Adipose Tissue Insulin Resistance Predicts the Severity of Liver Fibrosis in Patients With Type 2 Diabetes and NAFLD.

CONTEXT: Although type 2 diabetes (T2D) is a risk factor for liver fibrosis in nonalcoholic fatty liver disease (NAFLD), the specific contribution of insulin resistance (IR) relative to other factors is unknown. OBJECTIVE: Assess the impact on liver fibrosis in NAFLD of adipose tissue (adipose tissue insulin resistance index [adipo-IR]) and liver (Homeostatic Model Assessment of Insulin Resistance [HOMA-IR]) IR in people with T2D and NAFLD. DESIGN: Participants were screened by elastography in the outpatient clinics for hepatic steatosis and fibrosis, including routine metabolites, cytokeratin-18 (a marker of hepatocyte apoptosis/steatohepatitis), and HOMA-IR/adipo-IR. SETTING: University ambulatory care practice. PARTICIPANTS: A total of 483 participants with T2D. INTERVENTION: Screening for steatosis and fibrosis with elastography. MAIN OUTCOME MEASURES: Liver steatosis (controlled attenuation parameter), fibrosis (liver stiffness measurement), and measurements of IR (adipo-IR, HOMA-IR) and fibrosis (cytokeratin-18). RESULTS: Clinically significant liver fibrosis (stage F ≥ 2 = liver stiffness measurement ≥8.0 kPa) was found in 11%, having more features of the metabolic syndrome, lower adiponectin, and higher aspartate aminotransferase (AST), alanine aminotransferase, liver fat, and cytokeratin-18 (P < 0.05-0.01). In multivariable analysis including just clinical variables (model 1), obesity (body mass index [BMI]) had the strongest association with fibrosis (odds ratio, 2.56; CI, 1.87-3.50; P < 0.01). When metabolic measurements and cytokeratin-18 were included (model 2), only BMI, AST, and liver fat remained significant. When fibrosis stage was adjusted for BMI, AST, and steatosis (model 3), only Adipo-IR remained strongly associated with fibrosis (OR, 1.51; CI, 1.05-2.16; P = 0.03), but not BMI, hepatic IR, or steatosis. CONCLUSIONS: These findings pinpoint to the central role of dysfunctional, insulin-resistant adipose tissue to advanced fibrosis in T2D, beyond simply BMI or steatosis. The clinical implication is that targeting adipose tissue should be the priority of treatment in NAFLD.

Medical Tourism and Postoperative Infections: A Systematic Literature Review of Causative Organisms and Empiric Treatment.

BACKGROUND: Medical tourism has become increasingly globalized as individuals travel abroad to receive medical care. Cosmetic patients in particular are more likely to seek surgery abroad to defray costs. Unfortunately, not all procedures performed abroad adhere to strict hygienic regulations, and bacterial flora vary. As a result, it is not uncommon for consumers to return home with difficult-to-treat postoperative infections. METHODS: A systematic literature review of PubMed, Ovid, Web of Science, and Cumulative Index to Nursing and Allied Health Literature databases was performed to assess the microbiology patterns and medical management of patients with postoperative infections after undergoing elective surgery abroad. RESULTS: Forty-two cases of postoperative infections were reported among patients who underwent elective surgery abroad. Most cases were reported from the Dominican Republic, and the most common elective procedures were abdominoplasty, mastopexy, and liposuction. Rapidly growing mycobacteria such as Mycobacterium abscessus, Mycobacterium fortuitum, and Mycobacterium chelonae were among the most common causes of postoperative infection, with M. abscessus involving 74 percent of cases. Most cases were treated with surgical débridement and a combination of antibiotics. Clarithromycin, amikacin, and moxifloxacin were the most common drugs used for long-term treatment. CONCLUSIONS: When encountering a patient with a history of medical tourism and treatment-refractory infection, rapidly growing mycobacteria must be considered. To increase the likelihood of yielding a diagnostic organism, multiple acid-fast bacilli cultures from fluid and débridement content should be performed. There has been reported success in treating rapidly growing mycobacterial infections with a combination of antibiotics including clarithromycin, amikacin, and moxifloxacin.

Lactobacillus rhamnosus GG increases cyclooxygenase-2 expression and prostaglandin E2 secretion in colonic myofibroblasts via a MyD88-dependent mechanism during homeostasis.

Prostaglandin E2 (PGE2 ) plays a critical role in intestinal mucosal tolerance and barrier integrity. Cyclooxygenase-2 (COX-2)-dependent PGE2 production involves mobilisation of arachidonic acid. Lactobacillus rhamnosus GG (LbGG) is one of the most widely used probiotics reported to colonise the colonic mucosa. LbGG contributes to the protection of the small intestine against radiation injury through the repositioning of mucosal COX-2 expressing cells. However, it is unknown if LbGG modulates PGE2 production in the colonic mucosa under homeostasis and the major cellular elements involved in these processes. Colonic epithelial and CD90+ mesenchymal stromal cells, also known as (myo) fibroblasts (CMFs), are abundant innate immune cells in normal colonic mucosa able to produce PGE2 . Herein, we tested the hypothesis that under colonic mucosal homeostasis, LbGG modulates the eicosanoid pathway resulting in increased PGE2 production in both epithelial and stromal cells. Among the five tested human colonic epithelial cell lines, only exposure of Caco-2 to LbGG for 24 hr led to the mobilisation of arachidonic acid with concomitant increase in the components within the leukotriene and COX-2-dependent PGE2 pathways. By contrast, CMFs isolated from the normal human colonic mucosa responded to LbGG with increased expression of COX-2 and PGE2 in the prostaglandin pathway, but not 5-LO in the leukotriene pathway. Oral gavage of C57BL/6 mice for 5 days with LbGG (5 × 108 Colony-Forming Unit (CFU)/dose) increased COX-2 expression in the colonic mucosa. The majority of cells upregulating COX-2 protein expression were located in the colonic lamina propria and colocalised with α-SMA+ cells corresponding to the CMF phenotype. This process was myeloid differentiation factor-88-dependent, because silencing of myeloid differentiation factor-88 expression in CMFs abrogated LbGG-induced upregulation of COX-2 in culture and in vivo. Taken together, our data suggest that LbGG increases release of COX-2-mediated PGE2 , contributing to the maintenance of mucosal homeostasis in the colon and CMFs are among the major contributors to this process.

Intravascular Papillary Endothelial Hyperplasia (Masson's Tumor): Diagnosis the Plastic Surgeon Should Be Aware of.

Intravascular papillary endothelial hyperplasia (IPEH) or Masson's tumor is a rare benign entity commonly found on the head, neck, and upper extremities. It usually arises within a blood vessel but is considered to be a nonneoplastic reactive process often associated with vascular injury. Typically, IPEHs cause no symptoms and present as slowly growing soft-tissue masses. Given their prevalent location and indolent clinical presentation, the plastic surgeon should be familiar with this rare entity. We are presenting a case of IPEH of the forehead with unusual clinical and pathologic characteristics. Differential diagnosis, special considerations regarding preoperative work-up, and treatment options are discussed.