Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0024523 (malabsorption)
 7,319 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Giardia lamblia has a cosmopolitan distribution. The organism exists in two stages--the trophozoite and the cystic stage. Infected children may have acute or chronic diarrhea, crampy abdominal pain, anorexia, malasorption and poor weight gain and may be misdiagnosed as celiac disease. Infection may be selflimited or chronic even over years. Diagnosis is usually made by finding the characteristic cyst in stool specimens or by duodenal aspiration. Histological sections and impression smears (AMENT) of intestinal mucosa biopsies have been proved to be the most reliable method for detecting giardiasis. Evaluation of impression smears for parasites is easier and quicker than examining serial sections of biopsies. Out of 175 selected patients with intestinal complaints which were undergone small intestinal biopsy 11 were infected with giardia lamblia (6.2%). All infected children were symptomatic, malabsorption could be demonstrated in 5/8, lactase levels were reduced in most children. Examination of duodenal aspirates, stool specimens and histological sections (routine histology) alone would not have been diagnostic in every case. Evaluation of impression smears proved to be a reliable method in detecting giardia lamblia infection and is recommended whenever an intestinal biopsy is performed.
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PMID:[The value of the "impression smear" in detecting giardia lamblia infection (author's transl)]. 64 94

A 47-year-old man had diarrhea in 1965. Four years later, malabsorption syndrome was diagnosed and the patient was found to have mild lymphocytosis. Abdominal lymphoma was suspected, but exploratory laparotomy was normal except for partial villous atrophy of small intestine and slightly enlarged mesenteric lymphnodes which were normal microscopically. In vitro lymphocyte blastformation with phytohemagglutinin was depressed markedly throughout the course and the result predicted the developement of malignancy of the lymphocytic system. Infection of Isospora belli was found thereafter, and sulfamethoxazole was quite effective for diarrhea. In August, 1974, he noticed cervical lymphadenopathy for the first time and it was diagnosed as undifferentiated type of malignant lymphoma. He died in December, 1974. In this case diarrhea was most probably caused by the intestinal infection of Isospora belli without obvious lymphoma. The symptom was swept away by peroral sulfamethoxazole. In this patient coccidiosis was presumably induced and prolonged by suppression of cellular immunity which might have already begun to progress at the onset of diarrhea.
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PMID:Malignant lymphoma initiated with malabsorption syndrome due to Isospora belli infection and lymphocytosis. 96 Jan 6

Medical records of 38 horses less than 1 year of age and diagnosed as having a fracture of the femoral diaphysis, metaphysis or distal physis were evaluated. Twenty-six foals had fractures of the femoral diaphysis or metaphysis with the most common fracture configuration being comminuted. Twelve foals had distal physeal fractures with the most common fracture configuration being a Salter-Harris type II. Twenty-one foals with fractures of the capital femoral physis, neck or greater trochanter during the same time period were excluded from this study. Surgical repair was attempted in 16 diaphyseal and 2 distal physeal fractures. Most of the diaphyseal fractures were repaired by placing plates on the lateral and cranial surfaces of the bone. Dynamic condylar screw plates or angle blade plates were used for increased bone purchase in 4 foals with short distal fragments. Five foals with distal physeal fractures were treated; 2 were surgically treated by placing an angle blade plate on the lateral cortex, and 3 foals with minimally displaced distal physeal fractures were managed with stall confinement. Eight of the 16 surgically repaired diaphyseal fractures healed. Fracture location and configuration was not a determinant of outcome, but the mean age of foals with successfully repaired diaphyseal fractures was 2 months compared with 4 months for the unsuccessful cases, indicating that the age and size of the foal was important. Long-term follow up revealed that 6 of the 8 successfully repaired diaphyseal fractures had no residual effects of the fracture observed during performance of the horse for its intended use. Only 1 of the 2 surgically repaired distal physeal fractures healed, but this horse was eventually killed because of unthriftiness related to a malabsorption syndrome. Some form of complication developed in 13 of the 18 surgically repaired fractures. Infection was the primary cause of failure. The greatest determinant associated with infection was the inability to control post-surgical seroma formation.
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PMID:Retrospective study of 38 cases of femur fractures in horses less than one year of age. 139 3

Mongolian gerbils were infected with a human pathogenic Giardia lamblia strain and compared with sham-treated control animals 6 days after inoculation. Infection resulted in crypt hyperplasia associated with an increased enterocyte migration rate. Villus height was decreased in the duodenum, unchanged in the jejunum, and increased in the ileum of infected animals. Epithelial microvilli were markedly shortened, and brush border surface area decreased in the jejunum and ileum of infected animals. Thymidine kinase activity was increased in isolated duodenal villus enterocytes but did not differ in the jejunum and ileum. In vitro and in vivo experiments showed that the infection resulted in decreased jejunal glucose-stimulated electrolyte, water, and 3-O-methyl-D-glucose absorption, whereas in the ileum in vitro electrolyte and 3-O-methyl-D-glucose absorption was similar in infected and control animals. Thus, in the jejunum infection causes electrolyte, solute, and fluid malabsorption associated with decreased brush border surface area. The results indicate that the diarrhea associated with giardiasis is caused by malabsorption rather than active secretion.
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PMID:Pathophysiology of small intestinal malabsorption in gerbils infected with Giardia lamblia. 851 55

Infection with Giardia lamblia often causes only minor mucosal changes to the small intestine yet frank fat malabsorption may still occur. Some evidence suggests abnormal pancreatic exocrine function in subjects with giardiasis although the mechanism and significance of this is unclear. Studies were conducted in vitro to determine the effect of G. lamblia trophozoites or culture filtrates from the organism on lipolysis of triglyceride by porcine pancreatic lipase. Live trophozoites significantly inhibited lipolysis. The degree of inhibition increased with longer duration of lipase exposure to trophozoites. Total amounts of enzyme inhibited were proportional to enzyme concentration, while the percentage inhibition was greatest at lowest concentration. At a lipase concentration of 1.7 i.u./ml, enzyme activity was reduced by 89.7% compared to controls after incubation for 4 h with trophozoites. The effect was abolished using killed, intact trophozoites. Culture filtrates of G. lamblia did not inhibit lipolysis. Specificity of the effect was suggested by the failure of another flagellate protozoan, Trichomonas vaginalis, to inhibit lipase. In this assay system the inhibition of lipolysis was not dependent on the bile salt concentration present. The impact of this effect in vivo remains to be determined but it may contribute to fat malabsorption in giardiasis.
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PMID:The effect of Giardia lamblia trophozoites on lipolysis in vitro. 194 23

Unremitting diarrhea with malabsorption is associated with Cryptosporidium parvum infection of the small intestine in patients with AIDS. The lack of a well-defined in vitro model of C. parvum infection has severely hampered research into the biology of cryptosporidial invasion of the host epithelial cell and development of new pharmacologic and immunologic therapies. The adherent human intestinal epithelial cell line HT29 when grown in glucose-free medium develops morphologic and functional characteristics of the small intestine enterocyte and was used to develop an in vitro model of infection. Cryptosporidium oocysts obtained from AIDS patients were applied to a monolayer of cloned, differentiated HT29.74 cells. Cells were fixed and stained to estimate the degree of parasite infection. Schizonts were easily distinguished from the host cell by light microscopy. Twenty-four hours after 10(5) oocysts were added to approximately 10(6) HT29.74 cells, Cryptosporidium infection rates varied from 50 to 120 schizonts per 1,000 cells. Among 14 different experiments, the mean infection rate was 91 (+/- 18) schizonts per 1,000 cells. Electron microscopy at 6 and 24 h confirmed intracellular localization and development of schizonts. The morphologic features of the cryptosporidial schizonts within HT29.74 cells, which included the presence of a dense band and feeder layer, were identical to those described during cryptosporidial infection of human enterocytes in patients with AIDS. Fewer schizonts were observed at 5 days and beyond. Infection of differentiated HT29.74 cells (62 and 65 schizonts per 1,000 cells at 24 and 72 h, respectively) was over five times more efficient than infection of undifferentiated HT29.74 cells (9 and 5 schizonts per 1,000 cells at 24 and 72 h, respectively). In vitro infection of differentiated HT29.74 cells will allow a better understanding of the mechanisms by which C. parvum infects the small intestinal epithelium and will allow a systematic evaluation of new therapeutic agents.
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PMID:Asexual development of Cryptosporidium parvum within a differentiated human enterocyte cell line. 198 37

Giardia lamblia, the protozoan parasite, first described by Von Leewenhoek in 1681, has come into prominence in last quarter century because of mounting awareness that it may cause significant morbidity and loss of man power. Earlier thought to be a commensal organism, it has been recognised as a true intestinal pathogen in the past three decades. Nevertheless, the mechanism of the disease caused by this protozoan parasite (in the human host's small intestine) continues to remain unexplained. The infection with G. lamblia is worldwide with an average prevalence of 12.5 per cent and is especially common in children and may cause failure of child to thrive. The G. lamblia infection has been implicated in a number of water borne epidemics and is important cause of traveller's diarrhoea all over the world. Infection with G. lamblia may be entirely asymptomatic, may produce a mild, self limiting illness or chronic diarrhoea with or without malabsorption. The reasons for such variations in severity are not clearly understood. However, interplay of virulence of parasite, nutritional status and type of the host immune responses and its effect on intestinal mucosa appear to modulate the infection.
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PMID:Gut associated immune responses in clinical and experimental giardiasis: an overview. 219 84

Maintaining optimal nutrition in the pediatric patient with Acquired Immune Deficiency Syndrome (AIDS) is challenging, but it may be one of the most effective therapies. Patients experience numerous complications that compromise nutritional status. Infection, fever, diarrhea, feeding problems, and decreased intake all contribute to malnutrition, which in turn predisposes the patient even more to infection and malabsorption. Nutrition assessment should be done routinely so that new problems may be identified and treated. High-calorie, high-protein feedings, vitamin supplementation, and, when necessary, gavage feedings or parenteral nutrition are recommended to improve nutritional status and prevent further deficits. Maintaining optimal nutrition in the pediatric patient with Acquired Immune Deficiency Syndrome (AIDS) poses a significant challenge to the health care team. Patients may experience numerous complications that compromise nutritional status. The patient is at high risk for opportunistic infections, especially of the lungs, central nervous system, gastrointestinal (GI) tract, and skin. Such infections are common causes of morbidity and mortality. Impaired nutritional status may further impair the patient's immunocompetence. A study by Kotler and Gaety demonstrated severe progressive malnutrition in adult AIDS patients, with the lowest measures of lean body mass occurring in those patients close to death at the time of the study. While no studies of children with AIDS have been done to date, we have subjectively observed feeding problems, weight loss, and malnutrition in most of the patients we have seen.
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PMID:Nutrition support of the pediatric patient with AIDS. 243 78

Infection with Capillaria philippinensis has not been reported in Taiwan before. It is characterized by chronic diarrhea, abdominal pain and muscle wasting. Because the infection results in a severe disease with a high mortality, early diagnosis is very important. A 58-year-old housewife from Ar-Lien village, Kao-Hsiung County, was admitted to the National Taiwan University Hospital in July 1988, after suffering from diarrhea, lower leg edema and weight loss for one year. The initial symptom was epigastric pain followed by watery diarrhea. Thereafter borborygmus, frequent loose stool passage and weakness persisted. The cause of her malabsorption syndrome went undetected until the ova, larvae and adult worms of C. philippinensis were detected in the direct smear of the patient's stool in August 1988. She received mebendazole 200mg b.i.d. for 20 days. Capillaria ova were no longer detected following the third day of medication. At the second month follow-up, her body weight returned to her pre-morbid state and all laboratory findings returned to normal with the exception of mild anemia. The infection source was not clear.
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PMID:Intestinal capillariasis: report of a case. 279 62

Seven-day-old mice were infected orally with murine rotavirus (EDIM) and regions of the gut examined at 24 h intervals up to 7 days by electron microscopy. Structural changes were correlated with data on viral antigen production, thymidine kinase activity, and clinical signs of diarrhea. No pathological changes were detected in the colon. Infection and structural damage were confined to the small intestine, with middle regions showing the most pronounced changes. Constriction of villus bases, edema of the lamina propria, and vacuolation of enterocytes occurred at 24 h postinfection (PI), i.e., before evidence of major virus replication. Transient villus atrophy occurred at 48 h PI. Recovery of villus length was evident by 72 h PI accompanied by evidence of marked enterocyte replication at villus bases. Many enterocytes were damaged with little evidence for the presence of virus particles. By 96 h PI, villi had almost recovered from infection although some enterocytes were still damaged; no virus particles were detected in these cells. A second phase of villus damage and edema of the lamina propria occurred at 120 h PI; the pathology resembled that at 24-48 h PI. By 144 to 168 h PI, recovery of the mucosa from infection was virtually complete. We suggest that many of the pathological features following rotavirus infection result from rotavirus-induced ischemia of villi and that diarrhea results from malabsorption of fluid by damaged villi and hypersecretion of ions released from increased numbers of dividing cells at villus-crypt borders.
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PMID:An electron microscopic investigation of time-related changes in the intestine of neonatal mice infected with murine rotavirus. 283 83


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