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Tropical sprue

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Tropical sprue
Other namesPostinfectious tropical malabsorption[1]
SpecialtyGastroenterology Edit this on Wikidata
SymptomsDiarrhoea, abdominal pain, weight loss
ComplicationsMalabsorption, anaemia
Diagnostic methodIntestinal histology
Differential diagnosisCoeliac disease, environmental enteropathy
TreatmentAntibiotics, folate replacement

Tropical sprue is a malabsorption disease commonly found in tropical regions, marked with abnormal flattening of the villi and inflammation of the lining of the small intestine.[1][2] It differs significantly from coeliac sprue. It appears to be a more severe form of environmental enteropathy.[3][4]

Signs and symptoms

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The illness usually starts with an attack of acute diarrhoea, fever and malaise following which, after a variable period, the patient settles into the chronic phase of diarrhoea, steatorrhoea, weight loss, anorexia, malaise, and nutritional deficiencies.[1][2][3] The symptoms of tropical sprue are:

Left untreated, nutrient and vitamin deficiencies may develop in patients with tropical sprue.[1][2] These deficiencies may have these symptoms:

Cause

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The cause of tropical sprue is not known.[2] It may be caused by persistent bacterial, viral, amoebal, or parasitic infections.[5] Folic acid deficiency, effects of malabsorbed fat on intestinal motility, and persistent small intestinal bacterial overgrowth may combine to cause the disorder.[6] A link between small intestinal bacterial overgrowth and tropical sprue has been proposed to be involved in the aetiology of post-infectious irritable bowel syndrome (IBS).[7] Intestinal immunologic dysfunction, including deficiencies in secretory immunoglobulin A (IgA), may predispose people to malabsorption and bacterial colonization, so tropical sprue may be triggered in susceptible individuals following an acute enteric infection.[1]

Diagnosis

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Diagnosis of tropical sprue can be complicated because many diseases have similar symptoms. The following investigation results are suggestive:[1]

  • Abnormal flattening of villi and inflammation of the lining of the small intestine, observed during an endoscopic procedure.
  • Presence of inflammatory cells (most often lymphocytes) in the biopsy of small intestine tissue.
  • Low levels of vitamins A, B12, E, D, and K, as well as serum albumin, calcium, and folate, revealed by a blood test.
  • Excess fat in the feces (steatorrhoea).
  • Thickened small bowel folds seen on imaging.

Tropical sprue is largely limited to within about 30 degrees north and south of the equator. Recent travel to this region is a key factor in diagnosing this disease in residents of countries outside of that geographical region.[2]

Other conditions which can resemble tropical sprue need to be differentiated.[4] Coeliac disease (also known as coeliac sprue or gluten sensitive enteropathy), has similar symptoms to tropical sprue, with the flattening of the villi and small intestine inflammation and is caused by an autoimmune disorder in genetically susceptible individuals triggered by ingested gluten. Malabsorption can also be caused by protozoan infections, tuberculosis, HIV/AIDS, immunodeficiency, chronic pancreatitis and inflammatory bowel disease.[2] Environmental enteropathy is a less severe, subclinical condition similar to tropical sprue.[2]

Prevention

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Preventive measures for visitors to tropical areas where the condition exists include steps to reduce the likelihood of gastroenteritis. These may comprise using only bottled water for drinking, brushing teeth, and washing food, and avoiding fruits washed with tap water (or consuming only peeled fruits, such as bananas and oranges). Basic sanitation is necessary to reduce fecal-oral contamination and the impact of environmental enteropathy in the developing world.[2]

Treatment

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Once diagnosed, tropical sprue can be treated by a course of the antibiotic tetracycline or sulphamethoxazole/trimethoprim (co-trimoxazole) for 3 to 6 months.[2][8] Supplementation of vitamins B12 and folic acid improves appetite and leads to a gain in weight.[4][9]

Prognosis

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The prognosis for tropical sprue may be excellent after treatment. It usually does not recur in people who get it during travel to affected regions. The recurrence rate for natives is about 20%,[2] but another study showed changes can persist for several years.[10]

Epidemiology

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Tropical sprue is common in the Caribbean, Central and South America, and India and southeast Asia. In the Caribbean, it appeared to be more common in Puerto Rico and Haiti. Epidemics in southern India have occurred.[2]

History

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The disease was first described by William Hillary[11] in 1759 in Barbados.[12] Tropical sprue was responsible for one-sixth of all casualties sustained by the Allied forces in India and Southeast Asia during World War II.[2] The use of folic acid and vitamin B12 in the treatment of tropical sprue was promoted in the late 1940s by Dr. Tom Spies of the University of Alabama, while conducting his research in Cuba and Puerto Rico.[13][14][15]

References

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  1. ^ a b c d e f Wanke, Christine A. (2015). "Tropical Sprue: enteropathy". In Bennett, John E.; Dolin, Raphael; Blaser, Martin J. (eds.). Mandell, Douglas, and Bennett's Principles and Practice of Infectious Diseases (8 ed.). pp. 1297–1301. doi:10.1016/B978-1-4557-4801-3.00104-1. PMC 7151975.
  2. ^ a b c d e f g h i j k l Ramakrishna BS, Venkataraman S, Mukhopadhya A (2006). "Tropical malabsorption". Postgrad Med J. 82 (974): 779–87. doi:10.1136/pgmj.2006.048579. PMC 2653921. PMID 17148698.
  3. ^ a b Korpe PS, Petri WA (2012). "Environmental enteropathy: critical implications of a poorly understood condition". Trends Mol Med. 18 (6): 328–36. doi:10.1016/j.molmed.2012.04.007. PMC 3372657. PMID 22633998.
  4. ^ a b c Ghoshal UC, Srivastava D, Verma A, Ghoshal U (2014). "Tropical sprue in 2014: the new face of an old disease". Curr Gastroenterol Rep. 16 (6): 391. doi:10.1007/s11894-014-0391-3. PMC 7088824. PMID 24781741.
  5. ^ Cook GC (1997). "'Tropical sprue': some early investigators favoured an infective cause, but was a coccidian protozoan involved?". Gut. 40 (3): 428–9. doi:10.1136/gut.40.3.428. PMC 1027098. PMID 9135537.
  6. ^ Cook GC (1984). "Aetiology and pathogenesis of postinfective tropical malabsorption (tropical sprue)". Lancet. 1 (8379): 721–3. doi:10.1016/s0140-6736(84)92231-1. PMID 6143049. S2CID 41146323.
  7. ^ Ghoshal UC, Gwee KA (2017). "Post-infectious IBS, tropical sprue and small intestinal bacterial overgrowth: the missing link". Nat Rev Gastroenterol Hepatol. 14 (7): 435–441. doi:10.1038/nrgastro.2017.37. PMID 28513629. S2CID 33660302.
  8. ^ Batheja MJ, Leighton J, Azueta A, Heigh R (2010). "The Face of Tropical Sprue in 2010". Case Rep Gastroenterol. 4 (2): 168–172. doi:10.1159/000314231. PMC 2929410. PMID 20805939.
  9. ^ Klipstein FA, Corcino JJ (1977). "Factors responsible for weight loss in tropical sprue". Am. J. Clin. Nutr. 30 (10): 1703–8. doi:10.1093/ajcn/30.10.1703. PMID 910746.
  10. ^ Rickles FR, Klipstein FA, Tomasini J, Corcino JJ, Maldonado N (1972). "Long-term follow-up of antibiotic-treated tropical sprue". Ann. Intern. Med. 76 (2): 203–10. doi:10.7326/0003-4819-76-2-203. PMID 5009590.
  11. ^ Bartholomew C (November 1989). "William Hillary and sprue in the Caribbean: 230 years later". Gut. 30 (Special issue): 17–21. doi:10.1136/gut.30.spec_no.17. PMC 1440696. PMID 2691344.
  12. ^ Hillary, William (1759). Observations on the Changes of the Air and the Concomitant Epidemical Diseases in the Island of Barbados: To which is Added a Treatise on the Putrid Bilious Fever, Commonly Called the Yellow Fever. pp. 277–281.
  13. ^ Spies TD, Suarez RM, Suarez RM, Hernandez-Morales F (1946). "The Therapeutic Effect of Folic Acid in Tropical Sprue". Science. 104 (2691): 75–6. Bibcode:1946Sci...104...75S. doi:10.1126/science.104.2691.75. PMID 17769104.
  14. ^ SUAREZ RM, SPIES TD (1949). "A note on the effectiveness of vitamin B12 in the treatment of tropical sprue in relapse". Blood. 4 (10): 1124–30. doi:10.1182/blood.V4.10.1124.1124. PMID 18139385.
  15. ^ "Dr. Spies Receives Distinguished Service Medal". Journal of the American Medical Association. 164 (8): 878. 1957. doi:10.1001/jama.1957.02980080048013.