Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023890 (cirrhosis)
42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cell and humoral immunological tests were used in clinical examination of 47 patients suffering from cirrhosis of the liver; a mixed character of autoallergy was revealed in this form of pathology. Reproduction of passive anaphylaxis on guinea pigs with the aid of the sera and leukocytes of these patients pointed to the prevalence of cell allergy. Passive transmission of increased sensitivity to human hepatocytes from guinea pigs, preliminarily sensitized with salt extracts from human hepatocytes, to intact animals was realized. Active sensitization was accompanied by the formation of mixed allergy to the antigen obtained from the liver of a person who died accidentally, with the prevalence of the immediate type of reaction.
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PMID:[Study of the mechanisms of autoallergic reactions in cirrhosis of the liver]. 108 96

Acquired hemosiderosis resulting from massive iron deposits in various organs, including heart, liver, and pancreas, may lead to architectural and functional disturbances of these organs. Even though iron overload can occur in nonuremic as well as in uremic individuals, the dialysis patient is at particular risk for developing hemosiderosis. Many dialysis patients receive exogenous iron from either oral iron therapy or blood transfusions. In addition, these patients seem to be at high risk for retaining iron. A diagnosis of excess iron deposition should be considered if the patient has unexplained cardiomyopathy, hepatic cirrhosis, proximal myopathy, diabetes mellitus, arthropathy, or immune dysfunction such as listeriosis. Several techniques are available for determining iron overload. Diagnostic tests include measuring serum ferritin levels, staining bone marrow preparations for excess iron, measuring tissue hemosiderin concentrations, magnetic resonance imaging, and the deferoxamine (DFO; Desferal) "challenge test." The simplest treatment for iron overload in nonuremic patients is removal of iron by venesection. However, in patients in whom venesection is not feasible, the chelating agent DFO can effectively remove excess iron. In the dialysis patient, DFO therapy can be combined with either dialysis or hemoperfusion to remove the iron-DFO complex that would otherwise be removed by the kidney. DFO therapy in the nondialyzed individual has proven to be successful, but before treatment, the benefits of the treatment must be weighed against possible adverse side effects such as cataracts, changes in color vision, and anaphylaxis. In the dialysis patient, indications for iron removal are less clearly defined.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Management of iron overload in dialysis patients. 329 89

Topically applied thrombin was known to be effective in hemostasis of local bleeding, but complications of shock, anaphylaxis or disseminated intravascular coagulation (DIC) have been reported recently in rare cases. In this experiment, the possibility of DIC was examined by intraperitoneal injection of topical thrombin (Parke-Davis) to rabbits with liver cirrhosis or acute liver damages induced by CCl4. No significant changes in the coagulation parameters were found in the groups of liver cirrhosis or the untreated control, but the injection of thrombin induced decreases of platelet count and fibrinogen and prolongation of prothrombin time and partial thromboplastin time in the groups of acute liver damages, 24 or 48 hr after CCl4 injection. When the "junk" prepared from the topical thrombin was injected to the 48 hr-damage group, no change was noted in these parameters. It was concluded that DIC could be induced by the intraperitoneal injection of topical thrombin only in cases of acute liver damages, where the increased permeability of peritoneum was postulated. However, such an immediate or marked change in coagulation was not found in our experiment as encountered in the clinical cases, which suggested the involvement of the anaphylactic reaction to the topical application of thrombin in the development of DIC in these clinical cases.
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PMID:[Effect of intraperitoneal injection of topical thrombin on the coagulation and fibrinolysis of rabbits with experimental liver damages]. 398 69

Graft versus host disease (GVHD) is an uncommon complication following liver transplantation. In the present case report, a 53-year-old male hepatitis B virus carrier was diagnosed with primary liver cancer with post-hepatitis cirrhosis. Preoperative cytomegalovirus (CMV), Epstein-Barr virus, coxsackievirus, herpes simplex virus and autoimmune antibody series were negative. Preoperative human leukocyte antigen type was also negative. Following classic orthotropic liver transplantation, postoperative treatment included immunosuppression therapy, infection protection, anti-human immunodeficiency virus therapy and CMV infection protection therapy. Chemotherapy was initiated at day 16 following surgery. At day 26 following the transplantation, the patient developed a fever of unknown cause, and a scattered red rash was observed behind the left ear and on the neck. The patient presented with a fever of unknown cause, rash, symptoms of the digestive tract, leukocytopenia and pancytopenia. A diagnosis of GVHD was confirmed following a skin biopsy. Symptomatic therapies, including antivirals, anti-anaphylaxis drugs and steroids were administered. However, the patient succumbed to infection, acute respiratory distress syndrome and multiple organ failure at day 46 following surgery. Therefore, an effective therapeutic strategy for the treatment of GVHD following liver transplantation is yet to be established, and further research is required prior to such a regimen being developed.
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PMID:Graft versus host disease following liver transplantation: A case report. 2518 16

A 63-year-old female patient with recent diagnosis of hepatitis C and cirrhosis and no other comorbidities, on no medications, was found to have Barcelona Clinic Liver Cancer stage C hepatocellular carcinoma and began systemic therapy with sorafenib 400mg twice daily. Five days after starting treatment, the patient went to an emergency department with pruritic, target-shaped, erythematous papules compatible with erythema multiforme, painful oral aphthous ulcers, and fever. Sorafenib was suspended and the patient underwent oral corticosteroid treatment for 5 days, showing significant improvement of the lesions. One month after discharge, the patient was reassessed at an outpatient clinic. As she was asymptomatic and had no skin lesions, sorafenib was resumed at a lower dose (200mg daily). Three hours after ingesting a single dose of sorafenib, the patient experienced chills, fever, rash, angioedema and stridor. She immediately sought the emergency department and was diagnosed with anaphylaxis. The patient received intravenous corticosteroid therapy, which improved her respiratory and cutaneous symptoms in 72h. Sorafenib was permanently suspended, and regorafenib could not be prescribed as second-line therapy. This is the first description of anaphylaxis to sorafenib.
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PMID:Anaphylaxis preceded by erythema multiforme with sorafenib: First case report. 3108 38