Tropical sprue is a poorly understood syndrome that affects both expatriates and natives in certain but not all tropical areas and is manifested by chronic diarrhea, steatorrhea, weight loss, and nutritional deficiencies, including those of both folate and cobalamin. This disease affects 5–10% of the population in some tropical areas.
Chronic diarrhea in a tropical environment is most often caused by infectious agents including G. lamblia, Yersinia enterocolitica, C. difficile, Cryptosporidium parvum, and Cyclospora cayetanensis, among other organisms. Tropical sprue should not be entertained as a possible diagnosis until the presence of cysts and trophozoites has been excluded in three stool samples. Chronic infections of the gastrointestinal tract and diarrhea in patients with or without AIDS are discussed in Chaps. 122 and 182.
The small-intestinal mucosa in individuals living in tropical areas is not identical to that of individuals who reside in temperate climates. Biopsies reveal a mild alteration of villous architecture with a modest increase in mononuclear cells in the lamina propria, which on occasion can be as severe as that seen in celiac sprue. These changes are observed both in native residents and in expatriates living in tropical regions and are usually associated with mild decreases in absorptive function, but they revert to "normal" when an individual moves or returns to a temperate area. Some have suggested that the changes seen in tropical enteropathy and in tropical sprue represent different ends of the spectrum of a single entity, but convincing evidence to support this concept is lacking.
Etiology
Because tropical sprue responds to antibiotics, the consensus is that it may be caused by one or more infectious agents. Nonetheless, the etiology and pathogenesis of tropical sprue are uncertain. First, its occurrence is not evenly distributed in all tropical areas; rather, it is found in specific locations, including southern India, the Philippines, and several Caribbean islands (e.g., Puerto Rico, Haiti), but is rarely observed in Africa, Jamaica, or Southeast Asia. Second, an occasional individual will not develop symptoms of tropical sprue until long after having left an endemic area. This is the reason why the original term for celiac sprue was nontropical sprue to distinguish it from tropical sprue. Third, multiple microorganisms have been identified on jejunal aspirate with relatively little consistency among studies. Klebsiella pneumoniae, Enterobacter cloacae, or E. coli have been implicated in some studies of tropical sprue, while other studies have favored a role for a toxin produced by one or more of these bacteria. Fourth, the incidence of tropical sprue appears to have decreased substantially during the past two decades. One speculation for the reduced occurrence is the wider use of antibiotics in acute diarrhea, especially in travelers to tropical areas from temperate countries. Fifth, the role of folic acid deficiency in the pathogenesis of tropical sprue requires clarification. Folic acid is absorbed exclusively in the duodenum and proximal jejunum, and most patients with tropical sprue have evidence of folate malabsorption and depletion. Although folate deficiency can cause changes in small-intestinal mucosa that are corrected by folate replacement, several earlier studies reporting that tropical sprue could be cured by folic acid did not provide an explanation for the "insult" that was initially responsible for folate malabsorption.
The clinical pattern of tropical sprue varies in different areas of the world (e.g., India vs Puerto Rico). Not infrequently, individuals in South India initially will report the occurrence of an acute enteritis before the development of steatorrhea and malabsorption. In contrast, in Puerto Rico a most insidious onset of symptoms and a more dramatic response to antibiotics is seen when compared to some other locations. Tropical sprue in different areas of the world may not be the same disease, and similar clinical entities may have different etiologies.
Diagnosis
The diagnosis of tropical sprue is best made by the presence of an abnormal small-intestinal mucosal biopsy in an individual with chronic diarrhea and evidence of malabsorption who is either residing or has recently lived in a tropical country. The small-intestinal biopsy in tropical sprue does not have pathognomonic features but resembles, and can often be indistinguishable from, that seen in celiac sprue (Fig. 288-4). The biopsy in tropical sprue will have less villous architectural alteration and more mononuclear cell infiltrate in the lamina propria. In contrast to celiac sprue, the histologic features of tropical sprue are present with a similar degree of severity throughout the small intestine, and a gluten-free diet does not result in either clinical or histologic improvement in tropical sprue.
Tropical Sprue: Treatment
Broad-spectrum antibiotics and folic acid are most often curative, especially if the patient leaves the tropical area and does not return. Tetracycline should be used for up to 6 months and may be associated with improvement within 1–2 weeks. Folic acid alone will induce a hematologic remission as well as improvement in appetite, weight gain, and some morphologic changes in small intestinal biopsy. Because of the presence of marked folate deficiency, folic acid is most often given together with antibiotics.
[ reference : Harrison's Internal Medicine (online), 17th ed. ]
Tropical sprue is a poorly understood syndrome that affects both expatriates and natives in certain but not all tropical areas and is manifested by chronic diarrhea, steatorrhea, weight loss, and nutritional deficiencies, including those of both folate and cobalamin. This disease affects 5–10% of the population in some tropical areas.
Chronic diarrhea in a tropical environment is most often caused by infectious agents including G. lamblia, Yersinia enterocolitica, C. difficile, Cryptosporidium parvum, and Cyclospora cayetanensis, among other organisms. Tropical sprue should not be entertained as a possible diagnosis until the presence of cysts and trophozoites has been excluded in three stool samples. Chronic infections of the gastrointestinal tract and diarrhea in patients with or without AIDS are discussed in Chaps. 122 and 182.
The small-intestinal mucosa in individuals living in tropical areas is not identical to that of individuals who reside in temperate climates. Biopsies reveal a mild alteration of villous architecture with a modest increase in mononuclear cells in the lamina propria, which on occasion can be as severe as that seen in celiac sprue. These changes are observed both in native residents and in expatriates living in tropical regions and are usually associated with mild decreases in absorptive function, but they revert to "normal" when an individual moves or returns to a temperate area. Some have suggested that the changes seen in tropical enteropathy and in tropical sprue represent different ends of the spectrum of a single entity, but convincing evidence to support this concept is lacking.
Etiology
Because tropical sprue responds to antibiotics, the consensus is that it may be caused by one or more infectious agents. Nonetheless, the etiology and pathogenesis of tropical sprue are uncertain. First, its occurrence is not evenly distributed in all tropical areas; rather, it is found in specific locations, including southern India, the Philippines, and several Caribbean islands (e.g., Puerto Rico, Haiti), but is rarely observed in Africa, Jamaica, or Southeast Asia. Second, an occasional individual will not develop symptoms of tropical sprue until long after having left an endemic area. This is the reason why the original term for celiac sprue was nontropical sprue to distinguish it from tropical sprue. Third, multiple microorganisms have been identified on jejunal aspirate with relatively little consistency among studies. Klebsiella pneumoniae, Enterobacter cloacae, or E. coli have been implicated in some studies of tropical sprue, while other studies have favored a role for a toxin produced by one or more of these bacteria. Fourth, the incidence of tropical sprue appears to have decreased substantially during the past two decades. One speculation for the reduced occurrence is the wider use of antibiotics in acute diarrhea, especially in travelers to tropical areas from temperate countries. Fifth, the role of folic acid deficiency in the pathogenesis of tropical sprue requires clarification. Folic acid is absorbed exclusively in the duodenum and proximal jejunum, and most patients with tropical sprue have evidence of folate malabsorption and depletion. Although folate deficiency can cause changes in small-intestinal mucosa that are corrected by folate replacement, several earlier studies reporting that tropical sprue could be cured by folic acid did not provide an explanation for the "insult" that was initially responsible for folate malabsorption.
The clinical pattern of tropical sprue varies in different areas of the world (e.g., India vs Puerto Rico). Not infrequently, individuals in South India initially will report the occurrence of an acute enteritis before the development of steatorrhea and malabsorption. In contrast, in Puerto Rico a most insidious onset of symptoms and a more dramatic response to antibiotics is seen when compared to some other locations. Tropical sprue in different areas of the world may not be the same disease, and similar clinical entities may have different etiologies.
Diagnosis
The diagnosis of tropical sprue is best made by the presence of an abnormal small-intestinal mucosal biopsy in an individual with chronic diarrhea and evidence of malabsorption who is either residing or has recently lived in a tropical country. The small-intestinal biopsy in tropical sprue does not have pathognomonic features but resembles, and can often be indistinguishable from, that seen in celiac sprue (Fig. 288-4). The biopsy in tropical sprue will have less villous architectural alteration and more mononuclear cell infiltrate in the lamina propria. In contrast to celiac sprue, the histologic features of tropical sprue are present with a similar degree of severity throughout the small intestine, and a gluten-free diet does not result in either clinical or histologic improvement in tropical sprue.
Tropical Sprue: Treatment
Broad-spectrum antibiotics and folic acid are most often curative, especially if the patient leaves the tropical area and does not return. Tetracycline should be used for up to 6 months and may be associated with improvement within 1–2 weeks. Folic acid alone will induce a hematologic remission as well as improvement in appetite, weight gain, and some morphologic changes in small intestinal biopsy. Because of the presence of marked folate deficiency, folic acid is most often given together with antibiotics.
[ reference : Harrison's Internal Medicine (online), 17th ed. ]