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)

Pediatric liver diseases usually manifest as jaundice, hepatomegaly, ascites or edema and can reflect a metabolic or nonmetabolic condition. In unconjugated hyperbilirubinemia, hemolysis can be distinguished from transient or inherited glucuronidation deficiencies. Jaundice with conjugated hyperbilirubinemia should suggest extrahepatic bile duct obstruction (requiring immediate surgery) or intrahepatic mechanical or metabolic cholestasis. Hepatomegaly or hepatocellular necrosis suggests diseases characterized by hepatocyte damage or overload. Appropriate investigations and a painstaking physical examination are essential to establish the diagnosis and to identify the cause, since immediate treatment is needed in some cases.
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PMID:[Pediatric liver diseases]. 1060 77

A 74-year-old man was admitted to hospital because of jaundice and malaise of several weeks' duration. Five years earlier he had sustained a stroke from which he had recovered almost completely. On physical examination he was overweight and had an enlarged liver. Laboratory values were consistent with cholestasis and hepatitis. An abdominal ultrasound showed multiple nodular abnormalities in the liver consistent with a malignancy. Rapidly developing abnormalities in blood coagulation were thought to be a contraindication to hepatic biopsy. The patient deteriorated and sustained a new stroke. The physicians were convinced that he had cancer and could not be cured. They planned further diagnostic studies, but at the same time made an advance directive for non-resuscitation. Three days after admission the patient was found dead; no consent for an autopsy was obtained. If it is suspected that a patient is suffering from a malignant disease, the malignancy should be demonstrated or excluded as quickly as possible in the least uncomfortable way. Also, the patient and his family should be informed of any restriction on the possibilities of treatment.
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PMID:[Clinical thinking and decision making in practice. A severely ill elderly man with icterus]. 1081 73

Due to the urgency in choosing either clinical treatment or immediate surgical intervention, the study of the prolonged neonatal cholestasis involves two basic aims: the differential diagnosis between biliary atresia and neonatal hepatitis and the research into the associated etiological agents. So, in a prospective trial carried out in the 70's, 77 children with prolonged neonatal cholestasis were studied in order to establish the differential diagnosis between biliary atresia and neonatal hepatitis, followed by the evaluation of 108 children towards a pathogenesis of the prolonged neonatal cholestasis. The results of the differential diagnosis showed that within 18 items examined only 8 proved to be good biliary atresia indicators. They are as follows (in decreasing order): ductular proliferation (portal tracts), fibrosis (portal tracts), cholestasis (portal tracts), stools colour--acholia, hepatomegaly, canalicular cholestasis (lobule), infiltrate (portal tracts), giant cells (lobule). These eight items were then gathered in a sole indicator of great discriminative power, with a confidence level of 99%. The figures regarding the pathogenesis are: rubella virus 0%, herpes simplex virus 0%, listeriosis 0%, cytomegalovirus 2.2%, hepatitis B virus 2.4%, toxoplasmosis 2.8%, alpha-1-antitrypsin deficiency 13.1%, syphilis 21.1%, autoantibodies against the liver 58.4%. Such work thus revealed that those eight most important factors when differentiating biliary atresia from neonatal hepatitis remain as fundamental indicators and, when employed alongside other diagnostic methods, can help in the assembling of a multifactorial strategy less and less invasive and more precise. The pathogenic study, with its heavy dependency on time and place, has become more complete with the introduction of new diagnostic methods, evolving to the ideal progressive reduction of idiopathic processes.
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PMID:[Prolonged neonatal cholestasis: prospective study]. 1088 10

Generalized pustular psoriasis (GPP) is uncommon in children, and serious renal and liver complications arising from GPP are rarely reported. We describe a Chinese boy who had suffered from recurrent exacerbations of GPP from the age of 1 year. He developed IgA nephropathy at the age of 9 years. He also had recurrent episodes of oliguric renal failure, hepatomegaly and cholestasis associated with severe exacerbations of GPP. These complications progressed despite early antibiotics and supportive therapy, but responded promptly to intravenous methylprednisolone therapy. Ultimately, acitretin was given and he has successfully been in remission for a year.
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PMID:Renal failure and cholestatic jaundice as unusual complications of childhood pustular psoriasis. 1207 99

Polycystic liver disease (PLD) may provoke massive hepatomegaly and severe physical and social handicaps. Data on orthotopic liver transplantation (OLT) for PLD are rare and conflicting. Conservative surgery (resection or fenestration) is indicated for large single cysts, but its value for small diffuse cysts is questionable. In addition, conservative surgery is not devoid of morbidity and mortality. OLT offers the prospect of a fully curative treatment, but controversy remains because those patients usually have preserved liver function. Thus, we reviewed our experience with OLT for PLD. Sixteen adult women underwent OLT for small diffuse PLD between 1990 and 1999. Mean age was 45 years (range, 34 to 56 years). Fourteen patients had combined liver and kidney cystic disease, but only 1 patient required combined liver and kidney transplantation, whereas 13 patients underwent OLT alone. Two patients had isolated PLD. Indications for transplantation were massive hepatomegaly causing physical handicaps (n = 16), social handicaps (n = 16), malnutrition (n = 4), and cholestasis and/or portal hypertension (n = 5). OLT caused no technical difficulty in 15 of 16 patients (surgery duration, 6.8 hours; range, 5 to 8 hours), with blood transfusions of 7.9 units (range, 0 to 22 units). One patient who underwent attempted liver-mass reduction pre-OLT died of bleeding and pulmonary emboli. Native liver weight was 10 to 20 kg. Posttransplantation immunosuppression consisted of cyclosporine or FK506, azathioprine, and steroids (discontinued at 3 months). Morbidity included biliary stricture (2 patients), revision for bleeding and hepatitis (1 patient), pneumothorax and subphrenic collection (1 patient), and tracheostomy (1 patient). One patient died of lung cancer 6 years posttransplantation. Both patient and graft survival rates are 87.5% (follow-up, 3 months to 9 years). Of 15 patients who underwent OLT alone, only 1 patient needed a kidney transplant 4 years after OLT. Kidney function has remained satisfactory in the other patients despite the use of cyclosporine or FK506 (last follow-up creatinine level, 1.55 mg/dL; range, 0.80 to 2.85 mg/dL). OLT had a dramatic impact on daily quality of life, enabling these patients to go back to a fully active life style. OLT offers the chance of a definitive treatment in patients with extensive, small, diffuse PLD that has evolved into severely handicapping hepatomegaly. In contrast to previous studies, combined liver and kidney transplantation is rarely needed. Patient symptoms and chances of definitive palliation offered by OLT must be balanced against the risks of transplantation and lifelong commitment to immunosuppression.
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PMID:Liver transplantation for polycystic liver disease. 1124 66

Primary systemic amyloidosis (AL) is an uncommon disease characterized by the extracellular deposition of a protein with a beta-fibrillar structure, consisting of monoclonal immunoglobulin light chains, lambda or kappa (ratio of lambda to kappa, 3:1). In systemic amyloidosis liver involvement is frequent but it rarely has clinical importance. The massive and localized liver deposition of amyloid, characterized by marked hepatomegaly and portal hypertension without hepato-cellular failure and by a severe prognosis, without systemic involvement, is less frequent. The authors describe an unusual case of primary hepatic amyloidosis with giant hepatomegaly, intrahepatic cholestasis, portal hypertension and splenomegaly, occurred in an elderly patient.
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PMID:Giant hepatomegaly and portal hypertension in an elderly patient with primary liver amyloidosis: an uncommon clinical occurrence. 1140 89

We describe a 36-year-old man with advanced multiple myeloma (Salmon and Durie stage III) who developed jaundice and severe cholestasis after a first cure with systemic chemotherapy of vincristine, doxorubicin, and oral dexamethasone (VAD). Serology for hepatitis A, B, and C and for CMV was negative. A liver ultrasound and CT scan showed mild hepatomegaly without evidence of extrahepatic or intrahepatic biliary tree dilatation. A percutaneous liver biopsy revealed perisinusoidal deposits of an abundant slightly eosinophilic, PAS-positive amorphous substance. Immunohistochemistry showed positivity for kappa-light chains and was negative for lambda-light chains, for IgA, IgG, IgM, and IgD immunoglobulins as well as for AA and AL proteins and for amyloid P component. A diagnosis of light chain deposition disease (LCDD) of the liver was made. The patient developed rapid deterioration of liver function, leading to a multisystem dysfunction and death. The occurrence of LCDD in multiple myeloma is close to 5% and myeloma is the underlying disease in two thirds of patients with LCDD. The kidneys are involved in almost all cases of LCDD and renal dysfunction usually reveals the disease. Only three patients with LCDD of the liver without overt renal involvement have been reported so far. This is the first observation of LCDD presenting with jaundice and severe cholestasis shortly after the diagnosis of high tumor mass myeloma, without overt renal involvement, leading rapidly to the patient's death.
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PMID:Light chain deposition disease of the liver without renal involvement in a patient with multiple myeloma related to liver failure and rapid fatal outcome. 1199

Dibutyl phthalate is a phthalate ester with extensive use in industry in such products as plastic (PVC) piping, various varnishes and lacquers, safety glass, nail polishes, paper coatings, dental materials, pharmaceuticals, and plastic food wrap. Concomitant with this extensive worldwide use is the high potential for human exposure to dibutyl phthalate in the workplace and the home environment through direct sources as well as indirectly, through contamination of water, air, and foodstuffs. Because existing toxicity information was considered inadequate, the effects of exposure to dibutyl phthalate were examined in male and female F344/N rats and B6C3F1 mice in 13-week feed studies. Furthermore, due to concern over the potential for pervasive exposure of humans to dibutyl phthalate, additional perinatal studies examined rats and mice exposed as pups in utero, for the 4 weeks of lactation, and for an additional 4 weeks postweaning. Additional studies examined the effects on rats of combining perinatal and adult subchronic exposure. Due to the recognized biologic activity of this and other phthalates, hepatic peroxisome proliferation during the in utero and lactational phases and testicular toxicity during the perinatal period were also examined. Finally, reproductive assessment by continuous breeding (including crossover mating trials and offspring assessment) and genetic toxicity studies were also conducted. In the maximum perinatal exposure (MPE) determination study in rats, dibutyl phthalate was administered in the diet to dams during gestation and lactation, and to the pups postweaning for four additional weeks, at concentrations of 0, 1,250, 2,500, 5,000, 7,500, 10,000, and 20,000 ppm. Decreased weight gains were noted in dams exposed to 20,000 ppm during gestation and to dams exposed to 10,000 ppm during lactation. The gestation index (number of live pups per breeding female) was significantly lower in the 20,000 ppm group than in the controls, and pup mortality in this group was marked (100% by Day 1 of lactation); however, survival was 89% or greater in all other treatment groups. The mean body weight of pups in the 10,000 ppm group at Day 28 of lactation was approximately 90% of the mean weight of control pups. Pups were weaned onto diets containing dibutyl phthalate at the same concentrations fed to dams. After an additional 4 weeks of dietary administration, final mean body weights of pups in the 10,000 ppm groups were 92% of the control value for males and 95% of the control value for females. Hepatomegaly (increased relative liver weight) was observed in males in all exposed groups and in females receiving 2,500 ppm or greater. No gross lesions were observed at necropsy. Moderate hypospermia of the epididymis was diagnosed in all male rats in the 7,500 and 10,000 ppm groups; mild hypospermia of the epididymis was diagnosed in 2 of 10 males in the 5,000 ppm group. No degeneration of the germinal epithelium was detected in the testis of these rats. Thus, although toxicologically important, the epididymal hypospermia was not considered to be life threatening, and 10,000 ppm was recommended as the MPE concentration for male and female rats. In the subsequent subchronic toxicity study of dibutyl phthalate with perinatal exposure, dams were administered diets containing 0 or the MPE concentration (10,000 ppm) during gestation and lactation, and weaned pups were administered the same diets as their dams received for an additional 4 weeks, until the beginning of the 13-week exposure phase. Male and female rats then received diets containing dibutyl phthalate at concentrations of 0, 2,500, 5,000, 10,000, 20,000, and 40,000 ppm for 13 weeks. No mortality or toxicity was observed in dams during the perinatal phase of the study; however, before pups were culled at 4 days postpartum, the percentage of live pups per litter was 86% to 93% that of the controls. Through weaning, litter weights of exposed pups ranged from 89% to 92% of the control values. Ten control and ten exposed pups per sex were examined at the time of trol and ten exposed pups per sex were examined at the time of weaning; hepatomegaly and markedly increased peroxisomal enzyme activities (approximately 9-fold greater than the control values) were observed in exposed pups. Body weights of the perinatally exposed pups remained lower than those of the controls throughout the 4-week period before the 13-week adult exposures began. During the 13-week adult exposure phase, the final mean body weight of males in the MPE: 0 ppm control group (MPE rats, returned to the base diet for 13 weeks), was 95% that of the controls. The body weight gain of females in the MPE:0 ppm group was greater than that of the unexposed controls, and the final body weights of these two groups were similar. Body weight gains of rats treated with dibutyl phthalate as adults decreased with increasing exposure concentration; for rats that received the MPE concentration followed by 40,000 ppm for 13 weeks, final body weights were 51% of the control value for males and 74% of the control value for females. Hepatomegaly apparently regressed in rats in the MPE:0 ppm groups but was observed in male rats receiving 5,000 ppm or greater and in females receiving 2,500 ppm or greater. In males that received 20,000 ppm as adults, testis and epididymal weights were less than in the controls; males in the 40,000 ppm group also had a lower testis weight than the controls. Results of hematologic analyses conducted at the end of the 13-week exposure period suggested a mild anemia in male rats administered 10,000 ppm or greater as adults and female rats administered 40,000 ppm as adults. Hypocholesterolemia and hypotriglyceridemia were observed in male and female rats at the higher exposure concentrations. Hypotriglyceridemia was detected in females receiving 20,000 or 40,000 ppm and in males receiving 10,000 ppm or greater. Elevations in alkaline phosphatase activities and bile acid concentrations in male and female rats receiving 20,000 or 40,000 ppm as adults were indicative of cholestasis. Microscopic examination revealed hepatocellular cytoplasmic alteration, consistent with glycogen depletion, in male and female rats receiving a concentration of 10,000 ppm or greater. In the liver of rats receiving 40,000 ppm, small, fine, eosinophilic granules were also observed in the cytoplasm of hepatocytes. Ultrastructural examination suggested the presence of increased numbers of peroxisomes. Lipofuscin accumulation was detected in rats that received 10,000 ppm or greater. Consistent with the regression of the hepatomegaly in rats in the MPE:0 and MPE:2,500 ppm groups, peroxisomal enzyme activity was not elevated in these groups. Marked elevations of peroxisomal enzyme activity were detected, however, in males receiving 5,000 ppm or greater and in females receiving 10,000 ppm or greater; at the 40,000 ppm concentration, the highest concentration tested, enzyme activities were approximately 20 fold greater than the control values. Histopathologic examination of the testes revealed degeneration of the germinal epithelium, a mild to moderate focal lesion in rats in the 10,000 and 20,000 ppm groups and a marked, diffuse lesion in all males receiving 40,000 ppm; at 40,000 ppm, an almost complete loss of the germinal epithelium resulted. Testicular zinc concentrations were lower in the 40,000 ppm group than in the controls, a finding consistent with the marked loss of germinal epithelium at this exposure concentration. Spermatogenesis was evaluated in rats in the 0, 2,500, 10,000, and 20,000 ppm groups; rats administered 20,000 ppm had fewer spermatid heads per testis than the unexposed controls, and epididymal spermatozoal concentration was less than that in the MPE:0 ppm group. For comparison with the perinatal subchronic study, a standard 13-week evaluation of the toxicity of dibutyl phthalate in male and female rats was also conducted. In this study, rats received dibutyl phthalate at the same dietary concentrations used in the 13-week exposure phase of the study with perinatal exposure: 0, 2,500, 5,000, 10,000, 20,000, and 40,000 ppm. No deaths occurred in the standard study. Markedly reduced final mean body weights were observed in males and females in the 40,000 ppm groups (45% and 73% of control body weights, respectively); final mean body weights of males receiving 10,000 ppm or greater and females receiving 20,000 ppm or greater were lower than those of the controls. Hepatomegaly was observed in males that received 5,000 ppm or greater and in females that received 10,000 ppm or greater. Testis and epididymal weights of males in the 20,000 and 40,000 ppm groups were lower than those of the controls. A minimal anemia was detected in male rats receiving 5,000 ppm or greater. Hypocholesterolemia was observed in male and female rats receiving 20,000 or 40,000 ppm, and hypotriglyceridemia was detected in males in all exposed groups and in females receiving 10,000 ppm or greater. Elevations in alkaline phosphatase activity and bile acid concentration in male and female rats were considered indicative of cholestasis. Morphologic evaluation again confirmed the toxicity of dibutyl phthalate to the liver and testes of rats. Microscopic examination of the liver revealed hepatocellular cytoplasmic alterations, consistent with glycogen depletion, in male and female rats receiving 10,000 ppm or greater. In the liver of rats in the 40,000 ppm groups, small, fine, eosinophilic granules were also observed in the cytoplasm of hepatocytes. Ultrastructural examination suggested the presence of increased numbers of peroxisomes, and peroxisomal enzyme activity was elevated in the livers of male and female rats administered 5,000 ppm or greater; the enzyme activities in the 40,000 ppm groups were approximately 13-fold greater than the control value for males and 32-fold greater than the control value for females. Lipofuscin accumulation was detected in rats receiving 10,000 ppm or greater. Histopathologic examination of the testes revealed degeneration of the germinal epithelium, a mild to marked focal lesion in the 10,000 and 20,000 ppm groups and a marked, diffuse lesion in all males in the 40,000 ppm group; at 40,000 ppm, an almost complete loss of the germinal epithelium resulted. Testicular zinc concentrations were lower in the 20,000 and 40,000 ppm groups than in the controls. Serum testosterone values were also lower at these concentrations than in the controls. Spermatogenesis was evaluated in males in the 0, 2,500, 10,000, and 20,000 ppm groups; at 20,000 ppm, spermatid heads per testis and per gram testis, epididymal spermatozoal motility, and the number of epididymal spermatozoa per gram epididymis were lower than in the controls. All of these findings are consistent with the marked loss of germinal epithelium at these exposure concentrations. In the continuous breeding study, Sprague-Dawley rats received 0, 1,000, 5,000, or 10,000 ppm dibutyl phthalate in feed. Mean body weights of exposed dams at delivery and during lactation generally decreased with increasing exposure concentration. The mean pup weight at birth in the 10,000 ppm group was significantly lower than the control pup weight. The average number of live pups per litter in all exposed groups was lower than in the controls. Crossover mating trials in the F(0) generation revealed no effects on the fertility of male or female rats receiving 10,000 ppm. In contrast to the F(0) rats, mating, pregnancy, and fertility indices of F(1) rats were lower in the 10,000 ppm group than in the controls. Germinal epithelial degeneration of the testes and absence or under development of the epididymides were noted in F(1) males in the 10,000 ppm group. Interstitial cell hyperplasia was noted in 7 of 10 males in the 10,000 ppm group. These effects document the male and female reproductive toxicity of dibutyl phthalate in F(1) rats receiving 10,000 ppm and do not exclude the possibility of developmental toxicity to F2 offspring. In the MPE determination study in mice, dams received 0, 1,250, 2,500, 5,000, 7,500, 10,000, or 20,000 ppm dibutyl phthalate in feed during gestation and lactation; pups were weaned onto the same diets as the dams received and were exposed for an additional 4 weeks. The gestation period was longer in dams that received 2,500 ppm or greater than in the controls, and gestational body weight gain depressions were noted in dams receiving 7,500 ppm or greater. Only 5 of 20 females in the 10,000 ppm group delivered live pups, and none of the 20 females receiving 20,000 ppm delivered live pups. Only one pup in the 10,000 ppm group survived past Lactation Day 1; the number of live pups per litter in the 7,500 ppm group also remained low throughout lactation. No deaths of either male or female pups occurred after weaning. Initial (postweaning) and final body weights of male pups receiving 2,500 ppm or greater were significantly less than those of the control group. The mean body weights of exposed female pups were similar to the control body weight at weaning and remained similar throughout the 4 weeks postweaning. Hepatomegaly was present in male mice in all exposed groups, and the absolute liver weight of males administered 7,500 ppm was greater than that of the controls; although a similar change was apparent in females, no statistical differences between the liver weights of exposed and control females were detected. No treatment-related gross lesions were identified at necropsy, and no histopathologic lesions definitively associated with treatment were observed in male or female mice in the 7,500 ppm groups. The one surviving male pup in the 10,000 ppm group had cytoplasmic alteration in the liver, consistent with peroxisome proliferation. Developmental toxicity and fetal and pup mortality were suggested at concentrations as low as 7,500 ppm. No subchronic toxicity study with prior MPE exposure was conducted with mice, although an MPE concentration of 5,000 ppm was suggested by the data. In a standard 13-week toxicity study, mice received 0, 1,250, 2,500, 5,000, 10,000, or 20,000 ppm dibutyl phthalate in feed. No deaths occurred during this study. Mean body weights and weight gains of male and female mice decreased with increasing exposure concentration, and the decreases were significant for males and females that received 5,000 ppm or greater. Relative liver weights were greater in males and females receiving 5,000 ppm or greater than in the controls. A minimal anemia was suggested in female mice in the 20,000 ppm group. Although no gross lesions were observed at necropsy, microscopic examination revealed hepatocellular cytoplasmic alterations, consistent with glycogen depletion, in male mice receiving 10,000 or 20,000 ppm and female mice receiving 20,000 ppm. Small, fine, eosinophilic granules, consistent with peroxisome proliferation, were also observed in the cytoplasm of hepatocytes in males and females in the 20,000 ppm groups. Lipofuscin accumulation in the liver was detected in mice receiving 10,000 ppm or greater. In a continuous breeding study using Swiss (CD-1®) mice, animals received 0, 300, 3,000, or 10,000 ppm dibutyl phthalate in feed. The fertility index, average number of litters per breeding pair, and average number of live pups per litter in the 10,000 ppm group were lower than in the controls. Crossover mating trials of mice receiving 10,000 ppm revealed effects on dams in the F(0) generation, with a lower fertility index, number of live pups per litter, and pup weight than in the controls. Liver weights were greater in males and females, and the uterine weight was less in exposed dams than in the controls. No other changes were observed at necropsy or on histopathologic examination. These data document the female reproductive toxicity of dibutyl phthalate in F(0) mice. Dibutyl phthalate was not mutagenic in Salmonella typhimurium strain TA98, TA100, TA1535, or TA1537 with or without exogenous metabolic activation but did induce mutations in L5178Y mouse lymphoma cells treated without metabolic activation. In peripheral blood samples obtained from male and female mice at the end of the 13-week study, frequencies of micronucleated normochromatic erythrocytes were similar between exposed and control mice. Together, the studies in rodents suggest that young rodents (in utero and perinatal) respond in a manner qualitatively similar to that of adult rats and mice. Dibutyl phthalate induced toxic effects in rodents as pups in utero and during the lactational phases of development and also affected young adults, as evidenced by fetotoxicity and lethality, body weight gain decrements, increased liver weights, hepatic peroxisome proliferation, testicular toxicity, and female reproductive toxicity. Dibutyl phthalate was lethal to rat fetuses and rat and mouse neonates at dietary concentrations that were not toxic to dams. Otherwise, there was no teratogenic or morphologic evidence that rodent young were uniquely sensitive to the effects of short-term dibutyl phthalate treatment. Synonyms: 1,2-Benzenedicarboxylic acid dibutyl ester; benzene-o-dicarboxylic acid di-n-butyl ester; o-benzenedicarboxylic acid dibutyl ester; butyl phthalate; n-butyl phthalate; DBP; dibutyl 1,2-benzene dicarboxylate; dibutylphthalate; di-n-butylphthalate; di(n-butyl) phthalate; dibutyl-o-phthalate; phthalic acid dibutyl ester. Trade Names: Celluflex DBP; Elaol; Ergoplast FDB; Ersoplast FDA; Genoplast B; Hexaplas M/B; Palatinol C; Polycizer DBP; PX 104; RC Plasticizer DBP; Staflex DBP; Uniflex DBP; Unimoll DB; Witcizer 300; Witicizer 300. (NOTE: These studies were supported in part by funds from the Comprehensive Environmental Response, Compensation, and Liability Act trust fund (Superfund) by an interagency agreement with the Agency for Toxic Substances and Disease Registry, U.S. Public Health Service.)
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PMID:NTP technical report on the toxicity studies of Dibutyl Phthalate (CAS No. 84-74-2) Administered in Feed to F344/N Rats and B6C3F1 Mice. 1220 94

Sonography is often the first imaging procedure performed in the evaluation of individuals with suspected liver disease. Evaluation for biliary dilatation is always performed, because bile duct obstruction can cause abnormal liver test results, raising the suspicion of liver disease. Ultrasound is a useful but imperfect tool in evaluating diffuse liver disease. We discuss the uses and limitations of sonography in evaluating parenchymal liver disease. Sonography can show hepatomegaly, fatty infiltration of the liver, and cirrhosis, all with good but imperfect sensitivity and specificity. Sonography is of limited usefulness in acute hepatitis. Increased parenchymal echogenicity is a reliable criterion for diagnosing fatty liver. Cirrhosis can be diagnosed in the correct clinical setting when the following are present: a nodular liver surface, decreased right lobe-caudate lobe ratio, and indirect evidence of portal hypertension (collateral vessels and splenomegaly). Ultrasound plays an important role in the imaging of conditions and procedures common in patients with diffuse liver disease.
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PMID:Sonography of diffuse liver disease. 1221 50

Possible hepatic effects of oral contraceptives (OCs) include tumors, intrahepatic cholestasis, and less well known vascular lesions such as Budd-Chiari syndrome and peliosis, a disseminated pseudocystic dilatation of the sinusoid capillaries of the liver. A 29-year-old woman with a history of 4 pregnancies, hypertension and diabetes both requiring daily medication, and use since April 1983 of an oral contraceptive (OC) containing .15 mg levonorgestrel and .03 mg of ethinyl estradiol complained in March 1984 of epigastric pain and increased abdominal volume. Ascitis was diagnosed and the patient was hospitalized. She had experienced a generalized pruritus for several months and had lost weight. The bilirubin, alcaline phosphatase, and Gamma GT levels were slightly elevated. Sonography showed a hypertrophied liver. Incipient esophageal varices were seen with gastric fibroscopy. The small subhepatic venous branches had a cloudy aspect. The peliosis hepatis was diagnosed by a transjugular puncture biopsy of the liver. With discontinuation of the OCs, the ascites did not reappear after puncture and the perturbations of the liver functioning normalized. On follow-up in April 1985, slight hepatomagaly persisted but the patient reported no further symptoms. She continued her medication for hypertension and diabetes. Peliosis hepatis was 1st described in 1964 and several cases related to OC use have been reported since 1972. Peliosis has the aspect of multiple small congestive cavities of 1-3 mm in diameter in the parenchyma. The lesions consist of areas of hepatocellular necrosis secondarily filled with blood. The cysts may be voluminous and subcortical, creating a risk of hemoperitoneum. The lesions may also be associated with a benign or malignant liver tumor. Regression of the lesions is possible with termination of the etiologic agent. Clinically, hepatomegaly, painful or not, sometimes associated with splenomegaly, is often found with peliosis. Moderate jaundice is very frequent. Ascites or edema of the legs are observed. Hyperbilirubinemia and augmentation of phosphatases and Gamma GT are the main laboratory findings. Transaminases may be slightly elevated, and the rate of prothrombin may be diminished. The condition is sometimes diagnosed with laparoscopy, celiomesenteric arteriography, or phlebography, but hepatic puncture biopsy usually establishes the diagnosis. The contition may improve if the etiologic agent is removed or it may worsen because of liver failure or a complication such as hemoperitoneum or an associated tumor.
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PMID:[Peliosis hepatis and oral contraceptives: a case report]. 1228 Oct 5


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