ Concurent parenteral support till max absorption is reached ▪ Start ASAP to avoid oral aversion ▪ 50% achieve enteral autonomy within 5yrs ▪ H2 blockers till 1 year ▪ Cholestyramine for explosive diarrhea + bile loss ▪ Antibiotics to control bacterial overgrowth
  30. 30. Surgical rx ▪ To slow intestinal transit , to increase mucosal surface area ▪ Small bowel transplant Complications - Cather related (long term), thrombosis , cirrhosis - Sepsis - Vit deficiency - Steatorrhea → hyperoxaluria → renal stones
  31. 31. ▪ When the normal bacterial flora of the Small intestine proliferates abnormally to cause significant derangement to the normal physiological processes of digestion and absorption. ▪ Mechanism to prevent overgrowth is lost (acidic ph , stagnation,obstruction,anamolies) ▪ Achlorhydria, dysmotility, fistulae, and strictures ,Chronic or high dose opioid therapy ▪ Loss of appetite ▪ Nausea ▪ Flatulence ▪ Diarrhea ▪ Fullness after a meal ▪ Fatty stools (steatorrhea) ▪ Unintentional weight loss ▪ Generalised weakness Vitamin B12 deficiency Folate deficiency Iron deficiency Vitamin E deficiency Rx – Tetracyclin , Rifaximin , metronidazole Sx management
  32. 32. ▪ CROHNS > ULCERATIVE COLITIS , small BOWEL is predominantly involved . ▪ Significant weight loss , growth failure , malabsorption → 85% in crohns pts ▪ Excessive levels of proinflammatory cytokines are implicated in causing anorexia ▪ multiple nutritional deficiencies + negative nitrogen balance ▪ Optimizing nutritional status and growth are key priorities ▪ Osteopenia / osteoporosis , low vit D , Bile acid malabsorption ▪ Oral > enteral feeding (max wt gain)> parenteral
  33. 33. ▪ Loss of proteins into GI TRACT 1) INFLAMED MUCOSA / ULCERATION – infection , IBD , Celiac , tropical sprue 2) LYPHATIC OBSTRUCTION – 1 , 2 intestinal lymphangiectasia, CHF , Pericarditis 3) EPITHELIAL CELL DYSFUNCTION Congenital disorders of glycosylation ,Enterocyte heparin sulfate deficiency LYPHATIC OBSTRUCTION → INC Lymphatic pressure , stasis → lymph loss into gi tract including lypmphocytes (lymphopenia) , Ig , protein , lipids
  34. 34. INTESTINAL LYMPHANGIECTASIA ▪ Protein losing gastroenteropathy d/t dilatation of intestinal lymphatics n loss of lymphatic fluid into GI tract . ▪ Hypoproteinemia , edema , immunological anomalies ▪ Asc with turner , noonan syn ▪ Manifest with ascites, peripheral edema and a low serum albumin. ▪ Fecal alfa 1 antitrysin raised ▪ Video capsule endoscopy ▪ Rx – restrict long chain fats , give protein n mct supplements ▪ MCT – no need of micelle formation , direct lymphatic absorption
  35. 35. ▪WHIPPLE’S DIESEASE Chronic systemic infection - TROPHERYMA WHIPPLEI ▪ Diarrhea, ▪ Abdominal pain, weight loss and joint pains, Malabsorption, steatorrhea ▪ Lymphadenopathy + ▪ skin hyperpigmentation, and neurologic changes . ▪ Doudenal biopsy - PAS-positive foamy macrophage inclusions ▪ Rx – IV CEFTRIAXONE / MEROPENAM – 14 days and COTRIMOXAZOLE – 1y
  36. 36. ▪IMMUNODEFICIENCY DISORDERS Selective Iga Deficiency Agammaglobulinemia, Common Variable Immunodeficiency Disease (CVID) Severe Combined Immunodeficiency(scid) Wiskott-aldrich Syndrome Chronic Granulomatous Disease. ▪HIV : Opportunistic infections by Cryptosporidium parvum, cytomegalovirus, Mycobacterium avium-intracellulare, Isospora belli ▪ Cancer chemotherapy : damage the bowel mucosa, leading to secondary malabsorption of disaccharides such as lactose. Are complicated by Chronic Rotavirus Giardiasis Bacterial Overgrowth, Protein-losing Enteropathy Villous Atropy Secondary Disaccharidase Def
  37. 37. ▪ AR ▪ AT BIRTH – profuse watery secretory diarrhea ▪ h/o polyhydramnios ▪ Persistent diarrhea → difficult fluid management → fatal ▪ Microscopy – diffuse thinning of mucosa with hypoplastic villi ▪ Electron microscopy – Apical cytoplasm contains electron dense secretory granules . ▪ Octreotide , steroid can be tried
  38. 38. ▪ photo
  39. 39. SYMPTOMS Undigested disaccharides → osmotic load → attracts water →LOOSE WATERY DIARRHEA Unabsorbed carbohydrates in large bowel → bacterial fermentation → H2 , CO2 , Methane EXCESSIVE FLATUS BLOATING DISTENSION PAIN LOOSE WATERY DIARRHEA Organic acids ACIDIC pH OF STOOLS
  40. 40. ▪ DISSACHARIDES ? ▪ Enzymes in mature brush border epithelial cells converts di → monosaccharides ▪ MALTOSE GLUCOSE + GLUCOSE ▪ LACTOSE GLUCOSE + GALACTOSE ▪ SUCROSE ,ISOMALTOSE 3 GLUCOSE + FRUCTOSE MALTASE LACTASE SUCRASE ISOMALTASE
  41. 41. ▪ Congenital lactase deficiency : very rare , < 50 cases , LCT gene mutation ▪ Primary adult type – lactate : ▪ physiologic decline in lactase activity that occurs following weaning in most mammals ▪ Peak lactase activity from term to 3 yr, after which levels gradually decrease with age and has ETHNIC variability ▪ Blacks > Asian > whites
  42. 42. ▪ Secondary lactase deficiency ▪ Seen in healthy individuals during episodes of acute illness ▪ In acute GE , coeliac disease, Crohn's disease, ulcerative colitis chemotherapy, intestinal parasites ▪ TEMPORARY
  43. 43. LACTOSE INTOLERANCE MILK ALLERGY LACTASE DEFICIENCY ALLERGY TO COW MILK PROTEIN lactose-free milk → NO SYMPTOMS SYMPTOMS +
  44. 44. ▪ To limit the intake of lactose to a level that can be tolerated ▪ usually able to consume at least 12 grams of lactose per sitting ▪ DAIRY that can be taken : Butter ,Yogurt , Cheese ▪ Substitutes : soy milk, almond milk, coconut milk ▪ Commercially available : lactase enzyme , β-galactosidase
  45. 45. ▪ Large quantity of juice rich in fructose, corn syrup, or natural fructose in fruit juices ▪ reduced levels GLUT-5 transporter on the surface of the intestinal brush- border membrane ▪ Different from Hereditary fructose intolerance → IEM , ALDOLASE B def hypogycemia , convulsion , jaundice , hepatomegaly ▪ Rx – restriction , Xylose isomerase (fructose → glucose )
  46. 46. HYDROGEN BREATH TEST Simple, non-invasive, and is performed after a short period of fasting (12hrs) Principle: ▪malabsorbed sugar passes into colon ▪bacteria produce hydrogen gas ▪H2 diffuses into blood and is excreted by lungs ▪ Baseline reading → lactose 25g → take readings every 15, 30 or 60 minutes for two to three hours ▪ If the level of hydrogen rises above 20 ppm → lactose malabsorber ▪ Also used for fructose / sucrose malabsorption , small intestinal bacterial overgrowth ▪ Drawback- 18% of people are hydrogen nonexcretors
  47. 47. ▪ Lipids – 90% triglycerides Problems asc with fat absorption ▪ Not water soluble ▪ Donot mix with intestinal contents ▪ Form fat droplets LIPASE LINGUAL GASTRIC PANCREATIC
  48. 48. ▪ MOST fat digestion occurs in DOUDENUM ▪ BILE SALTS EMULSIFY fat droplets → inc surface area for lipase to act ▪ Bile salts : syn from CHOLESTROL , secreted by liver , stored in GB , Secreted into duodenum
  49. 49. VIT A , D , E , K
  50. 50. ▪ Pancreatic insufficiency ▪ Bile acid deficiency ▪ Small intestinal bacterial overgrowth ▪ Loss of absorptive surface area ▪ Defective enterocyte function ▪ Lymphatic disorders
  51. 51. ▪ Pancreatic exocrine insufficiency ▪ Destruction of acini n ducts by own proteolytic enzymes ▪ Obstructive , Calcific type ▪ Reduced secretion of digestive enzymes(LIPASES) , bicarbonate ▪ Malabsorption of fat due to loss/inactivation of pancreatic enzymes Leads to weight loss ▪ Bulky, oily stool - STEATORRHEA ▪ Fat soluble vitamin deficiency may occur in long-standing cases ▪ Edema/hypoproteinemia ▪ Due to malnutrition with decreased hepatic synthesis of albumin/serum proteins
  52. 52. ▪ Bile salt deficiency: terminal ileum resection loss of bile salts in stool insufficient bile salts production ▪ Bacterial overgrowth: Deconjugation and loss of bile acids ▪ Gastric hypersecretion: Acid inactivation of pancreatic enzymes INV in acute pancreatitis ▪ LIPASE → > 130U ▪ Hyperglycemia , hyperbilirubinemia , hypertriglyceridemia , hypocalcemia
  53. 53. ▪ ABD XRAY : USG : atrophic, calcified or fibrotic (advanced stages) CT CONTRAST : dilatation of the main pancreatic duct , calcification , pseudocysts
  54. 54. ▪ Multisystem disease,AR, most common lethal genetic disease in Caucasians ▪ Cystic fibrosis transmembrane conductance regulator (CFTR) – chromosome 7 ▪ most common F508del – genotype ▪ Abnormality in CFTR blocks chloride transport, with inadequate hydration results in thick secretion of exocrine glands . Pancreatic insufficiency Pancreatic enzymes stay in ducts and are activated intraductally Autolysis of pancrease Inflammation, calcification, plugging of ducts, fibrosis Intestinal abnormality – Meconium ileus (15% newborns with CF) – Distal intestinal obstruction syndrome (DIOS) – Rectal prolapse • Malabsorption • Failure to thrive • Fat soluble vitamin
  55. 55. ▪ Hypoproteinemic edema ▪ Asc liver disease spectrum (30%) Mainly bile duct origin ▪ Shruken , cystic pancreas ▪ SWEAT CHLORIDE TEST ▪ ANC USG : Hyperechoic meconium , dilated small bowels , GB cant be seen properly Rx ▪ Proactive treatment of airway infection ▪ Pulmonary rehab ▪ 10% N – Acetylcysteine enema ▪ Liver transplantation ▪ Cholecystectectomy - Inc liver enzyme - Biliary cirrhosis - Portal hypertension Giant cell hepatitis Cholelithiasis Bile duct obs Recurrent pancreatitis
  56. 56. Fat input = 100 g/day Malabsorbed fat: Normal < 7 g/day Fat Absorption 72-hour Fecal Fat Test
  57. 57. ▪ Qualitative Fecal Fat Analysis - • Fat analysis by microscopic examination 2 drops NS + Stool sample + 95% ethanol + SUDAN III Upto 100 globules and diameter less than 4 mm/hpf is normal • Sudan staining of spot stool samples had a sensitivity of 78% and a specificity of 70% for the detection of steatorrhea. Grading of STAETORRHEA GRADE No of FAT droplets Diameter of fat droplets MODERATE <100 4 – 8 um SEVERE >100 6 – 75 um
  58. 58. ▪ Quantitative Fecal Fat Analysis ▪ Fecal Output Of Fat In Grams Per 24 Hours – GOLD STD ▪ Patients should consume 70 to 120 g/day of dietary fat. ▪ estimation of daily stool weight for 3 – 5 days Fecal fat excretion ▪ < 7 g per day with a fat intake of 100 g – NORMAL ▪ > 7g is pathological ▪ >20 g in steatorrhea
  59. 59. SERUM PROTEINS AS NUTRITIONAL MARKERS ALBUMIN – as long half life (20days) , doesn’t reflect current status PREALBUMIN (Transthyretin) SOMATOMEDICN C RETINOL – BINDING PROTEIN TRANSFERRIN
  60. 60. SMALL BOWEL BIOPSY Indicated When D-XYLOSE test is abnormal ie intestinal mucosal pathology By endoscopy , CROSBY CAPSULE USES - To study histology , microbiology - Enzymatic /metabolic / immunologic studies CAPSULE ENDOSCOPY - wireless miniature encapsulated video camera designed to image the entire small bowel. - noninvasive, painless , ambulatory and disposable - ingestible pill camera , 8 -12 hrs , thousands of photos - Diagnostic not for biopsy
  61. 61. ▪ Always reduces the weight gain before it slows down growth rate ▪ Loss of subcutaneous fat , muscle wasting ▪ Vit k → hemmoraghic manifestation d/t impaired gamma carboxylation (2,7,9,10) ▪ Crohns n celiac ds : anorexia > malabsorption ▪ Chronic inflammation , protein losing enteropathy → low IGF-1 but NORMAL GH leading to growth failure ▪ 13 vitamins → A ,D, E , K (fat soluble)
  62. 62. Deficiencies: Vitamin B-12 Iron Folate B vitamins
  63. 63. Glossitis Deficiencies of: Vitamin B-12 Iron Folate Niacin
  64. 64. Acrodermatitis enteropathica
  65. 65. ▪ Prognosis primarily depends on the cause of malabsorption ▪ Reasonably good in most cases, if medical and diet therapy is rigorously followed ▪ Infectious causes if treated adequately have excellent. How Long is Therapy Necessary? Most causes of malabsorption, except infections require continuous supervision by a doctor and necessitate prolonged therapy.
  66. 66. TAKE HOME POINTS APPROACH TO SUSPECTED MALABSORPTION ▪ History ,Dietary history ▪ Physical exam ▪ Routine “screening”labs ▪ Stool analysis ▪ Selective tests based on above findings ▪ Treat based on underlying disease or type of malabsorption H2 breath tests,Celiac Abs,Abd imaging,PFT, ERCP/MRCP/EUS,, Fecal 1-AT,
  67. 67. ▪ Etiology of MAS in tropical areas differs from that in temperate countries ▪ Tropical sprue ,tuberculosis - a common cause of MAS in India ▪ Celiac disease and inflammatory bowel disorders are emerging ▪ Detailed history ,physical examination mandatory ▪ The order of testing and choice of a particular test should be individualized ▪ Emphasis should be put on defining an underlying disease entity which then provides the basis for appropriate treatment.
  68. 68. ▪ Nelson textbook of paediatrics 20th edition ▪ Paediataric gastroenterology & hepatology – A RIYAZ

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