Autoimmune haemolytic anaemia and neuropathy with IgA osteosclerotic myeloma: a case report

Pathology ◽  
2017 ◽  
Vol 49 (6) ◽  
pp. 646-647 ◽  
Author(s):  
Philip J. Crispin ◽  
Poh Lin Cheah
2003 ◽  
Vol 24 (1) ◽  
pp. 34-36 ◽  
Author(s):  
N. Tuncer Elmaci ◽  
S. Ratip ◽  
D. ?nce-G�nal ◽  
T. Tanrida?

1996 ◽  
Vol 11 (5) ◽  
pp. 439-442 ◽  
Author(s):  
ERIC M YOSHIDA ◽  
STEPHEN H NANTEL ◽  
DAVID A OWEN ◽  
PAUL F GALBRAITH ◽  
BAKUL I DALAL ◽  
...  

Author(s):  
Md Nazmul Hasan ◽  
Chowdhury Adnan Sami ◽  
Md Rasul Amin ◽  
Abed Hussain Khan ◽  
Sunil Kumar Biswas

Autoimmune hemolytic anaemia (AIHA) can be caused by many diseases like connective tissue disease, lymphoproliferative disorder, certain infections and various medications. The coronavirus disease 19(COVID-19) can cause an increased risk of thrombosis. But, the association of AIHA with COVID-19 is not well understood. Here, in this case report a 45-year-old man who presented with fever, cough, anaemia and splenomegaly. On further investigation, he was confirmed as severe COVID-19 case with AIHA. Subsequently he was managed with prednisolone with good results. BSMMU J 2021; 14 (COVID -19 Supplement): 57-59


2021 ◽  
pp. 1289-1294
Author(s):  
Anna Carbó-Bagué ◽  
Roser Fort-Culillas ◽  
Helena Pla-Juher ◽  
Jordi Rubió-Casadevall

Autoimmune haemolytic anaemia (AIHA) is a rare immune-related adverse event and appears to be more common with anti-PD1/PDL1 than anti-CTLA4. Little is known about the safety of re-treating with anti-PD1/PDL1 or changing to anti-CTLA4. We present a case of grade 4 AIHA due to nivolumab (PD1-inhibitor) treatment in a patient with melanoma for adjuvant setting after surgery and the safeness of subsequent treatment with ipilimumab (anti-CTLA4). After the remission of AIHA with steroids, ipilimumab was started with the rationale of its different mechanism of action. Fortunately, AIHA did not recur. The mechanism by which checkpoint inhibitors cause AIHA is likely by augmenting or redirecting immune surveillance, especially by activating pre-existing red blood cell autoantibodies, but further studies must be done. To our knowledge, this is the first case published in the literature with the change of immunotherapy treatment to anti-CTLA4.


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