Telemedicine as an Option for Monitoring Metabolic Dysfunction-Associated Fatty Liver Disease (MAFLD) Patients Facing the COVID-19 Pandemic: A Systematic Review and Meta-Analysis.

Healthcare visits were reduced during the COVID-19 pandemic, causing disturbances in sustainable MAFLD monitoring. Telemedicine acts to maintain connectivity between patients and healthcare professionals. This review aimed to assess the role of telemedicine in monitoring MAFLD during the pandemic. Databases searched included l PubMed Central and ScienceDirect from 2020 to 2023. Assessment with The Cochrane Risk of Bias for randomized controlled trials (RCTs) and the Newcastle-Ottawa scale for non-RCTs systematic reviews. Meta-analyses employing a random-effect model were performed to determine the pooled mean difference (MD) and p-value. The results showed three RCT and two non-RCT (n = 239) with 56.9% males and a mean age of 51.3 years. The median intervention duration was 5.5 months. The parameters assessed included body weight (BW), body mass index (BMI), waist circumference, liver function (AST/ALT), lipid profile, HbA1c, and others. Meta-analysis revealed that telemedicine had a significant effect on improving outcomes for BW (MD -2.81: 95% CI, -4.11, -1.51, p < 0.0001) and BMI (MD -1.01: 95% CI, -1.47, -0.55, p < 0.0001) compared to standard care, while the AST/ALT levels were not significantly reduced. Some biochemical markers decreased based on the systematic reviews. In conclusion, telemedicine using mobile-based applications could be an option for monitoring lifestyle modification in MAFLD patients facing the COVID-19 pandemic.

Cell sheet transplantation for ischemic heart disease: a systematic review.

Objective: Cell sheet transplantation is emerging as an appealing alternative for ischemic heart disease patients as it potentially can increase stem cell viability and retention. But the outcomes and safety of this treatment are still limited in literature and the result varies widely. We conduct a systematic review to look at the efficacy and safety of this promising transplantation method. Methods: A systematic review was performed according to PRISMA guidelines. A comprehensive literature search was undertaken using the PubMed, Scopus, and Embase databases. Articles were thoroughly evaluated and analyzed. Results: Seven publications about cell sheet transplantation for ischemic heart disease patients were included. The primary outcomes measured were left ventricular ejection fraction (LVEF) and New York Heart Association (NYHA) class. Safety measurement was depicted by cardiac-related readmission and deaths. The follow-up time ranged from 3 to 36 months for clinical outcomes and 8.5 years for safety outcomes. Cell sheet transplantation showed improvement in LVEF and NYHA class in most studies. Cardiac-related readmission and adverse events of cell sheet transplantation range from 0 to 30.4%, all were nonfatal as no cardiac-related death was reported. Patient preoperative status seems can affect the patient's response to cell sheet therapy. Conclusion: Cell sheet transplantation can safely improve LVEF and NYHA class in ischemic heart disease patients, even in very low ejection fraction patients with unsuccessful standard therapy before. Further studies with better patient inclusion, larger population, and long-term follow-up required to confirm these results.

Parathyroid Adenoma in a Young Female Presenting Multiple Fractures and Postoperative Hungry Bone Syndrome.

A young 18-year-old female patient with general bone pain and history of multiple fractures brought her to our medical attention. Laboratory work showed hypercalcemia and high parathyroid hormone levels in the blood. Radiograph imaging revealed severe scoliosis with multiple vertebrae fractures with decreased bone mineral density. Sestamibi showed parathyroid adenoma. This case emphasizes the importance of maintaining a primary hyperparathyroidism as a differential diagnosis when a young patient presents with a multiple pathologic fractures history.

Improvement of Metabolic Parameters Resulted from Levothyroxine Therapy in Hypothyroid Type 2 Diabetes Mellitus Patient.

This is a case of 51 year-old woman with uncontrolled type 2 diabetes mellitus which was diagnosed 1.5 year earlier, obesity with body mass index 32.2 kg/m2, waist circumference of 113 cm, diffuse goiter with neck circumference 40 cm, and hypertension with blood pressure >140/90 mmHg. Since 6 months ago, she often seemed like having less concentration or daydreaming, chronic fatigue, depression, and low food intake. Her body weight had been increasing over time. Her hypothyroidism clinical scoring Billewicz and Zulewski criterias were 17 and 8 respectively, showing that she tended to experience hypothyroidism. From laboratory examination, fasting blood glucose was 216 mg/dL and 2-hour postprandial blood glucose was 320 mg/dL with level of HbA1c was 9.9%, triglyceride level was 486 mg/dL, HDL cholesterol 46 mg/dL, LDL cholesterol 157 mg/dL, and total cholesterol was 269 mg/dL. Thyroid ultrasound showed a diffuse goiter in both lobes of her thyroid gland.

GLP-1 analog liraglutide protects against cardiac steatosis, oxidative stress and apoptosis in streptozotocin-induced diabetic rats.

OBJECTIVE: Accumulating evidence has implicated that GLP-1 may have a beneficial effect on cardiovascular but the mechanism is not fully understood. Here we show that GLP-1 analog, liraglutide, inhibits cardiac steatosis, oxidative stress and apoptosis in streptozotocin (STZ)-induced type 1 diabetic rats, via activation of AMPK-Sirt1 pathway. METHODS: Diabetic rats were treated with subcutaneous injections of liraglutide (0.3 mg/kg/12 h) for 4 weeks. Myocardial steatosis (detected by oil red O staining and myocardial triglyceride and diacylglycerol (DAG) contents assay), expression of protein kinase C (PKC), heart NAD(P)H oxidase activity, oxidative stress markers (8-hydroxy-2'-deoxyguanosine staining), apoptosis (TUNEL analysis) and genes that affect apoptosis and lipid metabolism were evaluated. RESULTS: Administration of liraglutide did not affect plasma glucose and insulin levels or body weights in STZ-induced diabetic rats, but normalized myocardial steatosis, expression of PKC, NAD(P)H oxidase activity, oxidative stress markers and apoptosis, all of which were significantly increased in diabetic hearts. Additionally, expression of genes mediating lipid uptake, synthesis and oxidation were increased in the diabetic hearts, and these increases were all reduced by liraglutide. In addition, liraglutide increased expression of Sirt1 and phosphorylated AMPK in the diabetic hearts. CONCLUSIONS: Liraglutide may have a beneficial effect on cardiac steatosis, DAG-PKC-NAD(P)H pathway, oxidative stress and apoptosis via activation of AMPK-Sirt1 pathway, independently of a glucose-lowering effect.

GLP-1 analog liraglutide protects against oxidative stress and albuminuria in streptozotocin-induced diabetic rats via protein kinase A-mediated inhibition of renal NAD(P)H oxidases.

Accumulating evidence has implicated that GLP-1 may have a beneficial effect on cardiovascular and renal diseases but the mechanism is not fully understood. Here we show that GLP-1 analog, liraglutide, inhibits oxidative stress and albuminuria in streptozotocin (STZ)-induced type 1 diabetes mellitus rats, via a protein kinase A (PKA)-mediated inhibition of renal NAD(P)H oxidases. Diabetic rats were randomly treated with subcutaneous injections of liraglutide (0.3 mg/kg/12 h) for 4 weeks. Oxidative stress markers (urinary 8-hydroxy-2'-deoxyguanosine and renal dihydroethidium staining), expression of renal NAD(P)H oxidase components, transforming growth factor-ß (TGF-ß), fibronectin and urinary albumin excretion were measured. In vitro effect of liraglutide was evaluated using cultured renal mesangial cells. Administration of liraglutide did not affect plasma glucose levels or body weights in STZ diabetic rats, but normalized oxidative stress markers, expression of NAD(P)H oxidase components, TGF-ß, fibronectin in renal tissues and urinary albumin excretion, all of which were significantly increased in diabetic rats. In addition, in cultured renal mesangial cells, incubation with liraglutide for 48 h inhibited NAD(P)H-dependent superoxide production evaluated by lucigenin chemiluminescence in a dose-dependent manner. This effect was reversed by both PKA inhibitor H89 and adenylate cyclase inhibitor SQ22536, but not by Epac2 inhibition via its small interfering RNA. Liraglutide may have a direct beneficial effect on oxidative stress and diabetic nephropathy via a PKA-mediated inhibition of renal NAD(P)H oxidase, independently of a glucose-lowering effect.

Chymase inhibition prevents myocardial fibrosis through the attenuation of NOX4-associated oxidative stress in diabetic hamsters.

UNLABELLED: Aims/Introduction: Diabetic cardiomyopathy entails the cardiac injury induced by diabetes, independent of vascular disease or hypertension. Despite numerous experimental studies and clinical trials, the pathogenesis of diabetic cardiomyopathy remains elusive. Here, we report that chymase, an immediate angiotensin II (AngII)-forming enzyme in humans and hamsters, and NOX4-induced oxidative stress have pathogenic roles in myocardial fibrosis in diabetic hamsters. MATERIALS AND METHODS: Expression of chymase was evaluated in the hearts of streptozotocin (STZ)-induced diabetic hamsters. The impact of chymase-specific inhibitors, TEI-E00548 and TEI-F00806, on myocardial fibrosis, and increased levels of intracardiac AngII, accumulation of 8-hydroxy-2'-deoxyguanosine (an oxidative stress marker in urine and heart tissue) and expression of heart NOX4 in diabetic hamsters were investigated. RESULTS: Myocardial chymase expression was markedly upregulated in STZ hamsters in a glucose-dependent manner. A total of 8 weeks after STZ administration, the diabetic hamsters showed enhanced oxidative stress and NOX4 expression in the heart, in parallel with increased myocardial AngII production. Oral administration of chymase-specific inhibitors, TEI-F00806 and TEI-E00548, normalized heart AngII levels, and completely reversed NOX4-induced oxidative stress and myocardial fibrosis in STZ-induced diabetic hamsters, although they did not affect the activity of the systemic renin-angiotensin system or systolic blood pressure. CONCLUSIONS: Chymase inhibition might prevent oxidative stress and diabetic cardiomyopathy at an early stage by reducing local AngII production. (J Diabetes Invest, doi: 10.1111/j.2040-1124.2012.00202.x, 2012).