Increased levels of soluble forms of E-selectin and ICAM-1 adhesion molecules during human leptospirosis.

Leptospirosis is a multisystemic zoonotic disease with infiltration of visceral organs by Leptospira. The capacity of the vascular endothelium to grant immune cell recruitment and activation in target organs during the disease course remains poorly characterized. We ascertained the levels of expression of several soluble cell adhesion molecules (CAM) notably expressed by endothelial cells in human leptospirosis. We prospectively enrolled 20 hospitalized patients and compared them to 10 healthy controls. Disease severity was defined by one or more organ failures, or death. Plasmatic concentrations of soluble CAM were assessed by multiplex bead assay at the time of patient presentation (M0) and 1 month after hospital discharge. The levels of soluble E-selectin (sCD62E) and soluble intercellular adhesion molecule 1 (sICAM-1, sCD53) were significantly increased in patients compared to controls (p<0.0001) and at 1 month (p<0.0001) with median values at 978 ng/ml (interquartile ranges 787-1164; sCD62E) and 1021 ng/ml (690-1428; sCD53). At M0, Soluble P-selectin level (sCD62P) was found to be decreased with levels at 60 ng/ml (0-631) versus 711 ng/ml (343-1113) for healthy controls (p<0.05). Levels of sICAM-3 (sCD50), sVCAM-1 (vascular cell adhesion molecule, sCD106) and sPECAM-1 (platelet endothelial cell adhesion molecule, sCD31) were not different from healthy subjects at M0. This study shows that two adhesion molecules, shed as soluble forms, are elevated during the acute phase of leptospirosis: E-selectin and s-ICAM1. These molecules may interfere with the process of immune cell recruitment to clear Leptospira at tissue levels.

Ameboma: an unusual cause of gastrointestinal bleeding during severe leptospirosis.

BACKGROUND: Severe leptospirosis occurs mainly in a tropical environment and includes icterus, acute renal failure and hemorrhages. These bleedings, which are mainly a consequence of acute homeostatic disturbances, can also reveal simultaneous diseases. Coinfections with other tropical diseases have been previously reported during leptospirosis. To our knowledge, invasive amebiasis, which can induce gastrointestinal bleedings, has never been described in the course of severe leptospirosis. CASE PRESENTATION: In this report, we describe a case of a 60 year-old man living in Reunion Island (Indian Ocean, France) admitted to our intensive care unit for severe Leptospira interrogans serovar icterohaemorrhagiae infection with neurological, renal, liver and hematological involvement. Two lower gastrointestinal bleedings occurred 7 and 15 days after admission. The first episode was promoted by hemostatic disturbances while the second bleeding occurred during low-dose heparin therapy. Colonoscopy revealed a pseudo-tumoral inflammatory mass of the recto-sigmoid junction. Histological examination found trophozoites inside mucinous exudate suggestive of Entamoeba histolytica. Amoebic serology was strongly positive whereas careful detection of cysts or trophozoites on saline-wet mount was negative in three consecutive samples of stools. Amoxicillin followed by metronidazole therapy, combined with supportive care, led to an improvement in the clinical and biological patient's condition and endoscopic appearances. CONCLUSION: Clinicians should be aware that gastrointestinal bleeding during severe leptospirosis could not solely be the consequences of hemostatic disturbances. Careful endoscopic evaluation that may reveal curable coinfections should also be considered.

Impact of very early high doses of recombinant erythropoietin on anemia and allograft function in de novo kidney-transplant patients.

After kidney transplantation, occurrence of anemia in the early post-transplant period (<1 month) is high and arises out of issues that are multifactorial. We performed a retrospective single-center study to assess whether delivery of high doses of erythropoietin-stimulating agents (ESA) within the first week of kidney transplantation, translates at 1 month post-transplant, in to causing less anemia and whether it has an impact on allograft function. Ninety-nine patients were not given ESA (group I), whereas 82 were (250 IU/kg/week; group II). All patients had similar pretransplant and baseline (day 0) variables. Similar numbers of group II patients were still receiving ESA by day 14 (97.5%) and day 30 (89%). Respective figures for group I were 27% and 27%. Independent factors for anemia at 1 month post-transplant included: being male subject, treatment for hypertension at pretransplant, anemia at transplant, a higher mean corpuscular volume at transplant, and an induction therapy using antithymocyte globulins. Independent predictive factors for lower creatinine clearance included being female subjects, having a donor aged >50 years, being a recipient aged >50 years, not treated for hypertension at pretransplant, and no post-transplant ESA therapy. High doses of ESA within the first month of kidney transplantation have no impact on anemia or renal function by 1 month post-transplant.