Recurrence of Diabetes After Diarrhea-Associated Hemolytic Uremic Syndrome

Casteels, Kristina; Damme‐Lombaerts, Rita Van

doi:10.2337/diacare.29.04.06.dc05-2542

Cited by 6 publications

(6 citation statements)

References 2 publications

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“…4 Relapse after initial resolution has been reported to occur 3, 7, 10, and 11 years after the acute illness. [12][13][14]22 In our review, given that almost 50% of recovering children were followed for less than 1 year, the rate of permanent DM may in fact be higher than reported.…”

contrasting

confidence: 71%

“…[5][6][7][8][9][10][11][12] This does not seem to be immune-mediated, as pancreatic autoantibodies were negative in all of the related eight case reports. 5,[8][9][10][11][12][13][14] However, the pathophysiology is likely related to microangiopathy of pancreatic microvasculature, resulting in b-cell death. Indeed, Gb3 receptors, associated with toxin binding in the kidney, 15 do exist in the pancreas.…”

mentioning

confidence: 98%

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Relationship between Escherichia coli O157:H7 and diabetes mellitus

Suri

Mahon

Clark

et al. 2009

Kidney International

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Ingestion of Escherichia coli O157:H7 can cause a spectrum of acute illness, ranging from overt hemolytic-uremic syndrome (HUS), to gastroenteritis with bloody diarrhea, to no symptoms. This organism has been responsible for dozens of outbreaks of gastroenteritis and HUS in industrialized nations, and thus is a major public health concern. Although the acute effects of E. coli O157:H7 ingestion are well understood, the long-term complications are less well known. Here, we review the biological and empirical evidence supporting a link between E. coli O157:H7 and long-term diabetes mellitus. Survivors with diarrhea-associated HUS have a significantly increased incidence of diabetes due to complete insulin deficiency, which may recur several years after the initial infection. However, less severe forms of infection, such as E. coli O157:H7 gastroenteritis without overt HUS, do not appear to result in an increased risk of type 2 diabetes.

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contrasting

confidence: 71%

mentioning

confidence: 98%

Relationship between Escherichia coli O157:H7 and diabetes mellitus

Suri

Mahon

Clark

et al. 2009

Kidney International

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Section: Discussionmentioning

confidence: 81%

“…Diabetes recurrence after diabetes HUS has been reported previously after a short or long period of time only in sporadic HUS cases (that were not part of an outbreak), and most of the cases reported negative islet cell antibodies ( Table 3). [3][4][5][6] Bendel-Stenzel reported two cases of diabetes recurrence after sporadic HUS who had also simultaneous pancreas-kidney transplant with subsequent good progress and insulin independence over 2 years follow-up. 7 The timing of the recurrence of diabetes after 8 years in our two cases may be explained by the onset of puberty and adrenarche ( Table 2) causing increased insulin resistance on the background of a reduction of functional β cell mass after HUS.…”

Section: Discussionmentioning

confidence: 99%

Diabetes recurrence after haemolytic uraemic syndrome outbreak in Adelaide

Peña

Graham

Rao

et al. 2016

J Paediatrics Child Health

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“…Pancreatic injury causes diabetes onset with hyperglycemia in 5-10% of patients during the acute phase, or afterwards during the recovery period. Some of these children remain permanently diabetic and require lifelong insulin 173,190,198,204,205 . Although lung and liver damage, manifested respectively by pulmonary thrombi with edema and hepatomegaly with elevated transaminases, are common they rarely cause severe dysfunction and are not associated with organ failure 83,173 .…”

Section: Clinical Aspects Of the Hemolytic Of Uremic Syndromementioning

confidence: 99%

The Path physiology of Renal Failure in a Shiga Toxin plus Lipopolysaccharide Induced Murine Model of Hemolytic Uremic Syndrome

Psotka¹

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Hemolytic uremic syndrome (HUS) is the primary cause of worldwide pediatric acute renal failure. The vast majority of HUS is due to gastrointestinal infection with Shiga toxin producing Escherichia coli (STEC), bacteria that produce the ribosomal protein synthesis inhibitor Shiga toxin (Stx). During the diarrheal prodrome, virulence factors lipopolysaccharide (LPS) and Stx cross into the systemic circulation and cause inflammation and apoptosis in many tissues. The multi-organ pathology that results from toxemia consists of microvascular thrombosis and tissue ischemia with parenchymal destruction. The clinical syndrome of HUS typically comprises microangiopathic hemolytic anemia, thrombocytopenia, acute renal failure, a complex inflammatory response, and neurologic dysfunction. The prognosis is variable; however death or significant lasting renal impairment occurs in up to half of cases. Current treatment consists only of supportive care with intravenous fluids and dialysis, and therapeutic advances have been unforthcoming. Due to the infrequent and sporadic nature of HUS, clinical and therapeutic advancement require an appropriate model system that will allow the underlying mechanisms of this disease to be elucidated. Thus far, only expensive and cumbersome large animal models mimic the human disease, and small animal models of HUS are either incomplete or inadequate. This work fully describes the renal failure that occurs in the mouse model of Shiga toxin mediated HUS. Intraperitoneal injection of Shiga toxin 2 (Stx2) plus LPS into mice causes systemic toxemia and results in death over 96 hours. Acute renal failure, thrombocytopenia, inflammation and neurologic dysfunction develop xii Abbreviations A/E Attaching and Effacing ACE Angiotensin Converting Enzyme ADP Adenosine Diphosphate AKI Acute Kidney Injury ARF Acute Renal Failure ß-TG ß-Thromboglobulin BUN Blood Urea Nitrogen CBC Complete Blood Count CCL2 CC Chemokine Ligand 2 (MCP-1) CCL4 CC Chemokine Ligand 4 (MIP-1ß) Cer Ceramide CD 50 50% Cytotoxic Dose CDH Ceramide Dihexoside CMH Ceramide Monohexoside CNS Central Nervous System CXCL1 C-X-C Chemokine Ligand 1 (Gro-α) CXCL5 C-X-C Chemokine Ligand 5 (ENA-78) D+HUS Diarrhea associated Hemolytic Uremic Syndrome DAF Delay Accelerating Factor DB Dutch Belted (Rabbit) Chapter 2: A Murine Model of HUS: Shiga Toxin with Lipopolysaccharide Mimics the Renal Damage and Physiologic Response of Human Disease This chapter was originally published as a co-authorship with Tiffany R. Keepers.

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Recurrence of Diabetes After Diarrhea-Associated Hemolytic Uremic Syndrome

Cited by 6 publications

References 2 publications

Relationship between Escherichia coli O157:H7 and diabetes mellitus

Relationship between Escherichia coli O157:H7 and diabetes mellitus

Diabetes recurrence after haemolytic uraemic syndrome outbreak in Adelaide

The Path physiology of Renal Failure in a Shiga Toxin plus Lipopolysaccharide Induced Murine Model of Hemolytic Uremic Syndrome

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