Studies on the antidiarrhoeal activity of Aegle marmelos unripe fruit: Validating its traditional usage

<p>Abstract</p> <p>Background</p> <p><it>Aegle marmelos </it>(L.) Correa has been widely used in indigenous systems of Indian medicine due to its various medicinal properties. However, despite its traditional usage as an anti-diarrhoeal there is limited information regarding its mode of action in infectious forms of diarrhoea. Hence, we evaluated the hot aqueous extract (decoction) of dried unripe fruit pulp of <it>A. marmelos </it>for its antimicrobial activity and effect on various aspects of pathogenicity of infectious diarrhoea.</p> <p>Methods</p> <p>The decoction was assessed for its antibacterial, antigiardial and antirotaviral activities. The effect of the decoction on adherence of enteropathogenic <it>Escherichia coli </it>and invasion of enteroinvasive <it>E. coli </it>and <it>Shigella flexneri </it>to HEp-2 cells were assessed as a measure of its effect on colonization. The effect of the decoction on production of <it>E. coli </it>heat labile toxin (LT) and cholera toxin (CT) and their binding to ganglioside monosialic acid receptor (GM1) were assessed by GM1-enzyme linked immuno sorbent assay whereas its effect on production and action of <it>E. coli </it>heat stable toxin (ST) was assessed by suckling mouse assay.</p> <p>Results</p> <p>The decoction showed cidal activity against <it>Giardia </it>and rotavirus whereas viability of none of the six bacterial strains tested was affected. It significantly reduced bacterial adherence to and invasion of HEp-2 cells. The extract also affected production of CT and binding of both LT and CT to GM1. However, it had no effect on ST.</p> <p>Conclusion</p> <p>The decoction of the unripe fruit pulp of <it>A. marmelos</it>, despite having limited antimicrobial activity, affected the bacterial colonization to gut epithelium and production and action of certain enterotoxins. These observations suggest the varied possible modes of action of <it>A. marmelos </it>in infectious forms of diarrhoea thereby validating its mention in the ancient Indian texts and continued use by local communities for the treatment of diarrhoeal diseases.</p

Infantile cirrhosis an analytic review of the literature and a report of 50 cases

Infantile cirrhosis is a very serious, often fatal, liver disease, largely limited to India or to descendants of Indians residing in the region of southern Asia. It occurs most frequently in children between 1 and 3 years of age and affects both sexes with about equal frequency; familial instances are not uncommon. The clinical picture is characterized by irritability, gastrointestinal upsets, jaundice, anemia and retarded development. In a number of cases there is a history of fever in some stages of the disease. Children with advanced cases develop hepatosplenomegaly, a sharp and hard anterior edge of the liver, and evidence of effects of progressive portal hypertension. The basic pathogenetic process leading to this liver disease is characterized histopathologically by evidence of profound injury to individual liver cells, resulting in severe degenerative changes and dissociation of the cytoplasmic contents; marked swelling; partial hyalinization of the cytoplasm (Mallory bodies); "bird's eye" nuclei, indicating difficulty in protein synthesis; and satellitosis about Mallory bodies-probably an attempt to remove the necrobiotic liver cells. In certain cases there is massive progressive degeneration and necrosis of liver cells, causing hepatic insufficiency without formation of regenerative pseudolobules and without development of portal hypertension. This course is interpreted as the result of a severe, diffuse injury of hepatic cells, which are unable to regenerate. This condition can perhaps be compared with the experimental massive acute necrosis due to thiamin deficiency in animals and with the diffuse hepatic necrosis seen in "florid cirrhosis" in human beings. In the majority of cases, however, there is development of a portal type of cirrhosis with formation of unilobular, regenerative islets, followed by rising portal hypertension with its usual consequences; not infrequently the regenerated elements are again destroyed by the persisting injurious process. Evidence of a causal relationship between viral hepatitis and infantile cirrhosis cannot be considered established; neither epidemiologic features nor histopathologic findings are thought to be compatible with the effects of viral hepatitis. The familial occurrence appears to be related to environmental factors rather than to a common source of infection from a silent carrier or to heredity. The nonspecific inflammatory infiltrates (satellites) accompanying this process are interpreted as a scavenger reaction secondary to the injury, degeneration, and necrosis of liver cells. Regeneration of liver cells can take place only if there are viable hepatic elements. The resulting cirrhosis of the liver is characterized by regenerated pseudolobules developing from such surviving liver cells, embedded in and surrounded by the collapsed pre-existent parenchymal stromal elements, including the surviving tissues from the portal canals. The role of the supporting tissue is considered to be entirely passive and incidental to the primary process of cell destruction. The necrobiotic changes of individual liver cells, with formation of Mallory bodies, the progressive destruction of the hepatic parenchyma, and the development of a portal type of cirrhosis are quite indicative of a nutritional cause, despite the absence of fatty metamorphosis. The histologic changes are unlike those described in persistent viral hepatitis or in the developing stages of posthepatitic (coarse, nodular) cirrhosis. The obliterative vascular changes of advanced infantile cirrhosis are interpreted as secondary phenomena accompanying the complete reorganization of the liver parenchyma. Electron microscopic studies of liver tissue from cases of histologically established infantile cirrhosis demonstrate profound disorganization of ultramicroscopic structures of liver cells, with reduction in number, distortion and partial obliteration of mitochondria, secretory granules and microsomes; deformity and distention of the channels of the intracytoplasmic reticulum; and alteration of nuclei and nuclear components. The "alcoholic hyalin" of the Mallory body appears to be the result of condensation and fusion of damaged, distorted and obliterated mitochondria