Myocarditis and haemolytic uraemic syndrome.

Abu‐Arafeh, Ishaq; Gray, Ernest D.; Youngson, George; Auchterlonie, Ian A; Russell, Graham

doi:10.1136/adc.72.1.46

Cited by 35 publications

(20 citation statements)

References 14 publications

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“…The diagnosis of cardiac TMA can be challenging because HUS-associated cardiac dysfunction may result from several etiologies: electrolytic disorders, systemic hypertension, fluid overload, and TMA-associated myocarditis. 10 The ejection fraction reduction, transient pericardial effusion, and increases in troponin levels and ECG repolarization anomalies seen in our patient are not pathognomonic of ischemic cardiac involvement. However, the persistence of cardiac abnormalities despite complete correction of cardiovascular overload and the normalization of cardiac function and of the ECG observed after eculizumab initiation strongly points toward aHUSrelated cardiac TMA.…”

Section: Discussionmentioning

confidence: 42%

Eculizumab in Anti-Factor H Antibodies Associated With Atypical Hemolytic Uremic Syndrome

et al. 2014

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Atypical hemolytic uremic syndrome (aHUS) is a life-threatening multisystemic condition often leading to end-stage renal failure. It results from an increased activation of the alternative pathway of the complement system due to mutations of genes coding for inhibitors of this pathway or from autoantibodies directed against them. Eculizumab is a monoclonal antibody directed against complement component C5 and inhibiting the activation of the effector limb of the complement system. Its efficacy has already been demonstrated in aHUS. The present article reports for the first time the use of eculizumab in a patient presenting with aHUS associated with circulating anti-complement Factor H autoantibodies and complicated by cardiac and neurologic symptoms. Our observation highlights the efficacy of eculizumab in this form of aHUS not only on renal symptoms but also on the extrarenal symptoms. It also suggests that eculizumab should be used very promptly after aHUS presentation to prevent life-threatening complications and to reduce the risk of chronic disabilities. To obtain a complete inhibition of the effector limb activation, the advised dosage must be respected. After this initial therapy in the autoimmune aHUS form, a long-term immunosuppressive treatment should be considered, to prevent relapses by reducing anti-complement Factor H autoantibody plasma levels.

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Section: Discussionmentioning

confidence: 42%

Eculizumab in Anti-Factor H Antibodies Associated With Atypical Hemolytic Uremic Syndrome

et al. 2014

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“…Myocarditis has been described in three patients with HUS [20,21], but was confirmed with biopsy in only one [21]. In the present case, profound cardiac dysfunction occurred on the 8th day after the onset of HUS, coincident with ongoing active disease.…”

Section: Discussionmentioning

confidence: 61%

Troponin I levels in a hemolytic uremic syndrome patient with severe cardiac failure

Askiti

Hendrickson

Fish

et al. 2004

Pediatric Nephrology

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Troponins are highly sensitive and specific biochemical markers of myocardial injury that are released into the circulation during myocardial ischemia. We describe changes in cardiac troponin I (cTnI) prior to and following clinical evidence of severe myocardial dysfunction in a child with hemolytic uremic syndrome (HUS). A previously healthy, 22-month-old girl presented with typical HUS and stool cultures positive for Escherichia coli O157:H7. She required dialysis, blood and platelet transfusions, and insulin for HUS-related diabetes mellitus. On the 6th hospital day she had sudden circulatory collapse with a blood pressure of 70/40 mmHg and an oxygen saturation of 88%. She responded rapidly to emergency resuscitation but had diminished left ventricular function (ejection fraction 18%). Four days after the acute event an echocardiogram showed normal ventricular size and contractility. She underwent hemodialysis for 22 days, and renal function was normal after 33 days. cTnI levels were measured with a microparticle enzyme immunoassay. cTnI was normal (>0.4 microg/l) 32 h prior to cardiac collapse, mildly increased (2.1 microg/l) 8 h before the cardiac collapse, severely elevated shortly after the cardiac event (43.1 microg/l), and peaked (140.6 microg/l) at 24 h. It then fell gradually and was normal at discharge. These results suggest that measurement of cTnI may be a useful predictor of cardiac involvement in severely affected children with HUS.

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“…Relatos de casos de miocardite após ITU são escassos, com apenas cinco casos até o momento, todos secundários a Escherichia coli. Uma explicação plausível para essa crescente associação é o poder invasivo e de produção de toxinas dos diversos gêneros da bactéria [4][5][6]8,9 . Não há consenso quanto ao diagnóstico de miocardite.…”

Section: Discussionunclassified

Miocardite aguda sob a forma de síndrome coronariana aguda após infecção do trato urinário

Carvalho¹,

Busato²,

Júnior³

et al. 2017

Clin. Biomed. Res.

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RESUMOA miocardite é cada vez mais diagnosticada, principalmente pela maior disponibilidade de métodos como a ressonância magnética cardíaca. A apresentação clínica é variável, geralmente posterior a uma infecção respiratória ou gastrointestinal, manifestando-se como síndrome coronariana aguda (SCA), insuficiência cardíaca aguda ou crônica, arritmias cardíacas ou mesmo choque cardiogênico inexplicável. Relatos de casos de miocardite após infecção do trato urinário (ITU) são escassos. Neste relato, descrevemos o caso de um paciente masculino de 24 anos com miocardite após ITU que se apresentou sob a forma de SCA. Palavras-chave: Miocardite; infecções urinárias; síndrome coronariana aguda ABSTRACTThe diagnosis of myocarditis has increased mainly due to greater availability of methods such as cardiac magnetic resonance (CMR). Its clinical presentation varies, usually following respiratory or gastrointestinal tract infection, in patients presenting with acute coronary syndrome (ACS), acute or chronic heart failure, cardiac arrhythmias, or even unexplained cardiogenic shock. Case reports of patients with myocarditis following urinary tract infection (UTI) are scarce. This is a case report of a 24-year-old male patient with myocarditis with symptoms of ACS following UTI. Keywords: Myocarditis; urinary tract infections; acute coronary syndromeA miocardite é cada vez mais diagnosticada, principalmente pela maior disponibilidade de métodos investigativos como a ressonância magnética cardíaca (RMC). Sua etiologia vai desde agentes infecciosos, principalmente os virais, até agentes tóxicos e imunológicos. A apresentação clínica é variável, geralmente posterior a uma infecção respiratória ou gastrointestinal, manifestando-se como síndrome coronariana aguda (SCA), insuficiência cardíaca (IC) aguda ou crônica, arritmias cardíacas ou mesmo choque cardiogênico inexplicável 1-3 . A miocardite bacteriana apresenta um campo em aberto por se tratar de uma doença rara, com poucos estudos sobre sua fisiopatologia e casos confirmados com realização de biópsia miocárdica ou necropsia. Os mecanismos de lesão propostos incluem invasão bacteriana direta, mediada por toxinas ou resposta imune [4][5][6] . Neste relato, descrevemos o caso de um paciente masculino de 24 anos com miocardite que se apresentou sob a forma de SCA após infecção do trato urinário (ITU).

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Myocarditis and haemolytic uraemic syndrome.

Cited by 35 publications

References 14 publications

Eculizumab in Anti-Factor H Antibodies Associated With Atypical Hemolytic Uremic Syndrome

Eculizumab in Anti-Factor H Antibodies Associated With Atypical Hemolytic Uremic Syndrome

Troponin I levels in a hemolytic uremic syndrome patient with severe cardiac failure

Miocardite aguda sob a forma de síndrome coronariana aguda após infecção do trato urinário

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