Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019209 (hepatomegaly)
 5,798 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Campylobacter coli is known to cause ulcerous enterocolitis, but hepatitis has not yet been reported. A 50-year-old woman without history of liver disease was admitted with diarrhoea, fever, poor general condition, subicterus and enlarged liver. Campylobacter coli was grown in haemoculture, and a specific antibiotic treatment resulted in complete cure. The results of haemoculture, the necrosis and polymorphonuclear infiltrates found in liver biopsies, the return to normal of biochemical tests and liver size under antibiotic therapy and the absence of any other cause of acute or chronic liver disease are strong arguments in favour of the hepatitis being caused by Campylobacter coli in this patient.
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PMID:[Hepatitis caused by Campylobacter coli (author's transl)]. 707 Sep 93

The case of a 7-year-old boy with virus-associated hemophagocytic syndrome (VAHS) and serologically proven parvovirus B-19 infection is described. The patient with VAHS presented with fever, hepatosplenomegaly, pancytopenia, and hyperlipidemia type IV. After induction therapy with VP-16 and prednisone, partial remission was achieved. Despite maintenance therapy, reinductions, and the addition of cyclosporine A for 3 months, several relapses occurred. The therapy was stopped because of life-threatening complications (Klebsiella sepsis, neutropenic enterocolitis, and stercoral peritonitis). The complications were treated successfully. The patient status was stabilized after splenectomy. However, hepatomegaly progressed slowly and the hyperlipidemia endured. Ten months after the diagnosis leukocytosis with absolute T lymphocytosis appeared. Reactivation of VAHS was suspected and intravenous immunoglobin and then antilymphocyte immunoglobulin ALG therapy were started. The resultant decrease in leukocytosis was prompt, but lymphopenia did not occur. Virostatic treatment with foscarnet was introduced based on human herpesvirus-6 seroconversion. Twenty-six months after the diagnosis, the patient is well, without any sign of VAHS or lymphoproliferation.
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PMID:Infection-associated hemophagocytic syndrome complicated by infectious lymphoproliferation: a case report. 872 Oct 28

The kallikrein-kinin (K-K) (contact) system is activated during acute and chronic relapsing phases of enterocolitis induced in genetically susceptible Lewis rats by intramural injection of peptidoglycan-polysaccharide (PG-APS). Using the selective plasma kallikrein inhibitor P8720, we investigate whether activation of the K-K system plays a primary role in chronic granulomatous intestinal and systemic inflammation in this model. Group I (negative control) received human serum albumin intramurally. Group II (treatment) received PG-APS intramurally and P8720 orally. Group III (positive control) received PG-APS intramurally and albumin orally. P8720 attenuated the consumption of the contact proteins, high molecular weight kininogen (P<0.03), and factor XI (P<0.04) in group II vs. group III. P8720 decreased chronic intestinal inflammation measured by blinded gross (P<0.01) and histologic (P<0.0005) scores as well as systemic complications (arthritis, splenomegaly, hepatomegaly, leukocytosis, and acute-phase reaction) (P<0.01) in group II as compared with group III. We conclude that relapsing chronic enterocolitis and systemic complications are in part due to plasma K-K system activation, and that inhibition of this pathway is a potential therapeutic approach to human inflammatory bowel disease and associated extraintestinal manifestations.
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PMID:Specific inhibition of plasma kallikrein modulates chronic granulomatous intestinal and systemic inflammation in genetically susceptible rats. 950 76

We report a 2-month-old boy without any immuno-compromised diseases, who suffered from the severe cytomegalovirus (CMV) infection after the subclavian flap aortoplasty and pulmonary artery banding for coarctation complex. He underwent the operation at 2 months old and received 2 units of irradiated packed red blood cells before and after the surgery. His postoperative course was uneventful but the interstitial pneumonitis, until he developed watery diarrhea 10 days after the surgery following hepatitis with the marked hepatomegaly 3 weeks after. Since CMV infection was confirmed as the cause of the pneumonitis, enterocolitis and hepatitis, he was initially treated by gamma-globulin with the high CMV titer at a dose of 200 mg/kg/day for 2 days and ganciclovir at a dose of 10 mg/kg/day for 14 days. Because of the persistent CMV infection, he needed two more treatments of ganciclovir at the same dosage and gamma-globulin once a week for 2 months. He finally recovered from severe CMV infection 5 months after the above treatments. In conclusion, the severe CMV infection can occur by blood transfusion even in the surgical case with normal immune system. If one finds pneumonitis, hepatitis or enterocolitis after any type of surgery with history of blood transfusion, CMV infection should be suspected as the cause of these diseases.
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PMID:[A case of severe cytomegalovirus infection after the repair of coarctation of aorta]. 974 11

The literature describes eight cases of mutations in the DPM1 gene generating DMP1-CDG, causing similar phenotype of early onset seizures, microcephaly and developmental delay. Investigations of these patients revealed associated abnormal findings on brain imaging, elevated CK, abnormal clotting factors and mildly deranged serum transaminases. We describe the ninth case of DMP1-CDG, whose clinical presentation includes severe gastrointestinal involvement, i.e. food protein induced enterocolitis syndrome (FPIES). Gastrointestinal manifestations (GIT) of the congenital glycosylation disorders have included deranged liver function, hepatomegaly, liver fibrosis, steatosis and protein-losing enteropathy. This is the first report of a congenital glycosylation disorder being associated with FPIES.
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PMID:DMP1-CDG (CDG1e) with Significant Gastrointestinal Manifestations; Phenotype and Genotype Expansion. 2748 10

Congenital syphilis is a severe disease that arises from the vertical transmission of Treponema pallidum. Clinical findings are related to the pregnancy stage, fetal gestational week, maternal treatment and fetal immunologic response. Prematurity, low birth weight, nonimmune hydrops fetalis, necrotizing enterecolitis, hepatomegaly, skin eruptions, thrombocytopenia, hemolytic anemia and fever can be detected in the symptomatic newborn. Postnatal respiratory insufficiency, hepatomegaly, anemia and thrombocytopenia were detected in a baby who was born at the 29th week of gestation, weighing 1.160 g and followed due to intestinal hyperechogenicity from the second trimester. Her and her mother's Venereal Disease Research Laboratory titers were positive, confirming test Treponema pallidum hemagglutination was reactive. After penicillin was administered for 10 days, anemia, and thrombocytopenia were regressed. In the 15th day of life, findings of perforated necrotising enterocolitis (NEC) suddenly appeared. The operation was performed due to NEC for three times but nonresponsive laboratory and clinical findings and died in the 54th day of life. We assumed that syphilis is the cause of both bowel hyperechogenicity and necrotising enterocolitis.
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PMID:Congenital Syphilis Presenting with Prenatal Bowel Hyperechogenicity and Necrotizing. 3237 45