ABSTRACT
Strongyloides stercoralis is an intestinal nematode that causes human infections and whose life cycle has special features, including autoinfection. Strongyloides infection may be asymptomatic for years, owing to a low parasite load. During immunosuppressive therapy, however, if cellular immunity is depressed, autoinfection can occur at a higher rate, resulting in hyperinfection syndrome. In this specific circumstance, it can become a fatal illness. We describe a case of hyperinfection syndrome in a liver transplant recipient and also review the literature.
Subject(s)
Immunosuppressive Agents/adverse effects , Liver Transplantation/adverse effects , Postoperative Complications/parasitology , Strongyloides stercoralis , Strongyloidiasis/etiology , Superinfection/etiology , Adult , Animals , Anthelmintics/therapeutic use , Fatal Outcome , Graft Rejection/prevention & control , Humans , Immunosuppressive Agents/therapeutic use , Male , Postoperative Complications/diagnosis , Postoperative Complications/drug therapy , Recurrence , Strongyloidiasis/diagnosis , Strongyloidiasis/drug therapy , Superinfection/diagnosis , Superinfection/drug therapyABSTRACT
The gut barrier monitors and protects the gastrointestinal tract from challenges such as microorganisms, toxins and proteins that could act as antigens. There is evidence that gut barrier dysfunction may act as a primary disease mechanism in intestinal disorders. The aim of the present study was to evaluate the barrier function towards sugars after the appropriate treatment of celiac disease and Crohn's disease patients and compare the results with those obtained with healthy subjects. Fifteen healthy volunteers, 22 celiac disease patients after 1 year of a gluten-free diet, and 31 Crohn's disease patients in remission were submitted to an intestinal permeability test with 6.0 g lactulose and 3.0 g mannitol. Six-hour urinary lactulose excretion in Crohn's disease patients was significantly higher than in both celiac disease patients (0.42 vs 0.15 percent) and healthy controls (0.42 vs 0.07 percent). Urinary lactulose excretion was significantly higher in celiac disease patients than in healthy controls (0.15 vs 0.07 percent). Urinary mannitol excretion in Crohn's disease patients was the same as healthy controls (21 vs 21 percent) and these values were significantly higher than in celiac disease patients (10.9 percent). The lactulose/mannitol ratio was significantly higher in Crohn's disease patients in comparison to celiac disease patients (0.021 vs 0.013) and healthy controls (0.021 vs 0.003) and this ratio was also significantly higher in celiac disease patients compared to healthy controls (0.013 vs 0.003). In spite of treatment, differences in sugar permeability were observed in both disease groups. These differences in the behavior of the sugar probes probably reflect different mechanisms for the alterations of intestinal permeability.
Subject(s)
Adult , Aged , Female , Humans , Male , Middle Aged , Young Adult , Celiac Disease/physiopathology , Crohn Disease/physiopathology , Intestinal Absorption/physiology , Lactulose/pharmacokinetics , Mannitol/pharmacokinetics , Case-Control Studies , Chromatography, High Pressure Liquid , Celiac Disease/drug therapy , Celiac Disease/metabolism , Crohn Disease/drug therapy , Crohn Disease/metabolism , Lactulose/urine , Mannitol/urine , Permeability , Young AdultABSTRACT
The gut barrier monitors and protects the gastrointestinal tract from challenges such as microorganisms, toxins and proteins that could act as antigens. There is evidence that gut barrier dysfunction may act as a primary disease mechanism in intestinal disorders. The aim of the present study was to evaluate the barrier function towards sugars after the appropriate treatment of celiac disease and Crohn's disease patients and compare the results with those obtained with healthy subjects. Fifteen healthy volunteers, 22 celiac disease patients after 1 year of a gluten-free diet, and 31 Crohn's disease patients in remission were submitted to an intestinal permeability test with 6.0 g lactulose and 3.0 g mannitol. Six-hour urinary lactulose excretion in Crohn's disease patients was significantly higher than in both celiac disease patients (0.42 vs 0.15%) and healthy controls (0.42 vs 0.07%). Urinary lactulose excretion was significantly higher in celiac disease patients than in healthy controls (0.15 vs 0.07%). Urinary mannitol excretion in Crohn's disease patients was the same as healthy controls (21 vs 21%) and these values were significantly higher than in celiac disease patients (10.9%). The lactulose/mannitol ratio was significantly higher in Crohn's disease patients in comparison to celiac disease patients (0.021 vs 0.013) and healthy controls (0.021 vs 0.003) and this ratio was also significantly higher in celiac disease patients compared to healthy controls (0.013 vs 0.003). In spite of treatment, differences in sugar permeability were observed in both disease groups. These differences in the behavior of the sugar probes probably reflect different mechanisms for the alterations of intestinal permeability.
