Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0015695 (fatty liver)
 13,941 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 30-year-old woman in the 36th week of her second pregnancy, suddenly developed jaundice with remarkable liver necrosis, accompanied by generalized bleeding due to disseminated intravascular coagulation (DIC). She underwent a caesarean and a dead foetus was extracted from the uterus. Heparin and frozen plasma infusion resulted in a prompt recovery from the haemostatic disorder. The course of the disease involved the successive appearance of haemorrhagic shock, intestinal ileus and pulmonary embolism all of which she recovered from. The liver biopsy showed severe cholestasis without derangement of the lobular structure. Hypotheses of acute veno-occlusive disease caused by the DIC, and acute fatty liver of pregnancy are discussed.
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PMID:[Disseminated intravascular coagulation and acute hepatic necrosis at the end of pregnancy. A case report]. 262 77

Portal hypertension, widely recognized as a complication of cirrhosis, may also develop as an intrahepatic consequence of numerous hepatic disorders in the absence of cirrhosis. When gastrointestinal bleeding occurs in such cases, ruptured esophageal varices must be considered. Among chronic liver diseases, some, such as schistosomiasis, are commonly associated with portal hypertension and its complications. In others, including tuberculosis, amyloidosis, and polycystic disease, well-documented portal hypertension has been reported in only a small minority of cases. Nevertheless, because of the ever-present possibility of variceal hemorrhage whenever portal hypertension occurs, clinicians should be aware of these disorders. Acute conditions associated with noncirrhotic intrahepatic portal hypertension include acute (and particularly fulminant) viral or drug-induced hepatitis, acute alcoholic hepatitis, acute veno-occlusive disease, and acute fatty liver of pregnancy. Portal hypertension may be reversible following recovery in these settings. Particular attention is called to the increasing frequency of acute veno-occlusive disease on bone marrow transplant units, presumably as a complication of high-dose chemo- and radiotherapy.
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PMID:Noncirrhotic intrahepatic portal hypertension. 354 26

Chemotherapy changes the appearance of liver tumours and may also affect the liver parenchyma. Tumours respond with changes in size, outline, and internal architecture. The accuracy of liver CT for detecting metastases is reduced after chemotherapy. Histologic studies have shown that some metastases which become invisible on follow-up CT are completely sterile at later resection, but most 'disappearing' lesions still contain active tumour. Hepatic steatosis becomes much more common after chemotherapy. Diffuse fatty change may conceal metastases on US and CT, whilst focal steatosis may mimic tumour. Chemical-shift MRI will distinguish fat from tumour. Fatty change is usually reversible, unless the liver receives a 'second hit' of damage from other causes. Sinusoidal obstructive syndrome (SOS), nodular regenerative hyperplasia, veno-occlusive disease and peliosis are manifestations of microvascular injury which can result from chemotherapy. SOS, the most common of these, is undetectable on US and CT, but can be shown on SPIO-enhanced MRI. Although SOS causes no symptoms in most patients, it may cause increased bleeding from the friable liver at surgery, and greater risk of peri-operative adverse events. Rarer complications of chemotherapy include pseudo-cirrhosis and sclerosing cholangitis.
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PMID:The effects of cancer chemotherapy on liver imaging. 1923 92