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)

Twelve children were included into the protocol, 5 in March 1989 and 7 in April 1993. All of them were HIV 1 positive and had diarrhoea, important adenopathy and opportunistic infections. Seven out of 12 patients had an immunological monitoring. One out of 12 children with B hepatitis died with liver cirrhosis. Eleven children had a clear improvement in their clinical course, during the treatment. Five out of 7 patients had a significant increase of the CD4 lymphocytes at 4 and 7 months follow-up. Four patients had an important and significant increase of the CD8 count at 4 months and 6 out of 7 patients at 7 months. Interestingly, in 4 out of 7 patients after 7 months treatment we observed higher than normal value of the CD8 count. Variations observed for CD8 population compared to CD4 were more important.
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PMID:Augmentation of CD8 and CD4 lymphocytes subsets in AIDS infected children after treatment with a non-toxic chelating agents compound--Rodilemid. 864 93

Inflammatory processes in organs frequently lead to hyperplasia of regional lymph nodes. In the present study, we investigated whether lymph node enlargement within the hepatoduodenal ligament may reflect the inflammatory activity within the liver of patients chronically infected with the hepatitis C virus (HCV). In 114 patients with chronic hepatitis C and 49 healthy controls, the total lymph node volume within the hepatoduodenal ligament was prospectively investigated by ultrasound. In patients with chronic hepatitis C, a liver biopsy was taken at the same occasion, and specimens were semiquantitatively evaluated by the histological activity index (HAI). Hepatitis C viremia was assessed by quantitative reverse transcription-polymerase chain reaction (RT-PCR). Genotyping was performed by a reverse hybridization assay. In 104 of 114 patients (91.2%) and in 45 of 49 healthy controls (91.8%), adequate visualization of the region of the hepatoduodenal ligament was achieved by ultrasound. Lymph nodes were detected in all patients with chronic hepatitis C and in 33 of 45 controls. The mean perihepatic lymph node volume in healthy controls (2.2 +/- 1.8 mL) was lower than in HCV-infected patients with mild to moderate inflammatory activity, severe inflammatory activity, and patients with cirrhosis (5.8 +/- 2.2 mL, 18.1 +/- 10.4 mL, and 22.8 +/- 18.8 mL, respectively). In patients with HCV-RNA levels of less than 10(6) copies/mL, the total lymph node volume was 5.8 +/- 1.6 mL and was significantly increased in patients with higher viremia (20.3 +/- 13.8 mL; P < 10(-6)). No correlation was found between the total lymph node volume within the hepatoduodenal ligament, HCV genotypes, and liver function test results. In conclusion, enlargement of perihepatic lymph nodes in patients with chronic hepatitis C is predictive for the presence of severe inflammatory activity. The mechanism of portal lymphadenopathy in patients with chronic hepatitis is unknown but appears to be related to viral replication within the liver and the immune-mediated inflammatory response of the host.
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PMID:Enlargement of perihepatic lymph nodes in relation to liver histology and viremia in patients with chronic hepatitis C. 925 60

We describe a case of a 73-year-old male with a rare T-cell lymphoma that presented deceptively as progressive hepatic failure with fever, weight loss, pancytopenia, mental confusion, splenomegaly, and no lymphadenopathy. An alcoholic history supported the diagnosis of cirrhosis, but a liver biopsy was not performed. A bone marrow biopsy was considered unremarkable. Death occurred after a course of four months. Postmortem examination showed hepatic, splenic, lymph node, and marrow infiltration by characteristically sparse, isolated, bizarre, medium-to-large sized neoplastic cells with extensive hepatic centrilobular necrosis, steatosis, and predominant splenic involvement. Immunohistochemical markers indicated a T-cell lymphoma consistent with either an alpha/beta peripheral T-cell lymphoma or a gamma/delta lymphoma. Definitive immunotyping was not available. However, the pathologic features are most consistent with a gamma/delta T-cell lymphoma. This case is an example of a rare, rapidly progressive lymphoma, which is a recognized clinical entity, easily missed, and treatable. Its diagnostic consideration must be explicitly communicated to pathologists, because the isolated or sparse tumor cells in a lymph node, liver, or bone marrow biopsy may easily be mistaken for variants of megakaryocytes or histiocytes.
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PMID:Case report: an autopsy study of a rare T-cell lymphoma clinically misdiagnosed as fulminant hepatic disease. 987 88

Sonographic detection of perihepatic lymphadenopathy by transabdominal ultrasound is helpful in the diagnosis of acute and chronic liver disease but differentiation between benign inflammatory and malignant disease is not possible. The diagnostic value of perihepatic lymphadenopathy has been evaluated in patients with chronic hepatitis C and primary biliary cirrhosis. In patients with chronic hepatitis C enlargement of perihepatic lymph nodes is associated with viremia and is predictive for the presence of severe inflammatory activity with and without cirrhosis. In retrospective studies it could be shown that patients with chronic hepatitis C without response to antiviral therapy do not normalize the size of perihepatic lymph nodes. Future prospective studies have to evaluate whether successful antiviral therapy together with histological improvement will be reflected in an decline of perihepatic lymph node size. In patients with primary biliary cirrhosis the total perihepatic lymph node volume reflect histological stages, i.e. larger lymph nodes are observed in more advanced disease. The mechanism of portal lymphadenopathy in patients with acute and chronic liver disease is unknown. Viral, bacterial infections, and immunological causes are potential etiopathological factors in periportal lympadenopathy. Malignant causes of perihepatic lymphadenopathy have also to be considered.
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PMID:[Sonographic detection of perihepatic lymph nodes: technique and clinical value]. 1019 Feb 47

We describe the case of a 18-year-old male patient who first presented with decompensated cirrhosis, fever and generalized lymphadenopathy. He had abnormal results for liver biochemical tests, with a hepatitic-like picture and high titre of antinuclear antibodies. According to the scoring system proposed by the International Autoimmune Hepatitis Group he had 'definite' autoimmune hepatitis and responded well to immunosuppressive treatment. One year later he developed pyoderma gangrenosum which was successfully treated with cyclosporine. Two years later he experienced bloody diarrhoea as a first presentation of ulcerative colitis. At that time both the cholestatic biochemical picture and the cholangiographic appearances of the biliary tree were consistent with primary sclerosing cholangitis. Despite the addition of azathioprine and ursodeoxycholic acid to his treatment regime he developed recurrent episodes of cholangitis and intractable pruritus for which he underwent successful liver transplantation.
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PMID:Overlapping syndrome of autoimmune hepatitis and primary sclerosing cholangitis associated with pyoderma gangrenosum and ulcerative colitis. 1065 5

Abdominal lymph node chains and route of lymph drainage of various organs (stomach, duodenum, liver, gallbladder, pancreas, small intestine, appendix, blind intestine, colon rectum) are analyzed according to their location. The role of conventional radiology and diagnostic imaging is evaluated in the study of abdominal lymphatic system with particular reference to lymphangiography and the new procedures of sonography, CT and MRI. Present methods used in inflammatory abdominal lymphadenopathy with special attention to tuberculous lymphadenitis, liver cirrhosis, neoplastic abdominal lymphadenopathy, colorectal and pancreatic cancer, are illustrated. Combined modality imaging is considered in gastric cancer based on the evolution of the classification of gastric lymph nodes. The role of sonography, endoscopic ultrasonography, spiral CT and MRI is assessed in gastric cancer N staging. A retrospective study is analyzed and perspectives for the application of a new CT protocol are proposed. PET potentialities in the study of abdominal lymph nodes are examined.
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PMID:Role of diagnostic imaging in abdominal lymphadenopathy. 1136 14

Imaging of hepatocellular carcinoma (HCC) is complicated because the tumor has a varied radiologic appearance and frequently coexists with cirrhotic regenerative and dysplastic nodules. In cirrhotic patients, any dominant solid nodule that is not clearly a hemangioma should be considered a HCC until proven otherwise, especially if the lesion is hypervascular, of high T2 signal intensity, or demonstrates venous invasion. Biopsy of HCC in cirrhosis is risky and surveillance is often preferable. The doubling time of HCC is 1 to 12 months, and a nodule that is stable over 4 months is very unlikely to be a HCC. However, stable nodules cannot be dismissed, since livers containing dysplastic nodules are at high risk to develop HCC. In noncirrhotic patients, any solid mass that is not clearly a hemangioma or focal nodular hyperplasia is potentially a HCC, and biopsy may be required. Venous invasion by tumor should be distinguished from bland thrombus. Imaging detection of nodal metastases is limited by the frequent finding of benign reactive lymphadenopathy in cirrhosis. Resection is the preferred treatment for HCC, but is contraindicated in the presence of tumors in both lobes, major venous invasion, invasion of adjacent organs other than the gallbladder, tumor rupture, nodal metastases, or distant metastases.
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PMID:Imaging of hepatocellular carcinoma: a practical approach. 1168 39

Portal vein thrombosis (PVT) is an uncommon cause for presinusoidal portal hypertension. PVT can be caused by one of three broad mechanisms: (1) spontaneous thrombosis when thrombosis develops in the absence of mechanical obstruction, usually in the presence of inherited or acquired hypercoagulable states; (2) intrinsic mechanical obstruction because of vascular injury and scarring or invasion by an intrahepatic or adjacent tumor; or (3) extrinsic constriction by adjacent tumor, lymphadenopathy or inflammatory process. Usually, several combined factors are necessary to result in PVT. The consequences of portal vein thrombosis are mostly related to the extension of the clot within the vein. Gastrointestinal bleeding from gastroesophageal varices is the most frequent presentation. Noninvasive imaging techniques are currently used for the screening of patients and the initial diagnosis of PVT. The invasive techniques are reserved for cases when noninvasive techniques are inconclusive, before percutaneous interventional treatment, or in preoperative assessment of patients who are candidates for surgery. Recanalization of the portal vein with anticoagulation alone may not be consistent or appropriate in highly symptomatic patients. Catheterization of the superior mesenteric artery (SMA) is helpful for diagnosis as well as for therapy by allowing the intra-arterial infusion of thrombolytic drugs in the same setting. Direct transhepatic portography allows precise determination of the degree of stenosis and extension within the portal vein, as well as pressure measurements. Thrombotic occlusions of the portal, mesenteric, and splenic veins can be managed by mechanical thrombectomy (MT) or pharmacologic thrombolysis. Underlying occlusions because of organized or refractory thrombus or fixed venous stenosis are best corrected by balloon angioplasty and stent placement. Access into the portal venous system can also be established through creating a transjugular intrahepatic portosystemic shunt (TIPS). Creating a TIPS is also important in the setting of PVT associated with cirrhosis to decompress portal hypertension and improve portal venous flow. PVT involving the portal, splenic, and/or mesenteric veins can also complicate a preexisting TIPS in which case the shunt can be readily used as therapy access. Several techniques may be used to recanalize the shunt and portal venous system, including thrombolytic therapy, balloon angioplasty/embolectomy, suction embolectomy, basket extraction of clots, and mechanical thrombectomy with a variety of devices. Advantages of MT include the potential to rapidly remove thrombus without the need for prolonged thrombolytic infusions, and reducing the potential life-threatening complications of thrombolytic therapy. Possible drawbacks include the risk of intimal or vascular trauma to the portal vein, which may promote recurrent thrombosis.
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PMID:Applications of percutaneous mechanical thrombectomy in transjugular intrahepatic portosystemic shunt and portal vein thrombosis. 1277 31

We report a case of systemic phaeohyphomycosis in a 13-year old girl. The clinical presentation was with fever, weight loss, cholestatic jaundice with hepatosplenomegaly and generalized lymphadenopathy. The patient was diagnosed initially as tuberculous adenitis and was on antituberculous therapy, but with worsening of symptoms. Lymph node and liver biopsy showed granuloma with fungal hyphae suggestive of phaeohyphomycosis. The patient responded to antifungal therapy. Later she developed secondary biliary cirrhosis with cholangitis due to long stricture of the common bile duct and common hepatic duct requiring biliary stenting. To the best of our knowledge, this is the first report on phaeohyphomycosis causing biliary cirrhosis in the English lilterature.
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PMID:Hepatobiliary phaeohyphomycosis with secondary biliary cirrhosis. 1591 77

Approximately 5% of patients with end-stage cirrhosis undergoing orthotopic liver transplantation have occult hepatocellular carcinoma. Careful follow up is required to detect recurrent tumour, and knowledge of the patterns of recurrence may avoid diagnostic confusion with other malignancies, such as post-transplantation lymphoproliferative disorder. This case report illustrates an unusual presentation of recurrent hepatocellular carcinoma in a 56-year-old man presenting with a para-aortic soft tissue mass, thought clinically and radiologically to represent lymphoma or post-transplantation lymphoproliferative disorder. This case demonstrates that recurrent hepatocellular carcinoma can present late after transplantation as retroperitoneal lymphadenopathy, and should alert physicians and radiologists to be aware of the radiological appearances of recurrence and of the need for early biopsy to avoid diagnostic confusion with other malignancies.
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PMID:Recurrent hepatocellular carcinoma after liver transplantation mimicking post-transplantation lymphoproliferative disorder. 1602 39


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