RESUMO
BACKGROUND Thrombotic thrombocytopenic purpura is mostly characterized by symptoms and signs of hemolytic anemia, thrombocytopenia, renal impairment, fever and neurologic dysfunction. It is not always necessary to have all 5 characteristic symptoms, and presentations can vary. It can be congenital or acquired by any etiology that causes deficiency or dysfunction of ADAMST13 enzyme. CASE REPORT We present a case of a 71-year-old man who presented to our hospital initially with abdominal pain. He was diagnosed with pancreatitis, and conservative management was started with pain control and hydration. During the hospital course, the patient developed anemia that was hemolytic in nature, acute kidney injury and thrombocytopenia. He was then diagnosed as having TTP secondary to pancreatitis with additive effect of clopidogrel, as he had recently been started on clopidogrel due to percutaneous coronary intervention. He was started on prompt treatment with plasma exchange and intermittent dialysis, and he achieved full recovery after that. CONCLUSIONS TTP is a potentially fatal disease with high mortality risk. It is judicious to recognize and have high suspicion of TTP being caused by such rare causes (pancreatitis and clopidogrel), as immediate recognition and treatment can enhance survival.
Assuntos
Clopidogrel/efeitos adversos , Pancreatite Necrosante Aguda/complicações , Troca Plasmática/métodos , Púrpura Trombocitopênica/etiologia , Púrpura Trombocitopênica/terapia , Dor Abdominal/diagnóstico , Dor Abdominal/etiologia , Idoso , Clopidogrel/uso terapêutico , Seguimentos , Humanos , Masculino , Pancreatite Necrosante Aguda/diagnóstico por imagem , Pancreatite Necrosante Aguda/terapia , Púrpura Trombocitopênica/fisiopatologia , Doenças Raras , Medição de Risco , Tomografia Computadorizada por Raios X/métodos , Resultado do TratamentoRESUMO
In avian smooth muscles, GTPgammaS produces a Rho kinase mediated increase in PHI-1 phosphorylation and force, but whether this correlation is causal is unknown. We examined the effect of phosphorylated PHI-1 (P-PHI-1) on force and myosin light chain (MLC(20)) phosphorylation at a constant [Ca(2+)]. P-PHI-1, but not PHI-1, increased MLC(20) phosphorylation and force, and phosphorylation of PHI-1 increased the interaction of PHI-1 with PP1c. Microcystin induced a dose-dependent reduction in the binding of PHI-1 to PP1c. These results suggest PHI-1 inhibits myosin light chain phosphatase by interacting with the active site of PP1c to produce a Ca(2+) independent increase in MLC(20) phosphorylation and force.