[Corrosions and frostbites].

Thermal burns are by far the most frequent and account for approx. 90% of all burns, while frostbites, chemical and electrical burns (CB) cover the remaining approx. 10%. This review gives an overview of the treatment of corrosions and frostbites. CB and frostbites are relatively rare and prompt initiation of proper treatment is essential for both. CB should be diluted as soon as possible, preferably with a neutralizing solution. Treatment of systemic hypothermia comes before management of peripheral frostbite. Frostbites involve thawing in warm water, followed by vasodilation, thrombolysis and amputation if indicated.

Reconstruction of columella and nasal vestibuli by bilateral nasolabial flaps - A case report.

INTRODUCTION AND IMPORTANCE: The nose is a common location for non-melanoma skin cancers. Resection of such cancers can result in large, multilayer defects that are challenging to reconstruct. The surgical approach is determined by multiple factors and the main goal is to obtain a satisfactory functional and aesthetic result. We present a case of reconstruction of the nasal vestibuli and columella by two transnasal nasolabial flaps. PRESENTATION OF CASE: A 66-year-old male underwent resection of a large squamous cell carcinoma in the right nasal vestibulum that extended through the columella into the left vestibulum. The resection resulted in a multilayer defect including the floor and roof of the right vestibulum, the entire columella, part of the septum cartilage and floor of the left vestibulum. The defect was reconstructed in two stages by bilateral nasolabial flaps, that were brought into the nasal cavity through incisions on the side of the nose and were used to line the vestibuli and sutured to each other medially to form the neocolumella. No complications or surgical site infections were observed. CLINICAL DISCUSSION: Transnasal nasolabial flaps can be used for larger columellar defects. The length of the flaps in our case provided enough tissue to reconstruct the columella as well as the entire vestibular linings. CONCLUSION: We describe a successful reconstruction of the nasal vestibuli and columella with two transnasal nasolabial flaps, which provided an acceptable aesthetic and functional result.

Hepatic microbiome in healthy lean and obese humans.

BACKGROUND & AIMS: Dysbiosis of the gut microbiota in response to an energy-rich Western diet and the potential leak of bacteria and/or bacterial products from the intestine to the liver is perceived as a potential risk factor for the development of non-alcoholic fatty liver disease (NAFLD). We investigated the microbiome in liver biopsies from healthy lean and obese individuals and compared it with their blood microbiome. METHODS: We examined liver biopsies from 15 healthy lean and 14 obese individuals (BMI of 18.5-25 and 30-40 kg/m2, respectively). Bacterial 16S ribosomal DNA (rDNA) was analysed by quantitative polymerase chain reaction (qPCR) and 16S metagenomic sequencing targeting the hypervariable V3-V4 region. Metagenomic analysis was performed using the linear discriminant analysis effect size (LEfSe) algorithm. Data are medians with IQRs in brackets. RESULTS: Histology revealed hepatic steatosis in 13 obese individuals and in 2 lean individuals. A robust signal from qPCR revealed significantly higher amounts of bacterial rDNA copies in liver samples from obese individuals compared with those from lean individuals (148 [118-167] vs. 77 [62-122] 16S copies/ng DNA, p <0.001). Liver biopsies from the obese group were characterised by lower alpha diversity at the phylum level (Shannon index 0.60 [0.55-0.76] vs. 0.73 [0.62-0.90], p = 0.025), and metagenomic profiling revealed a significantly higher proportion of Proteobacteria in this group (81.0% [73.0-82.4%] vs. 74.3% [68.4-78.4%], p = 0.014). CONCLUSIONS: We provide evidence for the presence of bacterial rDNA in the healthy human liver. Based on differences in the hepatic microbiome between obese individuals and healthy lean individuals, we suggest that changes in the liver microbiome could constitute an additional risk factor for the development of NAFLD. LAY SUMMARY: Non-alcoholic fatty liver disease (NAFLD) has become the most common liver disease globally, and new evidence suggests that obesity is associated with a disturbed gut bacterial composition, which may influence the development of NAFLD. We examined the composition of bacterial DNA in liver biopsies from healthy lean and obese individuals and found a different composition of bacterial DNA in liver biopsies from the obese group. We propose that the increased bacterial DNA load in the livers of obese individuals could constitute an early risk factor for the progression of NAFLD. CLINICAL TRIAL NUMBER: NCT02337660.

[Fat embolism syndrome after liposuction and lipoinjection].

Fat embolism syndrome (FES) after liposuction and lipoinjection especially gluteal augmentation is a rare, but potentially life-threatening complication. Plastic surgeons should only inject fat into the superficial planes and stay away from the gluteal veins. The three main symptoms include respiratory distress, neurological symptoms and petechial rash, but many patients fail to develop the classic triad, and there are no specific laboratory findings. As argued in this review, there is currently no specific therapy, so prevention, early detection and supportive care are the main strategies to prevent and treat FES.

Metabolic effects of 1-week binge drinking and fast food intake during Roskilde Festival in young healthy male adults.

AIMS/HYPOTHESIS: Metabolic effects of intermittent unhealthy lifestyle in young adults are poorly studied. We investigated the gluco-metabolic and hepatic effects of participation in Roskilde Festival (1 week of binge drinking and junk food consumption) in young, healthy males. METHODS: Fourteen festival participants (FP) were studied before, during and after 1 week's participation in Roskilde Festival. Fourteen matched controls (CTRL) who did not participate in Roskilde Festival or change their lifestyle in other ways were investigated along a similar timeline. RESULTS: The FP group consumed more alcohol compared to their standard living conditions (2.0 ± 3.9 vs 16.3 ± 8.3 units/day, P < 0.001). CTRLs did not change their alcohol consumption. AUC for glucose during OGTT did not change in either group. C-peptide responses increased in the FP group (206 ± 24 vs 236 ± 17 min × nmol/L, P = 0.052) and the Matsuda index of insulin sensitivity decreased (6.2 ± 2.4 vs 4.7 ± 1.4, P = 0.054). AUC for glucagon during oral glucose tolerance test (OGTT) increased in the FP group (1037 ± 90 vs 1562 ± 195 min × pmol/L, P = 0.003) together with fasting fibroblast growth factor 21 (FGF21) (62 ± 30 vs 132 ± 72 pmol/L, P < 0.001), growth differentiation factor 15 (GDF5) (276 ± 78 vs 330 ± 83 pg/mL, P = 0.009) and aspartate aminotransferase (AST) levels (37.6 ± 6.8 vs 42.4 ± 11 U/L, P = 0.043). Four participants (29%) developed ultrasound-detectable steatosis and a mean strain elastography-assessed liver stiffness increased (P = 0.026) in the FP group. CONCLUSIONS/INTERPRETATION: Participation in Roskilde Festival did not affect oral glucose tolerance but was associated with a reduction in insulin sensitivity, increases in glucagon, FGF21, GDF15 and AST and lead to increased liver stiffness and, in 29% of the participants, ultrasound-detectable hepatic steatosis.

Glucagon Resistance at the Level of Amino Acid Turnover in Obese Subjects With Hepatic Steatosis.

Glucagon secretion is regulated by circulating glucose, but it has turned out that amino acids also play an important role and that hepatic amino acid metabolism and glucagon are linked in a mutual feedback cycle, the liver-α-cell axis. On the basis of this knowledge, we hypothesized that hepatic steatosis might impair glucagon's action on hepatic amino acid metabolism and lead to hyperaminoacidemia and hyperglucagonemia. We subjected 15 healthy lean and 15 obese steatotic male participants to a pancreatic clamp with somatostatin and evaluated hepatic glucose and amino acid metabolism when glucagon was at basal levels and at high physiological levels. The degree of steatosis was evaluated from liver biopsy specimens. Total RNA sequencing of liver biopsy specimens from the obese steatotic individuals revealed perturbations in the expression of genes predominantly involved in amino acid metabolism. This group was characterized by fasting hyperglucagonemia, hyperaminoacidemia, and no lowering of amino acid levels in response to high levels of glucagon. Endogenous glucose production was similar between lean and obese individuals. Our results suggest that hepatic steatosis causes resistance to the effect of glucagon on amino acid metabolism. This results in increased amino acid concentrations and increased glucagon secretion, providing a likely explanation for fatty liver-associated hyperglucagonemia.

Don't Judge a Tumor by Its Biopsy!

Trichoblastomas (TBs) are extremely rare, benign hair germ tumors that can mimic basal cell carcinoma (BCC). They usually arise on the head or neck and have a potential for malignant transformation, albeit it is rare. We report a case of giant TB on the forehead of a 75-year-old otherwise healthy woman. Since the age of 20 she reported a bulge on her forehead, in which a superficial-looking wound had now developed. Initially a dermatologist biopsied the tumor suspecting a BCC, which the histological analyses confirmed. The patient was then referred to the Department of Plastic Surgery for complete excision of the carcinoma, including the large frontal bulge. Surprisingly, the concluding pathology report changed the diagnosis from a BCC to a TB. Current management of most skin lesions relies on the histopathological subtype of a single punch biopsy. Many benign and malignant dermatological entities may mimic BCC, and therefore misdiagnosis can lead to either unnecessary excision or delayed treatment of metastatic disease. Mimics may include various types of nonneoplastic processes, benign adnexal tumors, including TB, or cutaneous carcinomas with basaloid features. A single punch biopsy is not always adequate in making the correct diagnosis. Although it is considered the gold standard, the clinical assessment is just as important. Due to its potential for malignant transformation, it is recommended to excise TB with negative margins.

Hepatic transcriptome signatures in patients with varying degrees of nonalcoholic fatty liver disease compared with healthy normal-weight individuals.

Nonalcoholic fatty liver disease (NAFLD) represents a spectrum of conditions ranging from simple steatosis (NAFL), over nonalcoholic steatohepatitis (NASH) with or without fibrosis, to cirrhosis with end-stage disease. The hepatic molecular events underlying the development of NAFLD and transition to NASH are poorly understood. The present study aimed to determine hepatic transcriptome dynamics in patients with NAFL or NASH compared with healthy normal-weight and obese individuals. RNA sequencing and quantitative histomorphometry of liver fat, inflammation and fibrosis were performed on liver biopsies obtained from healthy normal-weight ( n = 14) and obese ( n = 12) individuals, NAFL ( n = 15) and NASH ( n = 16) patients. Normal-weight and obese subjects showed normal liver histology and comparable gene expression profiles. Liver transcriptome signatures were largely overlapping in NAFL and NASH patients, however, clearly separated from healthy normal-weight and obese controls. Most marked pathway perturbations identified in both NAFL and NASH were associated with markers of lipid metabolism, immunomodulation, extracellular matrix remodeling, and cell cycle control. Interestingly, NASH patients with positive Sonic hedgehog hepatocyte staining showed distinct transcriptome and histomorphometric changes compared with NAFL. In conclusion, application of immunohistochemical markers of hepatocyte injury may serve as a more objective tool for distinguishing NASH from NAFL, facilitating improved resolution of hepatic molecular changes associated with progression of NAFLD. NEW & NOTEWORTHY Nonalcoholic fatty liver disease (NAFLD) is the most common liver disease in Western countries. NAFLD is associated with the metabolic syndrome and can progress to the more serious form, nonalcoholic steatohepatitis (NASH), and ultimately lead to irreversible liver damage. Using gold standard molecular and histological techniques, this study demonstrates that the currently used diagnostic tools are problematic for differentiating mild NAFLD from NASH and emphasizes the marked need for developing improved histological markers of NAFLD progression.

Determinants of Fasting Hyperglucagonemia in Patients with Type 2 Diabetes and Nondiabetic Control Subjects.

BACKGROUND: Fasting hyperglucagonemia can be detrimental to glucose metabolism in patients with type 2 diabetes (T2D) and may contribute to metabolic disturbances in obese and/or prediabetic subjects. However, the mechanisms underlying fasting hyperglucagonemia remain elusive. METHODS: We evaluated the interrelationship between fasting hyperglucagonemia and demographic and biochemical parameters in 106 patients with T2D (31% female, age: 57 ± 9 years [mean ± standard deviation; body mass index (BMI): 30.1 ± 4.4 kg/m2; fasting plasma glucose (FPG): 9.61 ± 2.39 mM; hemoglobin A1c (HbA1c): 57.1 ± 13.1 mmol/mol] and 163 nondiabetic control subjects (29% female; age: 45 ± 17 years; BMI: 25.8 ± 4.1 kg/m2; FPG: 5.2 ± 0.4 mM; and HbA1c: 35.4 ± 3.8 mmol/mol). Multiple linear regression analysis was applied using a stepwise approach with fasting plasma glucagon as dependent parameter and BMI, waist-to-hip ratio (WHR), blood pressure, hemoglobin A1c, FPG, and insulin concentrations as independent parameters. RESULTS: Fasting plasma glucagon concentrations were significantly higher among patients with T2D (13.5 ± 6.3 vs. 8.5 ± 3.8 mM, P < 0.001) together with HbA1c (P < 0.001), FPG (P < 0.001), and insulin (84.9 ± 56.4 vs. 57.7 ± 35.3 mM, P < 0.001). When adjusted for T2D, HbA1c and insulin were significantly positive determinants for fasting plasma glucagon concentrations. Furthermore, WHR comprised a significant positive determinant. CONCLUSIONS: We confirm that fasting plasma glucagon concentrations are abnormally high in patients with T2D, and show that fasting plasma glucagon concentrations are influenced by WHR (in addition to glycemic control and fasting plasma insulin concentrations), which may point to visceral fat deposition as an important determinant of increased fasting plasma glucagon concentrations.