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Clinical Characteristics Whatever may be the etiology of tropical sprue, there is primary damage to the mucosa of the gastrointestinal tract resulting in malabsorption of nutrients, mainly vitamins, minerals, fats and carbohydrates. The disease may manifest itself clinically in a wide spectrum from a very mild condition with asymptomatic structural and/or functional abnormalities of the intestinal mucosa (subclinical enteropathy) to a very severe terminal illness with all the complications of malabsorption. The diagnosis of tropical sprue is based on five parameters: (1) the clinical picture, (2) biochemical tests for malabsorption, (3) jejunal biopsy, (4) radiological study of the small bowel and (5) the response to therapy. Classically, the disease can be divided into its acute and chronic forms. In the acute form, patients are typically tourists or military personnel traveling to the tropics and staying for a period of 1-2 weeks up to 1 year. Clinically, they develop acute diarrhea (with or without cramping), nausea, flatulence, alcohol intolerance, and systemic manifestations, including myalgias, weakness and fever. All will have malabsorption of fats. The chronic or classical form of tropical sprue occurs chiefly in the indigenous population and is divided into 3 stages: (1) Acute enteritis -- The earliest phase is characterized by fatigue, lassitude and mild diarrhea. The onset is often sharply defined. During the subsequent remissions and exacerbations, there is progressive illness characterized by marked weakness, weight loss, steatorrhea, bloating of the lower abdomen and crampy abdominal pains, followed by explosive release of bulky, foul smelling stools. These clinical findings are seen particularly in hyperendemic areas, such as south India. (2) Deficiency stage -- The malabsorption of fat and fat-soluble vitamins leads to a bleeding tendency, and skin and eye changes. Malabsorption of vitamin B complex leads to glossitis with sore tongue and mouth, cheilosis and stomatitis, as well as peripheral neuropathy. (3) Anemic stage -- Malabsorption of folic acid and vitamin B12 leads to a macrocytic megaloblastic anemia. It may take 2 to 4 years for patients to progress from the first to the third stage of disease. Loss of appetite and avoidance of food (because eating may worsen the symptoms) escalates the deficiency symptoms and signs. Dehydration, cardiac failure, and adrenal failure secondary to electrolyte loss are terminal states. Tropical sprue may remain latent for a long time in some individuals and present as folate and vitamin B12 deficiency, mimicking pernicious anemia. Clinical symptoms may develop in some people long after they have left the tropics. In patients who have recovered from their disease, it is not uncommon to find a persistent deficiency of lactase with symptomatic intolerance of milk. Several reports indicate decreases in a number of intestinal cell enzymes, especially disaccharidases, which correlate with the severity of the disease. |
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Copyright: Palmer and Reeder