Abhasnee Sobhonslidsuk

Portal vein thrombosis: a concise review

Portal vein thrombosis (PVT) is an uncommon cause for presinusoidal portal hypertension. Although several predisposing conditions are known to exist in the background of PVT, there still remains a proportion of patients in whom the etiology is not known and the pathogenesis is unclear. In this review we summarize the literature on PVT and present the current knowledge about the precipitating factors of PVT. Further, we discuss the advances in the radiological diagnosis that have improved diagnostic accuracy and are noninvasive. Finally, we discuss the treatment options for patients who have varying extents of thrombosis in the portal vein and specifically focus on PVT that is encountered before and after liver transplantation.

Competing Risks Analysis of Predictors of Delisting Owing to Tumor Progression in Liver Transplant Candidates with Hepatocellular Carcinoma

Orthotopic liver transplantation (OLT) is potentially curative for patients with early stage hepatocellular carcinoma (HCC). However, tumor progression before OLT remains a problem. Ninety‐three patients were listed for transplantation with HCC or diagnosed with HCC following listing between March, 1997 and September, 2001. Modified TNM Stage was I/II in 82 patients and III in 11 patients. Seventy‐one patients (76%) were transplanted with a median waiting time of 3.4 months, and 22 (24%) patients were delisted owing to tumor progression ( 14), noncompliance ( 5), and death from liver failure ( 3). Using a cox model competing risks approach, higher baseline alpha‐fetoprotein (AFP) ≥ 100 ng/mL was the only factor independently associated with a higher hazard rate of delisting owing to tumor progression (p = 0.00003), whereas four separate factors were independently associated with a lower hazard rate of transplantation: more recent listing year (1999–2001, p = 0.010), blood type O (p = 0.013), Stage I HCC (p = 0.029), and serum bilirubin < 4 mg/dL (p = 0.032). By logistic regression, AFP ≥ 100 ng/mL was the only factor that significantly influenced the probability of delisting owing to tumor progression (p = 0.001). In conclusion, the initial AFP level may be useful along with tumor stage in defining an urgency score for liver transplant candidates with HCC.

Liver Stiffness Measurement in Psoriasis: Do Metabolic or Disease Factors Play the Important Role?

Background. An increased prevalence of metabolic syndrome including nonalcoholic fatty liver disease (NAFLD) was reported in psoriasis. NAFLD can progress to nonalcoholic steatohepatitis and fibrosis. Transient elastography (TE) is a noninvasive liver fibrosis assessment. We evaluated the prevalence of significant liver fibrosis or high liver stiffness measurement (LSM) using the LSM cutoff over 7 kPa and its associated factors in psoriatic patients. Methods. Subjects underwent TE and ultrasonography. Univariate and multivariate analysis were performed for the associated factors. Results. One hundred and sixty-eight patients were recruited. Three patients were excluded due to TE failure. Mean BMI was 24.8 ± 4.7 kg/m2. NAFLD, metabolic syndrome, and diabetes were seen in 105 (63.6%), 83 (50.3%), and 31 (18.8%) patients. The total cumulative dose of methotrexate over 1.5 g was seen in 39 (23.6%) patients. Mean LSM was 5.3 ± 2.9 kPa. High LSM was found in 18 (11.0%) patients. Waist circumference (OR: 1.24; 95% CI: 1.11–1.38; P = 0.0002), diabetes (OR: 12.70; 95% CI: 1.84–87.70; P = 0.010), and AST (OR: 1.08; 95% CI: 1.02–1.16; P = 0.017) were associated with high LSM. Conclusion. 11% of psoriatic patients had significant liver fibrosis by high LSM. Waist circumference, diabetes, and AST level were the independent predictors.

Budd-Chiari-like presentation of hepatic adenoma.

Abstract  Hepatic adenoma is a benign tumor characterized by its hypervascularity. Hepatic adenoma tends to occur more frequently in women and is related to the use of contraceptive hormones, androgenic/anabolic steroids, pregnancy, glycogen storage diseases and hemochromatosis. Hepatic venous obstruction, or Budd–Chiari syndrome, is a condition of hepatic vein occlusion that has many causes. A 35‐year‐old woman presented shortly after pregnancy with a huge cystic lesion in the liver. The lesion compressed the hepatic vein and created an early stage of Budd–Chiari syndrome. Tumor resection was carried out successfully. The final diagnosis of this case was multiple hepatic adenomas.

Nucleotide Analogue-Related Proximal Renal Tubular Dysfunction during Long-Term Treatment of Chronic Hepatitis B: A Cross-Sectional Study.

Background. There have been few reports of nucleotide analogue-related renal tubular dysfunction (RTD) in CHB patients. We assessed the prevalence and presentation of nucleotide analogue-related proximal RTD. Methods. A cross-sectional study was performed in CHB patients taking nucleotide analogues. Inclusion criteria were patients who were on adefovir or tenofovir as mono- or add-on therapy with lamivudine (LAM) >1 year. Serum and urine were collected. Fractional excretion of phosphate (FEPO4), uric acid (FEUA), and potassium was calculated. Renal losses were defined based on the criteria: protein (24-hour urine protein >150 mg), glucose (glycosuria with normoglycemia), phosphate (FEPO4 >18%), uric acid (FEUA >15%), potassium (renal potassium losses with hypokalemia), and bicarbonate (normal gap acidosis). Subclinical and overt proximal RTD were defined when 2 and ≥3 criteria presented. Results. Ninety-two patients were enrolled. The mean duration of nucleotide analogue taking was 55.1 ± 29.6 months. Proximal RTD was found in 24 (26.1%) patients (subclinical 15 (16.3%) and overt 9 (9.8%)). The severity of RTD was associated with the duration of nucleotide analogue (P = 0.01). Conclusions. The prevalence of proximal RTD in CHB patients taking nucleotide analogues was 26%. The severity of RTD was associated with the treatment duration. Comprehensive testing is necessary for early detecting nucleotide analogue-related nephrotoxicity.

Urinary Metabolomic Profiling in Chronic Hepatitis B Viral Infection Using Gas Chromatography/Mass Spectrometry

Background: Chronic hepatitis B (CHB) can lead to cirrhosis and hepatocellular carcinoma. The metabolomic profiling has been shown to be associated with pathogenic mechanisms in many medical conditions including CHB. The purpose of this study was to investigate the urine metabolomic profiles in CHB patients by gas chromatography/mass spectrometry (GC/MS). Methods: Urine samples were collected from CHB patients (n = 20) and normal control subjects (n = 20). Metabolite profiles were assessed using GC/MS in conjunction with multivariate statistical analysis, in order to identify biomarker metabolites. Pathway analysis was performed by MetaboAnalyst 3.0 and KEGG database. Results: Twelve out of 377 metabolites were shown to be significantly different between the CHB and normal control groups (p < 0.05). These include palmitic acid, stearic acid, oleic acid, benzoic acid, butanoic acid, cholesterol, glycine, 3-heptanone, 4-heptanone, hexanal, 1-tetradecanol and naphthalene. Multivariate statistical analysis constructed using these expressed metabolites showed CHB patients can be discriminated from healthy controls with high sensitivity (95%) and specificity (85%). All the metabolic perturbations in this disease are associated with pathways of fatty acid, amino acid, bile acid and gut microbial metabolism. Conclusion: CHB patients have a specific urinary metabolomic profile. The abnormalities of fatty acid, amino acid, bile acid, and gut microbial metabolism lead to the development of disease progression. GC/MS-based assay is a promising tool for the metabolomic study in CHB.

Reversal of Proximal Renal Tubular Dysfunction after Nucleotide Analogue Withdrawal in Chronic Hepatitis B

Aims Proximal renal tubular dysfunction (PRTD) is an infrequent complication after nucleotide analogue therapy. We evaluated the outcomes of PRTD and nephrotoxicity after nucleotide analogue withdrawal in chronic hepatitis B (CHB). Methods A longitudinal follow-up study was performed in patients with PRTD after nucleotide analogue discontinuation. Serum and urine were collected at baseline and every 3 months for one year. The fractional excretion of phosphate (PO4), uric acid (UA), and potassium and tubular maximal reabsorption rate of PO4 to glomerular filtration rate (TmPO4/GFR) were calculated. Renal losses were defined based on the criteria of substance losses. Subclinical PRTD and overt PRTD were diagnosed when 2 and ≥3 criteria were identified. Results Eight subclinical and eight overt PRTD patients were enrolled. After nucleotide analogue withdrawal, there were overall improvements in GFR, serum PO4, and UA. Renal loss of PO4, UA, protein, and β2-microglobulin reduced over time. At one year, complete reversal of PRTD was seen in 13 patients (81.2%). Improvements in PRTD were seen in all but one patient. Conclusion One year after nucleotide analogue withdrawal, PRTD was resolved in most patients. Changes in TmPO4/GFR, urinary protein, and β2-microglobulin indicate that urinary biomarkers may represent an early sign of PRTD recovery.

The First Case Series of Combined Liver-Kidney Transplantation (CLKT) fromThailand

From the hospital database, four patients underwent CLKT. Three patients had ESRD and cirrhosis. Causes of cirrhosis were chronic hepatitis B and chronic hepatitis C in two and one patient. The fourth patient underwent CLKT due to subfulminant liver failure and prolonged acute renal failure with severely damaged kidney and required hemodialysis for 5 weeks. The waiting time ranged from 6 to 1988 days. After CLKT, one patient required hemodialysis for 45 days because of prolonged acute tubular necrosis. Mild early liver graft dysfunction occurred in one patient. Induction regimens were IL2-receptor blockers, steroids and tacrolimus in three patients, and steroids combining with tacrolimus in one patient. Maintenance regimens included tacrolimus, mycophenolate mofetil (with or without low-dose prednisolone). One-year graft and patient survival rate was 100%. Median follow-up time was 2.2 years. None developed liver or renal graft rejection. At 6 and 12 months, median creatinine levels were 1.30 and 1.13 mg/dl. At the last visits, median creatinine level was 1.05 mg/dl with median eGFR of 76.45 ml/min. CLKT may be done in the patients with ESRD and viral hepatitis-related cirrhosis even without portal hypertension. Other indication is for patients with acute liver failure with severely damaged ARF.