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Concurrent thrombotic thrombocytopenic purpura and Guillian Barre Syndrome post infectious diarrhea
Taimoor Hussain1, Jasvindar Kumar2, Sarab Jeet Singh3
1Bolan Medical College Quetta, Pakistan.
Thrombotic thrombocytopenic purpura (TTP) characterized by microangiopathic hemolytic anemia, thrombocytopenia and signs of organ dysfunction, is due to either congenital or acquired deficiency of ADAMTS13 gene. Guillian Barre Syndrome (GBS) is a post infectious disorder, most commonly associated with C. jejuni infection. Both conditions have high mortality if untreated and have been reported with other comorbid conditions. We found only one case report of sequential TTP and GBS. However, we report the first case of concurrent TTP and GBS infection in a 22 years old female after bloody diarrhea, successfully managed by symptomatic treatment, sessions of plasmapheresis, and hemodialysis. TTP and GBS have both been associated with bacterial and viral infections, and antibodies formed against them may result in cross reactivity due to molecular mimicry. It is suggested although unproven that in such cases, patients likely developed cross-reactivity against both platelet and neurogenic glycoproteins (the linking antigen) following predisposing infection.
Thrombotic thrombocytopenic purpura (TTP) characterized by microangiopathic hemolytic anemia, thrombocytopenia and signs of organ dysfunction, is due to either congenital or acquired deficiency of ADAMTS13 gene. Guillian Barre Syndrome (GBS) is a post infectious disorder, most commonly associated with C. jejuni infection. Both conditions have high mortality if untreated and have been reported with other comorbid conditions. We found only one case report of sequential TTP and GBS. However, we report the first case of concurrent TTP and GBS infection in a 22 years old female after bloody diarrhea, successfully managed by symptomatic treatment, sessions of plasmapheresis, and hemodialysis. TTP and GBS have both been associated with bacterial and viral infections, and antibodies formed against them may result in cross reactivity due to molecular mimicry. It is suggested although unproven that in such cases, patients likely developed cross-reactivity against both platelet and neurogenic glycoproteins (the linking antigen) following predisposing infection.
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