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

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

Transfusion-related acute lung injury (TRALI) is a serious complication of transfusion and has been ranked as one of the leading causes of transfusion-related fatalities. Nonetheless, many details of the immunopathogenesis of TRALI, particularly with respect to recipient factors are unknown. We used a murine model of antibody-mediated TRALI in an attempt to understand the role that recipient lymphocytes might play in TRALI reactions. Intravenous injection of an IgG2a antimurine major histocompatibility complex class I antibody (34-1-2s) into BALB/c mice induced moderate hypothermia and pulmonary granulocyte accumulation but no pulmonary edema nor mortality. In contrast, 34-1-2s injections into mice with severe combined immunodeficiency caused severe hypothermia, severe pulmonary edema, and approximately 40% mortality indicating a critical role for T and B lymphocytes in suppressing TRALI reactions. Adoptive transfer of purified CD8(+) T lymphocytes or CD4(+) T cells but not CD19(+) B cells into the severe combined immunodeficiency mice alleviated the antibody-induced hypothermia, lung damage, and mortality, suggesting that T lymphocytes were responsible for the protective effect. Taken together, these results suggest that recipient T lymphocytes play a significant role in suppressing antibody-mediated TRALI reactions. They identify a potentially new recipient mechanism that controls the severity of TRALI reactions.
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PMID:Recipient T lymphocytes modulate the severity of antibody-mediated transfusion-related acute lung injury. 2061 20