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Coeliac disease

It is T cell mediated autoimmune disorder in which prolamine (alcohol soluble protein in wheat, Rye and Barley) intolerance occur.
Also known as non tropical sprue, celiac disease and gluten-sensitive enteropathy.
Etiology – (Ref. Hari. 18th ed., Pg - 2469)
  1. Environmental factor- Gliadin, which is a component of gluten that is present in wheat, barley, and oats.
  2. Immunological factor-
    1. Anti endomysial antibody
    2. Anti tissue transglutaminase antibodies. (Most sensitive and most specific) (Ref. Nelson 22nd ed., Pg - 1592)
    3. Anti alpha gliadin antibody. Not used now a days
    4. IgA anti reticulin antibody. Not used now a days
  3. Genetic factors HLA DQ2 is present in 95% cases. Other have HLA DQ8 10% first degree relatives.
  4. Immunological factor-
    1. Anti tissue transglutaminase antibodies. (Most sensitive and most specific) (LQ 2012)
    2. Anti endomysial antibody
    3. Anti alpha gliadin antibody - Not done now a days
    4. IgA anti reticulin antibody - Not done now a days
  5. Genetic factors HLADQ2 is present in 95% cases. Other have HLA DQ8 10% first degree relatives.
Clinical Features – 2 age peaks (Infancy and 50 – 60 years) more common in females.
  1. Symptoms may appear at any age, but more typically they appear with the introduction of cereals in an infant’s diet.
  2. Usual clinical features are:
    1. Diarrhea - Due to
      1. Steatorrhea resulting from changes in jejunal mucosal function.
      2. Endogenous fluid secretion resulting from crypt hyperplasia
      3. Secondary lactose deficiency resulting from change in jejunal brush border enzymatic function.
      4. Bile acid malabsorption on-Due to involvement of ileum.
    2. Anemia - Due to
      1. Iron deficiency (Most common)Q
      2. Folate deficiency
      3. Vitamin B12 deficiency if ileum is involved.
    3. Edema - Due to protein loss.
    4. Osteomalacia.
Associated conditions - celiac sprue is associated with.
  1. Dermatitis herpetiformis Q
  2. Type 1 DM. Q
  3. IgA globulin deficiency Q
  4. Down syndrome
  5. Turner syndrome
Extra Edge (Ref. Hari. 18th ed., Pg - 2471)
  1. Celiac disease is also associated with diabetes mellitus type 1.
  2. The clinical importance of the association with diabetes is that although severe watery diarrhea without evidence of malabsorption is most often diagnosed as "diabetic diarrhea",
  3. Assay of antiendomysial antibodies and/or a small-intestinal biopsy must be considered to exclude celiac disease.
The changes seen on biopsy are
  1. Absence or reduced height of villi. (Flat appearance). Q
  2. Crypt hyperplasia Q
  3. Increased intra epithelial lymphocytes Q
  4. Cuboidal appearance of epithelial cells. Q
It is the reversion of histopathological appearance to normal following initiation of a gluten-free diet that establish the diagnosis.
  1. Removal of all gluten from the diet (Wheat, barley, Rye). (Ref. Hari. 18th ed., Pg - 2470)
  2. Rice, soya bean, potato and corn are given.
  1. Intestinal T cell lymphoma (10% cases) Q
  2. Intestinal ulceration Q
  3. Refractory sprue. Q
  4. Myopathy
  5. Neuropathy
  6. Hyposplenism
  7. Osteoporoses
  8. Increase chances of malignancy of stomach and esophagus
Tropical sprue (Ref. Hari. 18th ed., Pg - 2471)
Etiology – The etiology of tropical sprue is not known. The proposed etiological agents are.
  1. Infection- Klebsiella pneumoniae, Enterobacter cloacae, E. coli
  2. Nutrient deficiency – Folate deficiency.
  3. Toxins – Produced by bacteria.
Clinical features-
  1. Chronic diarrhea- It begin as acute diarrhea associated with fever.
  2. Anorexia with weight loss.
  3. Abdominal bloating.
  4. Prominent bowel sounds.
  5. Nutritional deficiency – Deficiency of folate, vitamin B12.
  1. Tetracycline for 6 months. Q
  2. Folic acid. Q
Bacterial overgrowth syndrome- (Ref. Hari. 18th ed., Pg - 2473)
Also known as stagnant bowel syndrome or blind loop syndrome,
Etiology- It is the proliferation of colon type bacteria within the small intestine. The cause is –
  1. Functional Stasis- Due to impaired peristalsis .e.g. scleroderma & DM.Q
  2. Anatomic stasis- Due to change in intestinal anatomy e.g. diverticula, stricture, jejunoileal bypass, dilatation.Q
  3. Direct Communication between small and large intestine e.g. enterocolic anastomosis.Q
Clinical features-
  1. Steatorrhea- Due to impaired micelle formation because of de conjugation of bile acids by the bacteria.
  2. Diarrhea- Due to
    1. Steatorrhea
    2. Bacterial enterotoxin causing fluid recreation.
  3. Macrocytic anemia- Due to cobalamin deficiency as it is utilized by the bacteria.
Whipple’s disease - (Ref. Hari. 18th ed., Pg - 2474)
It is a chronic multi system disease.
Etiology – Gram positive bacillus – Tropheryma whippelii.
Clinical features-
  1. Diarrhea steatorrhea, abdominal pain, weight loss, protein losing enteropathy with hypoalbuminemia.
  2. Migratory large joint polyarthritis is non-deforming
  3. Pleurisy, pulmonary infiltrates.
  4. Cardiac involvement – Coronary arteritis, pericarditis, conduction defects, endocarditis, valvular involvement.
  5. CNS involvement (10%)- Depression, seizures, myoclonus, meningitis, dementia (M/C), hypothalamic syndrome (Insomnia, hyperplasia, polydipsia).
  6. Ocular involvement- Ophthalmoplegia, Papilledema, scotoma, uveitis, nystagmus.
  7. Lymphadenopathy
  8. Chylous/serous ascites.
Laboratory diagnosis (It is diagnostic)-
  1. The diagnosis is established by histopathological examination of duodenum which demonstrate infiltration of the lamina propria with PAS-positive macrophages that contain gram positive bacilli.

Jejunal biopsy is done by Crosby’s Capsule

  1. Drug of choice is double strength trimethoprim/ sulfamethoxazole for 1 year.
  2. If trimethoprim/sulfamethoxazole is not tolerated, chloramphenicol is an appropriate second choice. (Ref. Hari. 18th ed., Pg- 2474)
Protein losing enteropathy - (Ref. Hari. 18th ed., Pg - 2475)
There is loss of both albumin and globulin in stool. Clinically patient develop généralisé anasarca.
Diagnosis: Radioactive alpha1 antitrypsin clearance in stool.
Table: Disease producing protein-losing enteropathy
Disease of the stomach e.g. Ménétrier’s disease
Disorders of intestinal lymphatics Intestinal lymphangiectasia, primary or secondary
Inflammatory disease of the gut
Inflammatory bowel disease
Parasitic infections
Blind loop syndrome
Tumours Gastric, small intestinal, colonic, familial polyposis
Coeliac disease
Radiation enteritis
Whipple’s disease
Constrictive pericarditis
Tropical sprue
Collagen-vascular disease
Allergic gastroenteropathy
Clinical features- The two important clinical features are-
  1. Peripheral edema due to hypoalbuminemia.
  2. Steatorrhea due to lymphatic block.
  1. Treatment of underlying cause.
Table: Consequences of small intestinal resection including ileal resection
Bile acids cannot be absorbed and enter the colon where they have a purgative effect. The remaining small intestine may act as a stagnant loop
Fat malabsorption
Steatorrhea Insufficient bile acids in the upper small intestine because of their loss in the Stool; fat malabsorption and fatty acid diarrhea
Gallstones Supersaturated bile because of diminished bile acid pool
Oxalate nephrolithiasis Increased absorption of oxalate because calcium, which normally binds to oxalic acids, binds instead to the excess fatty acids in the intestine.
Table: Causes of stagnant loop syndrome
Causes Mechanism
Gastric surgery Reduction in acidx
Duodenal blind loop after Polyp operation
Jejunal diverticula Diverticula act as blind loop
Enterocolic fistulas e.g. in Crohn’s disease Delivery of colonic bacteria to small intestine via the fistula
Strictures, e.g. in Crohn’s disease Delay of the fecal stream
Extensive bowel resection Proximity of remaining small intestine to the colon
Diabetic autonomic neuropathy Abnormal small intestinal motility
Scleroderma Abnormal small intestinal motility
Hypogammaglobulinemia Lack of antibody in the intestine

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