Insights on Skin Quality and Clinical Practice Trends in Asia Pacific and a Practical Guide to Good Skin Quality from the Inside Out

ObjectiveWe sought to examine the current skin quality trends and gaps in clinical practice in the Asia Pacific region and develop a practical guide to improve skin quality.MethodsMedical practitioners from 11 countries in the Asia Pacific region completed an online survey on current trends in skin quality treatment. A panel of 12 leading experts convened for a virtual meeting to develop a practical guide for skin quality improvement.ResultsA total of 153 practitioners completed the survey. The four most common skin quality issues were uneven skin tone, skin surface unevenness, skin laxity, and sebaceous gland hyperactivity and enlarged pores. Most practitioners reported using a combination of treatment modalities for each skin quality issue. It was also observed that each treatment modality could be used to treat several skin quality issues. A multimodal approach targeting different interrelated issues across the tissue planes was recommended for balanced results. The panel developed a practical guide for the appropriate combinations and sequence of treatments, and created treatment protocols for specific skin quality outcome goals. The guide employed an “inside-out” approach, treating the deeper tissue planes prior to the superficial layers to achieve harmonious results.LimitationsFuture studies are needed to support the recommended treatment protocols for skin quality improvement.ConclusionThese findings provide valuable insights on current skin quality trends and gaps in clinical practice. The practical guide provides a framework for practitioners to customize their treatment plan according to each patient’s needs.     

The Concept of Intrauterine Programming and the Development of the Neonatal Microbiome in the Prevention of SARS-CoV-2 Infection

The process of intrauterine programming is related to the quality of the microbiome formed in the fetus and the newborn. The implementation of probiotics, prebiotics, and psychobiotics shows immunomodulatory potential towards the organism, especially the microbiome of the pregnant woman and her child. Nutrigenomics, based on the observation of pregnant women and the developing fetus, makes it possible to estimate the biological effects of active dietary components on gene expression or silencing. Nutritional intervention for pregnant women should consider the nutritional status of the patient, biological markers, and the potential impact of dietary intervention on fetal physiology. The use of a holistic model of nutrition allows for appropriately targeted and effective dietary prophylaxis that can impact the physical and mental health of both the mother and the newborn. This model targets the regulation of the immune response of the pregnant woman and the newborn, considering the clinical state of the microbiota and the pathomechanism of the nervous system. Current scientific reports indicate the protective properties of immunobiotics (probiotics) about the reduction of the frequency of infections and the severity of the course of COVID-19 disease. The aim of this study was to test the hypothesis that intrauterine programming influences the development of the microbiome for the prevention of SARS-CoV-2 infection based on a review of research studies.     

Tuberculosis in Transplantation: Diagnosis, Prevention, and Treatment

Tuberculosis should always be taken into consideration as a possible infectious complication in transplant recipients. It is more frequent and fatal, and its diagnosis, prevention, and treatment are more challenging, in transplanted patients, as compared with the general population. Latent infection with M. tuberculosis is indirectly diagnosed by assessing the presence of a specific adaptive immune response, but depending on the assay used, the informative value of immunodiagnostic assays may be limited by the inhibitory action of immunosuppressive medication, and the positive predictive value for progression toward active tuberculosis is generally low. Diagnosis of active tuberculosis is challenging, since symptoms in immunocompromised patients are frequently less pronounced and atypical. Finally, treatment of tuberculosis is complicated by unpredictable drug interactions, drug-related organ toxicities, and development of drug resistance. This review provides an overview of the epidemiological characteristics of posttransplant tuberculosis and summarizes current knowledge on the prevention, diagnosis, and treatment of tuberculosis in transplant recipients.     

Impact of HLA-compatibilities in patients undergoing liver transplantation for HBV-cirrhosis

Liver transplantation (OLT) for end-stage chronic hepatitis-B-virus (HBV) infection is frequently complicated by HBV recurrence. In the present study we investigated whether human leucocyte antigen (HLA)-matching influences the outcome after OLT. In a retrospective analysis we reviewed 84 recipients of liver transplants for end-stage HBV-cirrhosis and complete HLA-typing for outcome after OLT. Follow-up ranges from 1 to 110 months (median = 55.6 months). Immunosuppression consisted of Cyclosporin A (CsA)-based quadruple induction therapy or Tacrolimus-based induction protocols. Immunoprophylaxis with hepatitis B immunoglobulin was started at OLT and continued long-term. Actuarial 1- and 5-yr graft survival figures were 90.5 and 80.4%, respectively. Hepatitis-B recurrence was responsible for 15 of 20 (75%) graft failures. We observed a significantly improved graft survival in patients with more HLA-A, -B compatibilities (p = 0.02), whereas the degree of HLA-DR compatibilities did not influence the outcome. The occurrence of HBV-reinfection was significantly lower in HLA-A, -B matched grafts (p < 0.05). Additionally, graft survival was prolonged in patients with HBV-reinfection and 1 or 2 HLA-B compatibilities when compared with patients with HBV-reinfection and a complete HLA-B mismatch (p = 0.02). In conclusion, this retrospective analysis shows that more HLA-A, -B compatibilities seems to be associated with an improved graft survival in patients after OLT for end-stage HBV infection.     

Glycemia Determines the Effect of Type 2 Diabetes Risk Genes on Insulin Secretion

OBJECTIVE

Several single nucleotide polymorphisms (SNPs) in diabetes risk genes reduce glucose- and/or incretin-induced insulin secretion. Here, we investigated interactions between glycemia and such diabetes risk polymorphisms.

RESEARCH DESIGN AND METHODS

Insulin secretion was assessed by insulinogenic index and areas under the curve of C-peptide/glucose in 1,576 subjects using an oral glucose tolerance test (OGTT). Participants were genotyped for 10 diabetes risk SNPs associated with β-cell dysfunction: rs5215 (KCNJ11), rs13266634 (SLC30A8), rs7754840 (CDKAL1), rs10811661 (CDKN2A/2B), rs10830963 (MTNR1B), rs7903146 (TCF7L2), rs10010131 (WFS1), rs7923837 (HHEX), rs151290 (KCNQ1), and rs4402960 (IGF2BP2).Furthermore, the impact of the interaction between genetic variation in TCF7L2 and glycemia on changes in insulin secretion was tested in 315 individuals taking part in a lifestyle intervention study.

RESULTS

For the SNPs in TCF7L2 and WFS1, we found a significant interaction between glucose control and insulin secretion (all P ≤ 0.0018 for glucose × genotype). When plotting insulin secretion against glucose at 120 min OGTT, the compromising SNP effects on insulin secretion are most apparent under high glucose. In the longitudinal study, rs7903146 in TCF7L2 showed a significant interaction with baseline glucose tolerance upon change in insulin secretion (P = 0.0027). Increased glucose levels at baseline predicted an increase in insulin secretion upon improvement of glycemia by lifestyle intervention only in carriers of the risk alleles.

CONCLUSIONS

For the diabetes risk genes TCF7L2 and WFS1, which are associated with impaired incretin signaling, the level of glycemia determines SNP effects on insulin secretion. This indicates the increasing relevance of these SNPs during the progression of prediabetes stages toward clinically overt type 2 diabetes.Type 2 diabetes is a disorder characterized by chronically elevated blood glucose levels due to insulin resistance and a relative lack of compensatory pancreatic insulin secretion. Environmental triggers such as a sedentary lifestyle, physical inactivity, and increased body weight play an important role in the development of the disease. In this regard, genetics and especially gene-environment interactions play an important role. Recent research revealed more than 25 gene variants leading to a higher risk for the development of type 2 diabetes (1). Interestingly, most of the diabetes risk genes alter β-cell function (1). This supports the hypothesis that the main genetic effect in the development of type 2 diabetes could be impaired insulin secretion. Neither environmental triggers nor genetics alone can explain the multifactorial disease type 2 diabetes, thus a close interaction between both is presumed (2–4). Hence, environmental influences may determine an individual''s susceptibility for single nucleotide polymorphism (SNP) effects, or vice versa genotype may designate a person''s susceptibility toward environmental factors.One “environmental” factor that plays a role early in the pathogenesis of type 2 diabetes is elevated glucose. It is well known that years before type 2 diabetes occurs, glucose control is altered, as reflected by higher fasting glucose and/or higher postprandial glucose (5). High glucose exerts unfavorable effects on insulin sensitivity and secretion, known as glucotoxicity (6,7). On the other hand, elevated glucose levels are needed for the incretin effect. Glucagon-like peptide 1–induced insulin secretion becomes fully active only in the hyperglycemic range (8,9). Incretin-dependent insulin secretion might therefore be of particular importance when compensatory insulin hypersecretion is required.The aim of this study was to investigate whether glycemia influences the effects of genetic variation associated with type 2 diabetes on insulin secretion. We therefore studied 10 genome-wide association study–derived variants that were furthermore found to influence β-cell function in subsequent studies (rev. in 1,10). Of these, 2 (in the TCF7L2 and WFS1 loci) are associated with incretin-stimulated insulin secretion (1). As the magnitude of incretin-stimulated insulin secretion is dependent on elevated glucose levels (8,9), we hypothesized that glucose levels specifically interact with the effect of those SNPs on insulin secretion both in cross-sectional and longitudinal intervention studies.