Hepatic Parenchymal Changes Research Articles

Imaging-based Quantification of Hepatic Fat: Methods and Clinical Applications

Fatty liver disease comprises a spectrum of conditions (simple hepatic steatosis, steatohepatitis with inflammatory changes, and end-stage liver disease with fibrosis and cirrhosis). Hepatic steatosis is often associated with diabetes and obesity and may be secondary to alcohol and drug use, toxins, viral infections, and metabolic diseases. Detection and quantification of liver fat have many clinical applications, and early recognition is crucial to institute appropriate management and prevent progression. Histopathologic analysis is the reference standard to detect and quantify fat in the liver, but results are vulnerable to sampling error. Moreover, it can cause morbidity and complications and cannot be repeated often enough to monitor treatment response. Imaging can be repeated regularly and allows assessment of the entire liver, thus avoiding sampling error. Selection of appropriate imaging methods demands understanding of their advantages and limitations and the suitable clinical setting. Ultrasonography is effective for detecting moderate or severe fatty infiltration but is limited by lack of interobserver reliability and intraobserver reproducibility. Computed tomography allows quantitative and qualitative evaluation and is generally highly accurate and reliable; however, the results may be confounded by hepatic parenchymal changes due to cirrhosis or depositional diseases. Magnetic resonance (MR) imaging with appropriate sequences (eg, chemical shift techniques) has similarly high sensitivity, and MR spectroscopy provides unique advantages for some applications. However, both are expensive and too complex to be used to monitor steatosis.

Hepatic parenchymal changes and histologic eosinophilia as predictors of subsequent acute liver allograft rejection

During the first episode of acute cellular rejection (ACR) after liver transplantation, centrilobular changes in liver biopsy specimens may be possible indicators of subsequent episodes of ACR, early chronic rejection, or acute graft loss. The purpose of this study was to identify differences between the histopathological findings in liver biopsy specimens obtained during the first rejection episode in patients who subsequently developed further episodes of ACR and those who did not. The histopathological findings in 22 patients who had a single episode of acute rejection (group 1) were compared with those in 23 patients who had multiple episodes of acute rejection (group 2). Only the first liver biopsy samples of the latter group were taken into consideration. We assessed the predictive value of centrilobular necrosis, central vein endothelialitis, pericentral inflammation, hepatocellular ballooning, cholestasis, hepatocellular apoptosis, lobular inflammation, the degree of portal eosinophilia, and characteristic portal tract features in poor responders to antirejection treatment. The time to the first episode of ACR and the rejection activity index were similar in patients in both groups. Hepatocellular apoptosis, hepatocellular ballooning, and central vein endothelialitis were common features of both groups. The incidences of pericentral inflammation, centrilobular necrosis, and portal eosinophilia were significantly higher in patients in group 2 than in those in group 1 (P < 0.05). Patients with pericentral inflammation, centrilobular necrosis, and marked portal eosinophilia during an initial episode of acute rejection may be more likely to develop subsequent episodes of ACR.

EXPERIMENTAL MODELS OF HEPATECTOMY AND LIVER REGENERATION USING NEWBORN AND WEANING RATS

Liver regeneration is a complex process that has not been completely elucidated. The model most frequently used to study this phenomenon is 70% hepatectomy in adult rats; however, no papers have examined this effect in developing animals. The aims of the present study were: 1) to standardize two models of partial hepatectomy and liver regeneration in newborn suckling and weaning rats, and 2) to study the evolution of remnant liver weight and histological changes of hepatic parenchyma on the days that follow partial hepatectomy. Fifty newborn and forty-four weaning rats underwent 70% hepatectomy. After a midline incision, compression on both sides of the upper abdomen was performed to exteriorize the right medial, left medial and left lateral hepatic lobes, which were tied inferiorly and resected en bloc. The animals were sacrificed on days 0 (just after hepatectomy), 1, 2, 3, 4 and 7 after the operation. Body and liver weight were determined, and hepatic parenchyma was submitted to histological analysis. Mortality rates of the newborn and weaning groups were 30% and 0%, respectively. There was a significant decrease in liver mass soon after partial hepatectomy, which completely recovered on the seventh day in both groups. Newborn rat regenerating liver showed marked steatosis on the second day. In the weaning rat liver, mitotic figures were observed earlier, and their amount was greater than in the newborn. Suckling and weaning rat models of partial hepatectomy are feasible and can be used for studies of liver regeneration. Although similar, the process of hepatic regeneration in developing animals is different from adults.

Arterioportal Fistulas: Introduction of a Novel Classification With Therapeutic Implications

Arterioportal fistulas (APFs) are arteriovenous communications between the splanchnic arteries and the portal vein that represent an infrequent cause of presinusoidal portal hypertension. They can be acquired or congenital. Penetrating hepatic trauma, including liver biopsies, represent the most common etiology. They can be asymptomatic or manifest with portal hypertension. An abdominal bruit is a valuable physical finding. Persistence of an APF can cause hepatoportal sclerosis and possibly portal fibrosis. A detailed radiologic evaluation is mandatory. One must differentiate between small peripheral intrahepatic APFs (type 1) and large central APFs (type 2). The former usually resolve spontaneously, whereas the latter can cause portal hypertension and hepatic parenchymal changes. Type 1 APFs caused by needle injury can be followed by Doppler ultrasound. All other fistulas need treatment. Arterioportal fistulas are first treated by transcatheter embolization. Surgical approaches are reserved for complex cases. Congenital APFs (type 3) are diffuse and intrahepatic and can be difficult to manage. Overall, the prognosis is good. Herein, we propose a novel classification for arterioportal fistulas with therapeutic implications.

Portal vein occlusion or stenosis in patients with hepatolithiasis: observation by multiphasic contrast-enhanced CT

To analyze the dynamic findings of multiphasic contrast-enhanced CT in hepatolithiasis and to elucidate occlusive changes in portal veins and other associated abnormalities. This was a retrospective study of 25 selected patients with hepatolithiasis who underwent various imaging examinations, including multiphasic contrast-enhanced CT. The following CT findings were evaluated in each of 71 hepatic segments: visualization of a calculus; biliary dilation or focal hepatic atrophy of the affected segment; areas that were abnormally enhanced in the hepatic arterial phase; degrees (normal, stenosis, occlusion) of portal vein calibre; and linear delayed enhancement along the bile-duct walls, suggesting cholangitis. On CT, calculi were depicted as a hyperdense structures in 61 of 71 segments (86%). Focal hepatic atrophy, which frequently accompanied CT findings suggesting compensatory hypertrophy of other segments, was seen in 50 of 71 segments (70%). Areas that were abnormally enhanced were recognized in 36 of 71 segments (51%). Stenosis or occlusion of portal venous branches was observed in 59 of 71 segments (83%), including 13 segments with occlusion. Findings indicating cholangitis were noted in 50 of 71 segments (70%). The degrees of portal vein calibre were significantly correlated with the presence of hepatic atrophy or cholangitis. Hepatolithiasis is associated with significant rates of stenosis or occlusion of adjacent portal veins as well as hepatic parenchymal changes in the affected area. Chronic deterioration of portal flow may cause these morphological changes.

`Nipped in the Budd'

Hepatic venous thrombosis (Budd-Chiari) in evolution is a rare phenomenon and carries a high morbidity and mortality. We describe the case of a 39-year-old Bangladeshi lady who presented with severe abdominal pain secondary to a perforated duodenal ulcer and during her hospital admission developed an asymptomatic Budd-Chiari syndrome (BCS). Our report highlights the important role of an inflammatory focus, and how this process with an associated reactive thrombocytosis may act as a trigger for the development of BCS in an individual with predisposing risk factors. Our patient had been on the contraceptive pill, and was homozygous for the C677T mutation of 5,10-methylenetetrahydrofolate reductase, which results in hyperhomocysteinaemia. These pro-thrombotic risk factors were compounded by the thrombogenic potential of subsequent laparoscopic surgery, and resulted in an evolving thrombus that progressed into the inferior vena cava causing hepatic infarction. A particular feature of this case was the radiological demonstration of complete regression of the thrombus and the hepatic parenchymal changes, upon resolution of the inflammation and normalization of the platelet count. These changes occurred with oral anticoagulation as the only treatment modality, since our patient declined systemic thrombolysis. The demonstration of complete radiological resolution raises the question of how long one should continue oral anticoagulants and, indeed, whether in some instances a conservative approach may be the best management strategy for evolving BCS.

Technique, Complications, and Therapeutic Efficacy of Percutaneous Transplantation of Human Pancreatic Islet Cells in Type 1 Diabetes: The Role of US

To retrospectively evaluate the role of ultrasonography (US) with regard to the technique, complications, and therapeutic efficacy of percutaneous intrahepatic transplantation of human pancreatic islet cells with combined US and fluoroscopic guidance. The institutional review board approved the study, and informed consent was obtained from all patients. After kidney transplantation, 34 uremic diabetic patients (20 men, 14 women; mean age, 40.9 years; age range, 29-61 years) underwent percutaneous intrahepatic transplantation of islet cells. Portal vein patency and liver echotexture were preliminarily assessed with color Doppler US. US also was used to identify early complications and presence (group A patients) or absence (group B patients) of hepatic parenchymal changes. Differences between the two groups in C peptide serum level and range were analyzed (Mann-Whitney test). Therapeutic efficacy of transplantation was assessed with regard to insulin independence period (rate and duration), exogenous insulin requirement, glycated hemoglobin, and C peptide level. A C peptide level of more than 0.5 ng/mL was considered to indicate well-functioning islet cells. Fifty-eight procedures were technically successful, with a single puncture used in 51 of 58 patients. Complications occurred in three of 58 patients (hemoperitoneum, hemothorax, and thrombosis in one patient each) and were conservatively treated and resolved. Duration of insulin independence in 12 patients was more than 3 months (mean, 21 months). Well-functioning islet cells at 6 years were found in 19 of 34 patients. Hyperechoic parenchymal changes were evident at US in 12 of 34. No statistically significant difference in C peptide level was found between groups (P > .05), but a wider range of values was recorded in group B. Complication rate of transplantation with US and fluoroscopic guidance was low. Well-functioning islet cells were found in about 50% of patients at 6 years of follow-up. Hepatic implantation of islet cells was evident on US images in more than one-third of patients.

Arterial and portal circulation and parenchymal changes in Budd-Chiari syndrome: A study in 17 explanted livers

Hepatic parenchymal changes associated with Budd-Chiari syndrome (BCS) have been tentatively explained by combined arterial and portal perfusion disturbances in addition to the complete occlusion of hepatic veins. The aim of this study was to correlate pretransplant course and vascular imaging with pathologic findings in livers explanted for BCS. Seventeen consecutive white patients who underwent transplantation for severe classic BCS were retrospectively analyzed. Pretransplant course was 1 year or less in 8 patients and more than 1 year in 9 patients. Thrombophilia was found in 16 patients (94%). Imaging showed decreased portal perfusion in 16 patients (94%) and increased arterial perfusion in 9 patients. Histology showed obstructive portal venopathy and nodular regenerative hyperplasia (NRH) aspects in all cases, large regenerative nodules resembling focal nodular hyperplasia (FNH) in 9 cases, and cirrhosis in 2 cases. Patients with increased arterial inflow had large regenerative nodules and a protracted pretransplant course. Patients with acute thrombi in portal veins had parenchymal infarcts (2 cases) and a short pretransplant course. In conclusion, patients with severe BCS have a constant impaired perfusion inflow unrelated to progression of cirrhosis but related to the outcome. An early decrease in portal perfusion is observed in the short term and is responsible for NRH or infarcts if complicated with large thrombi. An increase in arterial perfusion compensates impaired portal flow in chronic BCS. Arterial hyperemia contributes to the development of large regenerative nodules that are FNH-like. This pathologic situation offers an interesting vascular model to further understand the parenchymal response to changes in hepatic blood flow. (H EPATOLOGY 2003;37:510-519.)

Perfusion changes of hepatic parenchyma due to infectious hepatobiliary disease: demonstration by perfusion CT

We present two cases, in which perfusion CT demonstrated diffusely increased arterial and decreased portal perfusion of the liver parenchyma around liver abscess and infectious bilomas. These cases suggested that perfusion CT may be useful for a quantitative analysis of perfusion changes in infectious hepatobiliary diseases with good anatomical detail.

Experimental Monitoring of Hepatic Glucose, Lactate, and Glutamate Metabolism by Microdialysis during Surgical Preparation of the Liver Hilus

Mechanical liver manipulation can lead to hepatic microcirculation (MC) impairment. The pathobiochemical relevance of this phenomenon is not fully understood. Microdialysis (MD) allows a quantification of metabolic products in interstitial fluid, thus enabling analysis of the hepatic metabolic state during changes of liver perfusion. The aim of the study was to quantify the functional effects of standardized surgical liver preparation both on liver metabolism and microperfusion.Two groups of animals (pigs, n = 25) were formed: In the trial group (TG; n = 13) the liver was mobilized, followed by hilar preparation. In the control group (CG; n = 12) mobilization of the liver without hilar dissection was performed. Surgical manipulation was followed by an observation in both groups. Hepatic interstitial glucose, lactate, and glutamate concentrations were detected by MD and liver MC by thermodiffusion.During liver mobilization MC decreased significantly in both groups (TG; 86.7 ± 2.0 to 73.4 ± 2.3 ml/100 g min; and CG; 88.3 ± 3.1 to 71.9 ± 2.2 ml/100 g/min). In the trial group levels decreased further during hilar preparation reaching minimal values of 65.6 ± 2.8. After preparation MC recovered to baseline. Glucose, lactate, and glutamate concentrations increased significantly during liver mobilization in the trial (glucose; 0.52 ± 0.13 to 0.88 ± 0.19 mmol/L; lactate; 0.34 ± 0.07 to 0.54 ± 0.07 mmol/L; glutamate; 34.5 ± 3.6 to 52.6 ± 8.0 μmol/L) and control group (glucose; 0.58 ± 0.06 to 0.95 ± 0.13 mmol/L; lactate; 0.30 ± 0.06 to 0.49 ± 0.07 mmol/L; glutamate; 32.9 ± 2.36 to 56.1 ± 5.12 μmol/L). Throughout hilus preparation maximum values could be measured in TG (glucose; 1.69 ± 0.34; lactate; 0.90 ± 0.18; glutamate; 63.5 ± 7.2). After termination of mobilization or preparation baseline concentrations were reached again.MD allows monitoring of metabolic changes in hepatic parenchyma. Surgical liver preparation leads to changes of intrahepatic glucose, lactate, and glutamate levels (without alterations of parameters in systemic plasma) along with hepatic MC impairment. Reconstitution of hepatic MC was accompanied by rapid normalization of metabolic parameters. By measuring specific parameters, MD could prove to be of use for functional assessment of metabolic effects due to MC disturbances.

Bile duct injuries leading to portal vein obliteration after transcatheter arterial chemoembolization in the liver: CT findings and initial observations.

To document the computed tomographic (CT) findings of transcatheter arterial chemoembolization (TACE)-induced, localized bile duct injuries leading to portal vein branch obliteration in the liver and to elucidate the clinical implications with retrospective review of the authors' experiences. Follow-up CT scans obtained in 11 patients with TACE-induced intrahepatic bile duct dilatation were reviewed retrospectively to evaluate serial changes in the adjacent portal vein branches and hepatic parenchyma. Clinical data, including time between TACE and CT and serum alkaline phosphatase levels, also were analyzed. Of 11 patients with marked (n = 8) or mild (n = 3), lobar (n = 4) or segmental (n = 7) bile duct dilatation with or without bile collection in the tissue sheaths of the Glisson capsule or hepatic parenchyma, nine (82%) had bile duct changes at the first CT follow-up, within 1 month after TACE. Marked narrowing or obliteration of the adjacent intrahepatic portal vein branches in 10 (91%) patients resulted in progressive atrophy of the corresponding hepatic parenchyma in nine (82%) at variable times after TACE. The serum alkaline phosphatase level increased to more than 200 U/L in eight (89%) of nine patients 1 month after TACE. TACE-induced intrahepatic bile duct injury resulting in obliteration of the adjacent portal vein branch seems to be one cause of hepatic parenchymal atrophic changes after TACE.

CT appearance of hepatic parenchymal changes after percutaneous microwave coagulation therapy for hepatocellular carcinoma.

The purpose of this study was to evaluate the changes in the CT appearance of the hepatic parenchyma surrounding the necrotic area in the early period after percutaneous microwave coagulation therapy (PMCT) for hepatocellular carcinoma (HCC). We reviewed enhanced CT scans obtained before and within 2 weeks, at 1 month, and at 3 months after PMCT of 61 lesions in 47 patients with HCC. On dynamic CT, early enhancement of the hepatic parenchyma around the treated area was a frequent finding within 1 (87%) or 2 (68%) weeks after PMCT, but such enhancement disappeared on follow-up. Arterioportal shunts were also demonstrated by enhanced CT after treatment (21% at < or =2 weeks), and these shunts tended to persist for >1 month. We should evaluate the effect of PMCT by performing dynamic enhanced CT not only within 2 weeks to determine the end-point of treatment but also at 1 month or more after finishing treatment for definite assessment of tumor necrosis.

Changes in the liver parenchyma after proton beam radiotherapy: evaluation with MR imaging

The objective of this study was to describe magnetic resonance (MR) findings with a 1.5T imager for hepatic parenchymal changes after proton beam radiotherapy. Thirty-two patients who received proton radiotherapy with doses of 50–87 Gy underwent MR imaging 1–75 months (mean 22 months) after the start of irradiation. Axial T 2, T 1-weighted imaging, and a dynamic study after a gadolinium injection were performed. The irradiated areas showed hypointense in T 1-weighted images, hyperintense in T 2-weighted images, and intense and prolonged enhancement on the dynamic study (maximum relative enhancement 441.8% ± 263.3 vs. surrounding liver 145.6% ± 67.7, p < 0.0001). T 2 values of the irradiated areas were 50.6 to 65.8 msec greater than in the surrounding liver ( p < 0.005). The values increased with time, being significantly greater 13 months or longer after the beginning of the therapy than after a period of less than 3 months ( p < 0.05). Pathologic examinations ( n = 3) indicated that the irradiated areas were composed of collapsed lobules with hepatic small vein occlusions, and rich extracellular matrices which retained extracellular fluid. MR imaging can demonstrate hepatic parenchymal changes after proton beam radiotherapy, and show the changes are irreversible.

Perilesional enhancement of hepatic metastases: correlation between MR imaging and histopathologic findings-initial observations.

To correlate perilesional enhancement on gadolinium-enhanced magnetic resonance (MR) images with histopathologic findings in patients with hepatic metastases. In seven patients with histopathologically proved hepatic metastases, MR images obtained before and early and late after the administration of gadopentetate dimeglumine were retrospectively evaluated for perilesional enhancement. The thickness of hepatic parenchyma with intense perilesional enhancement was calculated. The thickness of the histologic tumor border (the zone separating the outermost border of the tumor nodule from the surrounding hepatic parenchyma) also was measured. In three patients, early gadolinium-enhanced images showed prominent perilesional enhancement, which correlated with a thick tumor border containing peritumoral desmoplastic reaction, peritumoral inflammation, and vascular proliferation at histopathologic examination. In one patient, mild perilesional enhancement was shown. At histopathologic examination, the lesion periphery showed moderate peritumoral changes. In the remaining three patients, no perilesional enhancement was observed, and at histopathologic examination there was a thin tumor border that contained minimal to mild perilesional changes. The thickness of hepatic parenchyma with intense perilesional enhancement on early gadolinium-enhanced images showed a strong positive correlation with tumor border thickness at histopathologic examination (r = 0.99). Intense perilesional enhancement of metastases on early gadolinium-enhanced MR images correlates with histopathologic hepatic parenchymal changes, which include peritumoral desmoplastic reaction, inflammatory cell infiltration, and vascular proliferation.

Dynamic MR follow-up of small hepatocellular carcinoma after percutaneous ethanol injection therapy.

For patients with small hepatocellular carcinomas (HCCs) treated by percutaneous ethanol injection (PEI) therapy, dynamic MRI has been performed to evaluate the therapeutic efficacy at our institute. In this pictorial essay, we illustrate the various dynamic MR findings of HCCs after PEI therapy, including complete necrosis, partial necrosis, local recurrence, and pathologic conditions such as arterioportal shunt and contractive changes of hepatic parenchyma. We also present the limitation of dynamic MRI in the evaluation of therapeutic effectiveness of PEI therapy.

MR signal intensity changes in hepatic parenchyma with ductal dilation caused by intrahepatic cholangiocarcinoma.

MR images of the liver in 13 patients with surgically proven intrahepatic cholangiocarcinoma were reviewed retrospectively and correlated to the histologic analysis of surgical specimens. We paid special attention to the peripheral liver tissue with ductal dilation but without tumorous involvement. High signal intensity was observed in the hepatic parenchyma with ductal dilation on T1-weighted spin-echo images (8 of 12) and spoiled gradient-recalled echo images (seven of seven), as compared with the contralateral hepatic lobe without duct dilation. The high signal intensity was not suppressed with fat saturation and showed enhancement after administration of contrast (11 of 12). Concurrent portal venous obstruction did not have significant effect on these findings (P < .05). Correlation with pathologic specimens suggested that this enhancement was associated with periportal fibrosis. The etiology of the high signal intensity on unenhanced spin echo or gradient-recalled T1-weighted image remains unclear. Radiologists should recognize these findings and should distinguish these from tumor involvement or the arterial buffer response caused by portal venous obstruction.

Hepatic parenchymal changes after ethanol injection in rabbits: correlation of conventional and dynamic MR imaging with pathologic findings.

The purpose of this study is to clarify the changes of peripheral normal liver parenchyma before and after ethanol injection, with respect to MR appearances and pathologic findings and, in so doing, to clinically evaluate the therapeutic effectiveness of percutaneous ethanol injection (PEI) therapy. The normal liver in 12 rabbits was injected with ethanol. We performed conventional and dynamic MR imaging and prepared the histopathologic specimens 1 week (group 1), 2 weeks (group 2), and 1 month (group 3) after ethanol injection. On conventional MR images, coagulative necrosis in the normal liver was demonstrated as an area of low signal intensity on T1-weighted images and high signal intensity on T2-weighted images in all groups. On dynamic MR images, contrast enhancement in the coagulative necrosis was not seen in groups 1 and 2; however, gradual and concentric enhancement was seen in the direction of the central necrotic portion from early-to-delayed phase image in group 3. Although signal intensity of the coagulative necrotic area in the normal liver after ethanol injection may mimic that of untreated or viable hepatocellular carcinoma (HCC) when clinically encountered on conventional MR images, coagulative necrosis of the normal liver parenchyma will be discriminated from viable HCC by using dynamic MR imaging.

Three cases of primary biliary cirrhosis associated with bronchial asthma

The association of primary biliary cirrhosis (PBC) and bronchial asthma was observed in three patients. All of these patients were female (53, 54, and 41 years old, respectively), and were positive for antimitochondrial antibodies. The patients fulfilled the diagnostic criteria of both PBC and bronchial asthma. Bronchial asthma preceded PBC in two patients, and the reverse order was seen in the other. Patient the clinical symptoms were mainly due to the bronchial asthma. Two patients had asymptomatic PBC and the third patient complained of pruritus. The liver histology showed mild to moderate eosinophilic infiltration in addition to the ductal and hepatic parenchymal changes characteristic of PBC. A survey of 266 cases of PBC referred to us disclosed that, in 6 of these, the PBC was associated with bronchial asthma, while no association with bronchial asthma was the material of found in 166 patients with viral hepatitis in our liver biopsy files. The 3 present cases we experienced suggest that bronchial asthma may be included in the list of extrahepatic diseases associated with PBC. The significance of this association is unclear and may merit further study. Steroid therapy, which is known to cause adverse effects in PBC, was employed for bronchial asthma in these 3 patients. Another therapeutic approach will have to be considered in patients with bronchial asthma associated with PBC.

Hepatic ultrasonic changes in workers exposed to perchloroethylene.

To determine if subclinical hepatotoxicity is associated with exposure to perchloroethylene at concentrations commonly experienced in the workplace, and whether surveillance with serum hepatic transaminase activity underestimates such effects. Hepatic parenchymal echogenicity on ultrasonography and serum hepatic transaminase activity were compared in 29 community based dry cleaning operators exposed to perchloroethylene, and a control group of 29 non-exposed laundry workers. Perchloroethylene exposure was assessed by work history and air monitoring. Mean hepatic transaminase activities were minimally increased in dry cleaners compared with laundry workers. Increased alanine aminotransferase activities, between 1.0 and 1.5 times the normal limits, were found in five of 27 (19%) dry cleaners compared with one of 26 (4%) laundry workers. In contrast, diffuse parenchymal changes in echogenicity, as determined by hepatic ultrasonography, were increased nearly twofold in dry cleaners, occurring in 18 of 27 (67%) dry cleaners compared with 10 of 26 (39%) laundry workers (P < 0.05), and were most strongly associated with increased perchloroethylene exposure in older dry to dry or wet transfer operations (odds ratio 4.2, 95% confidence interval 1.1-15.3). Mean eight hour time weighted average perchloroethylene exposure for dry cleaners was 16 ppm, which is less than the permissible exposure limit of 100 ppm in the United States. It was concluded that mild to moderate hepatic parenchymal changes occur more frequently in workers exposed to perchloroethylene than in populations not exposed to chemical solvents, and that these effects are underestimated by serum hepatic transaminase activity.

Hepatic ultrasound findings in the glycogen storage diseases

Hepatic ultrasonography was performed on 70 patients with the hepatic glycogen storage diseases (GSDs) to assess parenchymal echogenicity. 27 patients had GSD-I, 24 had GSD-III and 19 had GSDs-VI/IX; ages varied from 0.6 to 35.7 years (median 11.7). 31 (44%) had normal or mild parenchymal changes, and 41% (11/27) of those with GSD-I, 25% (6/24) with GSD-III and 11% (2/19) with GSDs-VI/IX had marked changes. No relationships were found between the ultrasonographic appearances and other indices of metabolic control, including plasma triglycerides, total cholesterol or height standard deviation score. Seven adult patients (21-29 years) were found to have hepatic tumours: six with GSD-I and one with GSD-III. Those with GSD-I and tumours tended to have the more severe hepatic parenchymal changes. We conclude that ultrasonography may be useful in identifying patients with GSD-I at risk of hepatic tumour formation.