Search

Background Variants of adiponutrin (PNPLA3) and adiponectin (ADIPOQ) genes were considered to be associated with non-alcoholic fatty liver disease (NAFLD). Although the prevalence of NAFLD is increasing, there are limited numbers of studies about the association in Indonesian population. Objective To confirm whether specific variants of adiponutrin (PNPLA3) and adiponectin (ADIPOQ) genes are associated with NAFLD in Indonesian patients. Methods Data and DNA of 152 participants were obtained from a previous study in Dr. Kariadi Hospital, Semarang, Indonesia. PCR-RFLP analysis was performed for detection of PNPLA3 rs738409 and ADIPOQ rs2241767 variants. The diagnosis and severity of NAFLD were assessed according to NAFLD activity score (NAS) based on histopathology assessment of liverbiopsy. Results Allele G of PNPLA3rs738409 was associated with NAFLD in both bivariate (p=0.009, OR 2.52, CI 95% 1.25–5.07) and multivariate (p=0.008, OR 2.62, CI 95% 1.29%–5.32%) analysis, while ADIPOQ rs2241767 had no significant association. In NAFLD participants, both genotypes showed allele G was higher in the group of possible non-alcoholic steatohepatitis (NASH) – NASH (NAS >2) than in the simple steatosis group (NAS

Background: Double coronary culprit lesions in ST-segment elevation myocardial infarction (STEMI) is uncommon. Despite successful primary percutaneous coronary intervention (PPCI) in all culprit lesions, the clinical outcome remains unfavorable and the possible factors for the outcome are not fully understood. Cases Presentation: We reported four cases of double culprit lesions STEMI underwent PPCI. Patient A, a 62 y.o. male with extensive anterior-inferior STEMI, had total occlusion (TO) at both proximal left anterior descending (LAD) and mid right coronary artery (RCA). Patient B, a 42 y.o. male with extensive anterior-inferior STEMI, had subtotal occlusion (STO) at proximal RCA and TO at proximal LAD. Both of them had RBBB ECG pattern. Patient C, a 67 y.o. male with inferior STEMI had 90% thrombus occlusion at proximal–mid LAD and TO at proximal RCA. Patient D, a 65 y.o. male with anteroseptal STEMI, had STO at proximal LAD and 80% thrombus occlusion at mid left circumflex. The cardiomyocyte infarction biomarkers increased in all patients. Although all of them underwent successful PPCI in all of culprit lesions, they suffered from acute heart failure and two of them experienced recurrent ventricular arrhythmia episodes. One of them (patient A) died two days post PPCI. He was only patient who suffering from total occlusion in LAD and RCA with TIMI thrombus 5 and experienced a total atrioventricular block post-PPCI. Conclusion: STEMI with coronary double culprits have severe clinical outcome, regardless of the successful PCI. The degree of coronary occlusions might be linked to the patient clinical outcome.

Serum uric acid level above 7 mg/dl is defined as hyperuricemia, which gives rise to the monosodium urate (MSU), causing gout and urolithiasis. Hyperuricemia is an independent risk factor as well as a marker for hypertension, heart failure, atherosclerosis, atrial fibrillation, and chronic kidney disease. MSU crystals, soluble uric acid (UA), or oxidative stress derived from xanthine oxidoreductase (XOR) might be plausible explanations for the association of cardio-renovascular diseases with hyperuricemia. In macrophages, MSU activates the Nod-like receptor family, pyrin domain containing 3(NLRP3) inflammasome, and proteolytic processing mediated by caspase-1 with enhanced interleukin (IL)-1β and IL-18 secretion. Soluble UA accumulates intracellularly through UA transporters (UAT) in vascular and atrial myocytes, causing endothelial dysfunction ad atrial electrical remodeling. XOR generates reactive oxygen species (ROS) that lead to cardiovascular diseases. Since it remains unclear whether asymptomatic hyperuricemia could be a risk factor for cardiovascular and kidney diseases, European and American guidelines do not recommend pharmacological treatment for asymptomatic patients with cardio-renovascular diseases. The Japanese guideline, on the contrary, recommends pharmacological treatment for hyperuricemia with CKD to protect renal function, and it attaches importance of the cardio-renal interaction for the treatment of asymptomatic hyperuricemia patients with hypertension and heart failure.