Over a two year period, 323 livers were examined using ultrasound. Majority of these cases were icteric and ultrasound could distinguish obstructive from non-obstructive jaundice. Primary and secondary liver tumours were also detected. Liver abscesses, and radiolucent gallstones were picked up by ultrasound, the areas under study being scanned using standard methods as outlined by various ultrasonographists.
The changes in serum prealbumin (transthyretin) and serum albumin in acute and chronic liver diseases were investigated. Albumin has long been used as a useful indicator of liver function but serum prealbumin has recently been noted for its clinical significance in acute liver diseases. Serum prealbumin concentrations and liver function tests (albumin, bilirubin, alanine aminotransferase) were determined on blood obtained from normal donors (n = 148) and from patients suffering from liver diseases (n = 78) such as acute viral hepatitis, chronic active hepatitis, cirrhosis and hepatoma. The mean serum prealbumin concentration in normal subjects was 29.6 +/- 4.82 mg/dl while the mean serum prealbumin concentration in patients with liver disease was greatly reduced (acute viral hepatitis = 15.3 +/- 7.4mg/dl; chronic active hepatitis = 10.2 +/- 6.6mg/dl; cirrhosis = 9.9 +/- 6.4mg/dl and hepatoma = 10.7 +/- 4.2). Albumin concentrations dropped slightly (13% compared to control) in acute viral hepatitis but dropped markedly (28% compared to control) in chronic liver diseases. The study suggests that serum prealbumin concentration might be a more sensitive indicator than albumin in assessing liver dysfunction in acute liver diseases.
A case of symptomatic polycystic liver disease treated by fenestration and segmental liver resection is reported. The intraoperative use of ultrasound to define the plane of liver resection is emphasised. No significant post-operative complication was encountered. The clinical presentation, management and treatment are discussed.
A pilot epidemiologic study of all cases of Reye and Reye-like syndromes was undertaken at 8 representative major hospitals in Peninsular Malaya from January 1st to December 31st 1986. The cases were classified as definitive Reye's syndrome, clinical Reye's syndrome and encephalo-hepatopathies. Less than 50% of cases reviewed fulfilled the National Center for Disease Control criteria for clinical Reye's syndrome. Causes of Reye-like syndromes/encephalo-hepatopathies included fulminant hepatitis, Japanese B encephalitis, dengue, septicaemia, and complex febrile fits. It was not possible to differentiate clinical Reye's syndrome from the other encephalo-hepatopathies by either the clinical features (except for jaundice) or biochemical parameters. Liver biopsy is necessary for a definitive diagnosis of Reye's syndrome in Malaysia, because of the high prevalence of Reye-like diseases. The mortality rate in the 2 groups of patients is similar. Ingestion of salicylates was not found to be significantly associated with Reye and Reye-like syndromes in this study.
Liver involvement, a common feature in childhood mitochondrial hepatopathies, particularly in the neonatal period, may manifest as neonatal acute liver failure, hepatic steatohepatitis, cholestasis, or cirrhosis with chronic liver failure of insidious onset. There are usually significant neuromuscular symptoms, multisystem involvement, and lactic acidemia. The liver disease is usually progressive and eventually fatal. Current medical therapy of mitochondrial hepatopathies is largely ineffective, and the prognosis is usually poor. The role of liver transplantation in patients with liver failure remains poorly defined because of the systemic nature of the disease that does not respond to transplantation. Several specific molecular defects (mutations in nuclear genes such as SCO1, BCS1L, POLG, DGUOK, and MPV17 and deletion or rearrangement of mitochondrial DNA) have been identified in recent years. Prospective, longitudinal multicenter studies will be needed to address the gaps in our knowledge in these rare liver diseases.
Primary tumours of the liver are uncommon in childhood. Of these, more than two-thirds are malignant. As such, benign hepatic tumours are often not considered in the differential diagnosis of a hepatic mass in childhood. We report a case of hepatic mesenchymal hamartoma, a rare benign tumour, in a 10-month-old infant. This tumour is characterised by an admixture of ductal structures within a copious loose connective tissue stroma. Only approximately 160 cases had been reported in the literature. Awareness of the ultrasound (U/S) and computed tomography (CT) features, although not diagnostic, is helpful in distinguishing it from the more common malignant tumours. A correct preoperative diagnosis is important as surgical excision is often curative.
The incidence of obesity is increasing in Asia, with implications on gastrointestinal (GI) and liver diseases. The Gut and Obesity in Asia Workgroup comprises regional experts with the aim of studying relationship between obesity and the GI and liver diseases in Asia. Through literature review and the modified Delphi process, consensus statements examining the impact of obesity on esophageal, gastric, pancreatic, colorectal, and liver diseases, exploring relationship between gut microbiome and obesity, and assessing obesity therapies have been produced by the Gut and Obesity in Asia Workgroup. Sixteen experts participated with 9/15 statements having strong consensus (>80% agreement). The prevalence of obesity in Asia is increasing (100% percentage agreement in brackets), and this increased prevalence of obesity will result in a greater burden of obesity-related GI and liver diseases (93.8%). There was consensus that obesity increases the risk of gastric cancer (75%) and colorectal neoplasia (87.5%). Obesity was also associated with Barrett's esophagus and esophageal adenocarcinoma (66.7%) and pancreatic cancer (66.7%) in Asia. The prevalence of non-alcoholic fatty liver disease (NAFLD) in Asia is on the rise (100%), and the risk of NAFLD in Asia (100%) is increased by obesity. Obesity is a risk factor for the development of hepatocellular carcinoma (93.8%). Regarding therapy, it was agreed that bariatric surgery was an effective treatment modality for obesity (93.8%) but there was less agreement on its benefit for NAFLD (62.5%). These experts' consensus on obesity and GI diseases in Asia forms the basis for further research, and its translation into addressing this emerging issue.
Transforming growth factor beta-1 (TGF-beta-1) is a multifunctional cytokine involved in the regulation of growth and differentiation of both normal and transformed cells. The main aim of this study was to determine whether TGF-beta-1 or alpha fetoprotein (AFP) or the combination of the two is a better indicator for hepatocellularcarcinoma (HCC). Serum TGF-beta-1 and AFP were measured by ELISA in 40 healthy subjects, 23 patients with hepatocellular carcinoma (HCC), 70 patients with hepatitis B, 26 patients with hepatitis C and 16 patients with liver cirrhosis (LC). Patients with liver diseases showed significantly higher serum TGF-beta-1 values (> 3 fold) compared to control subjects. As for serum AFP, significant elevation was only observed for HCC cases. Serum TGF-beta-1 exhibited higher percent sensitivity compared to serum AFP in all liver diseases. Combination of serum TGF-beta-1 and AFP increased specificities in all cases studied. In conclusion, serum TGF-beta-1 is a more sensitive marker for HCC when compared to serum AFP and its specificity is increased when combined with serum AFP.
Here the first case in the literature of both mesenchymal hamartoma and malignant mesenchymoma occurring in a 6-year-old male child, at different times and at different sites in the liver, and also the possible malignant transformation of a mesenchymal hamartoma is reported. The tumor developed from a lesion in the right lobe that was overlooked initially during a left lateral segmentectomy at 18 months of age for a mesenchymal hamartoma. Malignant mesenchymoma is a rare and aggressive tumor. The origin of this tumor is not well understood. There has been no direct support to the hypothesis that malignant mesenchymoma may be the malignant counterpart of mesenchymal hamartoma. The authors provide clinical and histopathologic evidence in our case that suggests the possibility of malignant mesenchymoma arising from a mesenchymal hamartoma. This case emphasizes the need for complete removal of mesenchymal hamartoma and the need for long-term follow-up to detect multifocal lesion or malignant transformation.