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Diarrhea and Malnutrition
Published in Fima Lifshitz, Childhood Nutrition, 2020
Andrea Maggioni, Fima Lifshitz
Hemorrhagic colitis caused by E. Coli 0157:H7 was first recognized in 1982 during outbreaks in Oregon and Michigan.32 A very young age was a significant risk factor among the reported risk factors for diarrhea caused by this microorganism, other than ingesting contaminated food or water and person-to-person spread. In a recent survey, the risk of infection in day care settings was inversely related to the age of the children who attended.33 Similarly, the severity of symptoms and the risk of developing serious complication as hemolytic uremic syndrome was higher in children less than five years of age.34
Fibrinolysis and Inflammation
Published in Pia Glas-Greenwalt, Fibrinolysis in Disease Molecular and Hemovascular Aspects of Fibrinolysis, 2019
In a series of patients with glomerulonephritis increased levels of t-PA: Ag but decreased plasma u-PA levels were demonstrated.22 A most intriguing observation was the impaired response of t-PA:Ag and u-PA:Ag to desmopressin infusion. A similar finding in patients with hemolytic uremic syndrome has been published by others,23 in agreement with our own experience.24 Several investigators have noticed elevated PAI-1 levels in plasma of patients with HUS (hemolytic uremic syndrome).25-27
Campylobacter jejuni
Published in Peter M. Lydyard, Michael F. Cole, John Holton, William L. Irving, Nino Porakishvili, Pradhib Venkatesan, Katherine N. Ward, Case Studies in Infectious Disease, 2010
Peter M. Lydyard, Michael F. Cole, John Holton, William L. Irving, Nino Porakishvili, Pradhib Venkatesan, Katherine N. Ward
In severe cases of enterocolitis, toxic megacolon may occur and rare cases of cholecystitis or pancreatitis have been reported. Three major extraintestinal complications are recognized. The commonest complication is reactive arthritis, which occurs in about 1% of cases and occurs several weeks after the initial infection.. It is more common in subjects who are HLA B27. The hemolytic uremic syndrome may also follow infection and usually comes on within a few days. Infection may be followed by the Guillain-Barre or the Miller Fisher syndrome variant. Although a rare complication, because campylobacteriosis is so common, an infection with C. jejuni is the cause of these immune pathologies in about 50% of cases. Other extraintestinal complications that have occasionally been reported are IgA nephropathy and interstitial nephritis.
Apyrase decreases phage induction and Shiga toxin release from E. coli O157:H7 and has a protective effect during infection
Published in Gut Microbes, 2022
Ida Arvidsson, Ashmita Tontanahal, Karl Johansson, Ann-Charlotte Kristoffersson, Sára Kellnerová, Michael Berger, Ulrich Dobrindt, Diana Karpman
Enterohemorrhagic Escherichia coli (EHEC) cause diarrhea, hemorrhagic colitis, and in certain cases the severe complication hemolytic uremic syndrome (HUS)1 characterized by nonimmune hemolytic anemia, thrombocytopenia, and acute kidney injury with up to 5% mortality. There are no specific or effective treatments for this infection and antibiotic treatment, during the prodromal pre-HUS phase, may increase the risk of developing HUS.2E. coli O157:H7 is the most common clinical isolate of EHEC.1 EHEC infects via oral intake of contaminated food or water and is a noninvasive bacterium.3 After ingestion EHEC colonize the intestine.4 In the intestine, EHEC release virulence factors such as Shiga toxin (Stx).5 During human EHEC infection Stx can be found within intestinal cells6 and massive intestinal inflammation and apoptosis have been reported.7 Similarly, mice inoculated intragastrically with EHEC exhibit goblet cell depletion,8 intestinal inflammation, and apoptosis particularly associated with the presence of Stx.7
Pharmacotherapeutic options for the prevention of kidney transplant rejection: the evidence to date
Published in Expert Opinion on Pharmacotherapy, 2022
Goce Spasovski, Lada Trajceska, Irena Rambabova-Bushljetik
Recently, immunosuppressant minimization strategies are considered, based on the associated complications (toxicity and/or adverse reactions) [10]. Thus, individual CNI concentration levels are monitored in order to prevent more frequent AR episodes while limiting their nephrotoxicity [11]. Steroid discontinuation resulted in somewhat increased AR possibilities, although with preserved graft function and survival [12]. MMF is frequently reduced alleviating gastrointestinal and hematological side effects and infections. Nowadays, a couple of new drugs (belatacept and alemtuzumab) may be a treatment of choice for induction of donor-specific immunotolerance or mixed chimerism [13–15]. Of note, the combined immunosuppression should minimize the individual impact on morbidity and mortality, while the overall drug effectiveness would be improved. However, the problem of unrecognized production of de novo or preexisting anti-HLA antibodies and development of chronic antibody-mediated rejection (cAMR) and transplant glomerulopathy (TG) as sequel that prevents long-term graft survival need further analysis and update in the treatment. Finally, therapeutical possibilities for the small proportion of patients with cancers and atypical hemolytic uremic syndrome (aHUS) should be further evaluated. The actual immunosuppressants with their mechanism of action and possible side effects are presented in Table 1.
Complement system network in cell physiology and in human diseases
Published in International Reviews of Immunology, 2021
Roberta Romano, Giuliana Giardino, Emilia Cirillo, Rosaria Prencipe, Claudio Pignata
The dysfunctional regulation of alternative complement pathway due to Factor H or I deficiency or C3 unresponsiveness to inhibition leads to the development of the atypical form of Hemolytic Uremic Syndrome. Usually caused, in its typical form, by Shiga-toxin producing Escherichia coli, atypical Hemolytic Uremic Syndrome is a thrombotic microangiopathy disease affecting mainly kidneys, in which deposits of C5b-C9 damage glomerular endothelium. Thereafter, intravascular hemolysis and platelets activation result in the formation of microthrombi [48]. Atypical forms account for 5 to 20% of cases of Hemolytic Uremic Syndrome and may be either due to mutations in one of more genes coding for regulatory or cascade proteins (loss of function mutations in CFH, CFI or gain of function mutations in CFB and C3) [49,50] or due to autoantibodies to factor H, detected in 5-13% of European atypical Hemolytic Uremic Syndrome patients. In such patients, genetic and autoantibodies testing are essential: the detection of anti-factor H autoantibodies may suggest the use of immunosuppressive drugs combined with plasma exchange, as therapeutic approach [51] as opposed to sero-negative atypical Hemolytic Uremic Syndrome forms in which the standard treatment choice is a humanized monoclonal antibody, Eculizumab, that binds the terminal complement component C5, as below described [51].