Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0034063 (pulmonary edema)
 10,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We reviewed 1500 acute transfusion reactions that were reported to the Auckland Regional Blood centre over a 7 year period, from approximately 440,000 transfusions. The majority of reactions were to red cells, and these had the highest reaction incidence per unit (0.73%) of all blood products. The reaction incidence per unit transfused for plasma was 0.1%, for stable plasma protein solution 0.01%, and for platelets 0.04%. The majority of symptoms reported were mild and transient. The commonest were fever (72%), rigors (33%), and rash or urticaria (30%). Although more serious reactions were reported such as angioedema, hypotension and pulmonary oedema, none of these were severe, as judged from the data reported to the centre. There were two transfusion related deaths during the study period, one due to an ABO incompatible transfusion, the other due to bacterial contamination of a unit of blood. Leucocyte agglutinins or antibodies were detected in 29% of those with a febrile reaction, but were also detected in 22% of those who remained afebrile. Serological abnormalities that may have accounted for the reaction were only detected in 12 patients six of whom had autoantibodies. As laboratory investigation reveals little that accurately defines the aetiology of a reaction, a rationalisation of the investigation into acute transfusion reactions is suggested.
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PMID:Acute transfusion reactions. 223 45

A 47-year-old Japanese man was transferred to our hospital because of acute-on-chronic hepatitis B virus infection. On admission, he was suffering from sepsis due to a catheter infection and respiratory failure caused by pulmonary edema and pneumonia, but, as a result of preoperative intensive care, we avoided septic shock. ABO-incompatible liver transplantation (ABO-I-LT) was performed. In accordance with our ABO-I-LT protocol, we administered, rituximab and performed plasma exchange, splenectomy as well as hepatic artery infusion. The patient was discharged 80 days after living donor transplantation (LDLT). However, 136 days after LDLT, he experienced recurrent respiratory failure due to severe pneumonia. At that time, the CD19(+) B-cell count in the peripheral blood flow remained below 1%. We suspected a mixed infection involving Streptococcus pneumonia, Pneumocystis carinii, and fungus. The cause of the complication was overwhelming postsplenectomy infection (OPSI). We started administration of sulfamethoxazole and trimethoprim, ciprofloxacin hydrochloride, and micafungin sodium therapy as well as gamma-globulin. Oxygenation improved gradually; the patient was discharged at 41 days after re-admission. Although this patient survived the OPSI, it was clear that some aspects of the ABO-I-LT protocol should also be altered.
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PMID:A survival case of ABO-incompatible liver transplantation complicated with severe preoperative infection and subsequent overwhelming postsplenectomy infection. 1991 18

Antibody-mediated rejection (AMR) in heart transplants in the absence of anti-HLA donor-specific antibody (DSA) is not well studied or documented. This case reviews hyperacute fulminant graft dysfunction suspected to be mediated by non-HLA antibodies. After cross clamp removal, the patient developed severe pulmonary edema, profound coagulopathy, and biventricular failure. The patient's presumed AMR, cardiogenic shock, and coagulopathy were treated with extracorporeal membrane oxygenation (ECMO), plasmapheresis, intravenous immunoglobulin (IVIG), multiple blood products, and prothrombin complex concentrate. The recipient was 0% panel-reactive antibody (PRA), ABO, and crossmatch compatible. Intraoperative biopsy sample revealed a thrombotic process suggestive of a coagulation pathway activated by AMR; however, no C4d deposition was detected. Postmortem biopsies also suggested AMR. Retrospective testing of the patient's pretransplant serum revealed strong antiangiotensin II type 1 receptor (AT1R) antibodies and a strongly positive endothelial cell crossmatch. Anti-AT1R antibodies are known to be AT1 receptor agonists and may trigger inflammation and activate the extrinsic coagulation pathway. Given the potential effects of signaling through the AT1R, the patient's preexisting anti-AT1R antibodies and procoagulant therapy may have adversely affected the patient's clinical course.
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PMID:Hyperacute graft dysfunction in an orthotopic heart transplant in the presence of non-HLA antibodies. 3140 Feb 58