مقالات پذیرفته شده در هفتمین کنگره بین المللی زیست پزشکی
A comprehensive review of the clinical findings of shiga toxin-induced HUS
A comprehensive review of the clinical findings of shiga toxin-induced HUS
Behzad Bahramzadeh,1Mohammad Aghazadeh,2,*
1. Department of Medical Microbiology, Faculty of Medicine, Tabriz University of Medical Sciences, Tabriz-Iran 2. Department of Medical Microbiology, Faculty of Medicine, Tabriz University of Medical Sciences, Tabriz-Iran
Introduction: HUS , disease that with triad of features thrombocytopenia, hemolytic anemia, and ischemic organ damage characterized. It is caused by gastrointestinal infection by a Shiga toxin-producing E.coli (and occasionally other pathogens). Functionally, the Shiga toxins belong to the family of ribosome-inactivating proteins. The O104:H4 sero type E.Coli stands out as one of the most virulent strains responsible for HUS and The O26:H11 serotype has emerged as the most common non-O157 serotype causing human disease. Route of transmission is mostly foodborne.
Methods: was conducted using the PubMed/MEDLINE , EMBASE databases using search terms "HUS” , “STEC" , “shiga toxin " Search restrictions included the English language and full text availability. A total of 42 articles were identified, and 25articles remained after removing duplications. Abstracts were screened for pertinent information.
Results: STEC-HUS is one of the most common diseases requiring emergency renal replacement therapy in children and is responsible for 2%–5% of mortality worldwide during the acute phase. Approximately 5%–10% of infected patients will develop STEC-HUS about a week after the onset of digestive signs. Rural areas also tend to be more affected than urban ones, and cases occur predominantly during summer months. age is also an important risk factor for HUS and also reported that female sex and a higher socio-economic status are associated with a higher risk of developing STEC-related disease. Gastric acidity is an important barrier to ingested pathogens. Hypochlorhydria, whether related to gastrectomy or to proton pump inhibitors, has been associated with an increased risk of STEC infection and STEC-HUS. Genetic factors, like erythrocyte and serum Gb3 level or presence of the platelet glycoprotein 1b alpha, could also influence the susceptibility to HUS. The presence of the intimin (eae) gene is associated with human disease and evolution towards hemorrhagic colitis and HUS. In any case, the estimated half-life of shiga toxin in serum is less than 5 min, as it rapidly diffuses to affected tissues. It is thus likely that by the time patients develop HUS, shiga toxin has disappeared from the serum. STEC-related diseases display a wide range of severity, from asymptomatic carriage to lethal HUS. STEC-HUS mainly occurs through large outbreaks. The disease being usually limited to the colon and not prone to bacteremia. STEC-HUS does not usually recur. The kidneys bear the brunt of most of the long-term sequelae. Need and duration of dialysis are seemingly the most reliable predictors of poor renal outcome. Next to renal sequelae, central nervous system involvement is one of the most dreaded complications of STEC-HUS. It is responsible for the majority of patient deaths and is an important contributor to the morbidity of the disease. For patients with renal sequelae after STEC-HUS, a low-sodium diet, early restriction of protein intake, seem to slow down the progression of chronic kidney disease.
Conclusion: Over 30 years after the description of Shiga toxins and Shiga toxin E. coli-associated HUS , the quest for a specific treatment remains elusive, despite major achievements in the understanding of the pathophysiology of the disease, and the encouraging results in preclinical models and ongoing clinical trials, a specific treatment is still absent. Supportive therapy is the cornerstone of the treatment of STEC-HUS patients.