scholarly journals Adalimumab as a potential cause of drug-induced thrombocytopaenic microangiopathy

2020 ◽  
Vol 13 (3) ◽  
pp. e233526 ◽  
Author(s):  
Lorenzo Falsetti ◽  
Mattia Sampaolesi ◽  
Francesca Riccomi ◽  
Cinzia Nitti
Keyword(s):  
Internal Medicine ◽  
Emergency Department ◽  
Shiga Toxin ◽  
Haemolytic Uraemic Syndrome ◽  
Laboratory Tests ◽  
Severe Diarrhoea ◽  
Drug Induced ◽  
Medicine Department ◽  
Atypical Haemolytic Uraemic Syndrome ◽  
Count Recovery

We report the case of a 63-year-old male patient admitted to our emergency department for dyspnoea, peripheral oedema, severe diarrhoea and asthenia. History revealed Crohn’s disease (CD) submitted to several intestinal surgical resections in the previous years. He recently started a treatment with adalimumab for the control of CD. Laboratory tests at the admission revealed severe haemolytic anaemia and thrombocytopaenia. Haptoglobin levels were low, schistocyte count was markedly increased. In the suspect of thrombotic microangiopathy, he was admitted to our internal medicine department where we urgently started plasma exchange (PEX). We observed normal ADAMTS-13 activity in absence of Shiga toxin or enterotoxic Escherichiacoli at stool tests. Despite a diagnosis of atypical haemolytic–uraemic syndrome, we observed full platelet count recovery and schistocytes normalisation after the fourth PEX. We then put a diagnosis of adalimumab-induced thrombocytopaenic microangiopathy. Adalimumab was withdrawn. We did not observe relapses in the following 3 months.

Carfilzomib-induced atypical haemolytic uraemic syndrome: a diagnostic challenge and therapeutic success

2021 ◽  
Vol 14 (2) ◽  
pp. e239091
Author(s):  
Alicia Darwin ◽  
Leonger Malpica ◽  
Jugraj Dhanoa ◽  
Hamza Hashmi
Keyword(s):  
Multiple Myeloma ◽  
Plasma Exchange ◽  
Haemolytic Anaemia ◽  
Haemolytic Uraemic Syndrome ◽  
Complement Protein ◽  
Diagnostic Challenge ◽  
Drug Induced ◽  
Therapeutic Success ◽  
Atypical Haemolytic Uraemic Syndrome ◽  
History Of

Haemolytic uraemic syndrome (HUS) is a thrombotic microangiopathy (TMA) that presents with renal insufficiency, thrombocytopaenia and microangiopathic haemolytic anaemia. Typical HUS is associated with Shiga toxin while atypical HUS (aHUS) is due to overactivation of the alternative complement pathway. aHUS has numerous causes, including drugs, with rare reports of carfilzomib, a proteasome inhibitor used in multiple myeloma, as causative agent. Cases vary in presentation, presenting a diagnostic challenge. Historically, TMAs were treated with plasma exchange. aHUS, however, is considered refractory to plasma exchange and best treated with eculizumab, a monoclonal antibody targeting C5, a terminal complement protein. We report a patient with history of multiple myeloma who presented with headaches, elevated blood pressure, petechiae, ecchymosis and haemolytic anaemia. His condition was determined to be carfilzomib-induced aHUS and he was successfully treated with eculizumab. Early detection and treatment of drug-induced aHUS is vital in reducing morbidity and mortality related to the condition.

scholarly journals Extra-corporeal membrane oxygenation and Eculizumab: Atypical treatments for typical haemolytic uraemic syndrome

2019 ◽  
Vol 21 (2) ◽  
pp. 191-193
Author(s):  
Matthew D Kelham ◽  
Liam Gleeson ◽  
Inma Alcalde ◽  
Rosalba Spiritoso ◽  
Alastair G Proudfoot ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Cardiogenic Shock ◽  
Shiga Toxin ◽  
Haemolytic Uraemic Syndrome ◽  
Intensive Therapy ◽  
Supportive Therapy ◽  
Neurological Involvement ◽  
Extra Corporeal Membrane Oxygenation ◽  
Membrane Oxygenation ◽  
Atypical Haemolytic Uraemic Syndrome

A 19-year-old female with no medical history presented with bloody diarrhoea. Investigations revealed an acute kidney injury, thrombocytopenia and microangiopathic haemolysis. A diagnosis of haemolytic uraemic syndrome secondary to Shiga toxin-producing Escherichia coli 055 was confirmed and supportive therapy commenced in the intensive therapy unit. On day 11 of her admission, she rapidly deteriorated with evidence of refractory cardiogenic shock and neurological involvement, both features associated with a poor prognosis. Cross-specialty collaboration prompted a trial of veno-arterial extra-corporeal membrane oxygenation and Eculizumab, a complement inhibitor normally reserved for atypical haemolytic uraemic syndrome, as a bridge to organ recovery. To our knowledge, herein we present the first adult patient with haemolytic uraemic syndrome induced cardiogenic shock successfully supported to cardiac recovery with extra-corporeal membrane oxygenation. The potential role for Eculizumab in Shiga toxin-producing Escherichia coli/typical haemolytic uraemic syndrome is also discussed.

Successful treatment with eculizumab in a patient with pregnancy-associated atypical hemolytic uremic syndrome

2021 ◽  
pp. 1753495X2110199
Author(s):  
Mehmet Nuri Duran ◽  
Fatma Beyazit ◽  
Mesut Erbaş ◽  
Onur Özkavak ◽  
Celal Acar ◽  
...  
Keyword(s):  
Haemolytic Uraemic Syndrome ◽  
Gestational Hypertension ◽  
Severe Renal Impairment ◽  
Post Partum ◽  
Atypical Hemolytic Uremic Syndrome ◽  
Kidney Injury ◽  
Rapid Improvement ◽  
Plasma Therapy ◽  
Elevated Liver Enzymes ◽  
Atypical Haemolytic Uraemic Syndrome

Pregnancy‐associated atypical haemolytic uraemic syndrome is a rare and potentially lethal complement-mediated disorder. It can mimic preeclampsia, gestational hypertension, thrombotic thrombocytopenic purpura and hemolysis, elevated liver enzymes and low platelets syndrome. Thus, it can be hard to distinguish pregnancy‐associated atypical haemolytic uraemic syndrome from other causes in peri/post-partum women presenting with features of microangiopathic haemolytic anemia, thrombocytopenia and acute kidney injury. We present a case of a 35-year-old woman in her third pregnancy at 32 weeks’ gestation who underwent caesarean section due to fetal distress. She developed severe renal impairment, thrombocytopenia and neurologic symptoms within 24 hours after delivery. A diagnosis of pregnancy‐associated atypical haemolytic uraemic syndrome was provided, and treatment with plasma therapy followed by eculizumab was initiated. A rapid improvement of both clinical and laboratory parameters was observed. This case demonstrates the significance of early initiation of anti-complement therapy to prevent irreversible renal damage and possible death in women with pregnancy‐associated atypical haemolytic uraemic syndrome.

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