Machine Learning Decision Support for Detecting Lipohypertrophy With Bedside Ultrasound: Proof-of-Concept Study.

BACKGROUND: The most common dermatological complication of insulin therapy is lipohypertrophy. OBJECTIVE: As a proof of concept, we built and tested an automated model using a convolutional neural network (CNN) to detect the presence of lipohypertrophy in ultrasound images. METHODS: Ultrasound images were obtained in a blinded fashion using a portable GE LOGIQ e machine with an L8-18I-D probe (5-18 MHz; GE Healthcare). The data were split into train, validation, and test splits of 70%, 15%, and 15%, respectively. Given the small size of the data set, image augmentation techniques were used to expand the size of the training set and improve the model's generalizability. To compare the performance of the different architectures, the team considered the accuracy and recall of the models when tested on our test set. RESULTS: The DenseNet CNN architecture was found to have the highest accuracy (76%) and recall (76%) in detecting lipohypertrophy in ultrasound images compared to other CNN architectures. Additional work showed that the YOLOv5m object detection model could be used to help detect the approximate location of lipohypertrophy in ultrasound images identified as containing lipohypertrophy by the DenseNet CNN. CONCLUSIONS: We were able to demonstrate the ability of machine learning approaches to automate the process of detecting and locating lipohypertrophy.

Ten-year remission rates in insulin-treated type 2 diabetes after biliopancreatic diversion with duodenal switch.

BACKGROUND: Biliopancreatic diversion with duodenal switch (BPD-DS) confers the highest rate of type 2 diabetes (T2D) remission compared with other bariatric procedures. Previous studies suggest that type of antidiabetic therapy used before surgery and duration of disease influence postsurgical glycemic outcomes. Short-term, progressive improvement in insulin sensitivity and beta-cell function after metabolic surgery in patients with noninsulin-treated T2D has been demonstrated. Whether patients with more advanced disease can achieve sustained remission remains unclear. OBJECTIVE: The aim of this study was to assess long-term glycemic outcomes in insulin-treated patients with T2D after BPD-DS and identify predictors of sustained diabetes remission or relapse. SETTING: University-affiliated tertiary care center. METHODS: Data from 141 patients with insulin-treated T2D who underwent BPD-DS between 1994 and 2006 with 10 years of follow-up data were collected from a prospective electronic database. RESULTS: Follow-up was available in 132 patients (91%). At 10 years after metabolic surgery, 90 patients (68.1%) had a complete remission of diabetes, 3 (2.3%) had a partial remission, 21 (15.9%) had an improvement, and 3 (2.3%) were unchanged in their diabetes status. Fourteen patients died during the 10-year follow-up period. Relapse after an initial period of remission occurred in 15 (11.4%) patients. Insulin discontinuation was achieved in 97%. Duration of diabetes was an independent predictor of nonremission at 10 years. CONCLUSIONS: The BPD-DS maintains remission at 10 years postoperatively in patients with more advanced diabetes. Long-term benefits of the BPD-DS on weight loss and glycemic control should be considered when offering metabolic surgery to patients with insulin-treated T2D.

Exploratory examination of inflammation state, immune response and blood cell composition in a human obese cohort to identify potential markers predicting cancer risk.

Obesity has reached epidemic proportions and is often accompanied by elevated levels of pro-inflammatory cytokines that promote many chronic diseases, including cancer. However, not all obese people develop these diseases and it would be very helpful to identify those at high risk early on so that preventative measures can be instituted. We performed an extensive evaluation of the effects of obesity on inflammatory markers, on innate and adaptive immune responses, and on blood cell composition to identify markers that might be useful in distinguishing those at elevated risk of cancer. Plasma samples from 42 volunteers with a BMI>35 had significantly higher CRP, PGE2, IL-1RA, IL-6 and IL-17 levels than 34 volunteers with normal BMIs. Of the cytokines and chemokines tested, only IL-17 was significantly higher in men with a BMI>35 than women with a BMI>35. As well, only IL-17 was significantly higher in those with a BMI>35 that had type 2 diabetes versus those without type 2 diabetes. Whole blood samples from participants with a BMI>35, when challenged with E. coli, produced significantly higher levels of IL-1RA while HSV-1 challenge resulted in significantly elevated IL-1RA and VEGF, and a non-significant increase in G-CSF and IL-8 levels. T cell activation of PBMCs, via anti-CD3 plus anti-CD28, resulted in significantly higher IFNγ production from volunteers with a BMI>35. In terms of blood cells, red blood cell distribution width (RDW), monocytes, granulocytes, CD4+T cells and Tregs were all significantly higher while, natural killer (NK) and CD8+ T cells were all significantly lower in the BMI>35 cohort, suggesting that obesity may reduce the ability to kill nascent tumor cells. Importantly, however, there was considerable person-to-person variation amongst participants with a BMI>35, with some volunteers showing markedly different values from controls and others showing normal levels of many parameters measured. These person-to-person variations may prove useful in identifying those at high risk of developing cancer.

Pheochromocytoma-Induced Takotsubo Syndrome Treated With Extracorporeal Membrane Oxygenation: Beware of the Apical Sparing Pattern.

A 45-year-old female presents with suspected acute myocardial infarction with cardiogenic shock requiring mechanical circulatory support. Pheochromocytoma-induced atypical Takotsubo syndrome is diagnosed. Clinicians should suspect high catecholamine states as a cause of the basal subtype of atypical Takotsubo syndrome. (Level of Difficulty: Beginner.).

Androgens and the Regulation of Adiposity and Body Fat Distribution in Humans.

The sexual dimorphism in human body fat distribution suggests a causal role for sex hormones. This is of particular importance when considering the role of excess visceral adipose tissue accumulation as a critical determinant of obesity-related cardiometabolic alterations. Scientific literature on the modulation of body fat distribution by androgens in humans is abundant, remarkably inconsistent and difficult to summarize. We reviewed relevant literature on this topic, with a particular emphasis on androgen replacement, androgen effects on selected parameters of adipose tissue function and adipose tissue steroid-converting enzymes. In men, low androgenic status mostly reflected by reduced total testosterone is a frequent feature of visceral obesity and the metabolic syndrome. Regarding testosterone therapy, however, studies must be appreciated in the context of current controversies on their cardiovascular effects. Analyses of available studies suggest that decreases in waist circumference in response to testosterone are more likely observed in men with low levels of testosterone and high BMI at study onset. In women with androgen excess, higher testosterone and free testosterone levels are fairly consistent predictors of increased abdominal and/or visceral adipose tissue accumulation, which is not the case in nonhyperandrogenic women. Regarding mechanisms, androgens decrease adipogenesis and markers of lipid storage in vitro in men and women. Evidence also suggest that local steroid transformations by adipose tissue steroid-converting enzymes expressed in a depot-specific fashion may play a role in androgen-mediated modulation of body fat distribution. Accumulating evidence shows that androgens are critical modulators of body fat distribution in both men and women. © 2018 American Physiological Society. Compr Physiol 8:1253-1290, 2018.

Surgery for Diabetes: Clinical and Mechanistic Aspects.

According to the most recent publication by the Canadian Public Health Agency, obesity affects 25% of adults. In addition, there is a clear association between the recent rise in obesity and the increased prevalence of type 2 diabetes. Medical therapy for obesity has shown limited long-term effectiveness, and surgical treatment is now recognized by medical authorities as part of the armamentarium for the management of type 2 diabetes in severely obese patients. The current indications for obesity surgery and postoperative management are reviewed. The choice of surgery should balance expected benefits associated with weight loss (including remission rate of type 2 diabetes), side effects and the risks for early and long-term complications. Long-term outcomes of metabolic surgery for diabetes vary according to the type of surgery (ranging between 20% and 90% remission rates) and the underlying metabolic changes. Several controlled trials have been published in recent years confirming the superiority of metabolic surgery over medical treatment for the management of type 2 diabetes associated with severe obesity. Some of the known underlying mechanisms of action include a combination of caloric restriction, hormonal changes, decreased nutrient absorption and changes in bile acids, microbiota and incretins. Further research is needed to clarify the mechanistic changes associated with each surgical procedure and their respective long-term outcomes.

Screening, detecting and enhancing the yield of previously undiagnosed hepatitis B and C in patients with acute medical admissions to hospital: a pilot project undertaken at the Vancouver General Hospital.

BACKGROUND: Hepatitis B virus (HBV) and hepatitis C virus (HCV) represent an increasing health burden and morbidity in Canada. Viral hepatitis, specifically HCV, has high prevalence among persons born between 1945 and 1965, with 45% to 85% of infected adults asymptomatic and unaware of their infection. Screening has been shown to be cost effective in the detection and treatment of viral hepatitis. OBJECTIVE: To quantify incidence and identify undocumented HBV and HCV infection in hospitalized patients at a single centre with secondary analysis of risk factors as part of a quality improvement initiative. METHODS: A one-time antibody test was conducted in patients admitted to the acute medicine and gastroenterology services. RESULTS: Over a 12-week period, hospital screening for HBV and HCV was performed in 37.3% of 995 admitted patients. There was identification of 15 previously undiagnosed cases of HCV (4%) and 36 undocumented cases of occult (ie, antihepatitis B core antigen seropositive) or active (ie, hepatitis B surface antigen seropositive) HBV (9.7%). Among patients with positive screens, 60% of seropositive HCV patients had no identifiable risk factors. CONCLUSIONS: The prevalence of HBV and HCV infection among hospitalized patients in Vancouver was higher than that of the general population. Risk factors for contraction are often not identified. These results can be used as part of an ongoing discussion regarding a 'seek and treat' approach to the detection and treatment of chronic blood-borne viral illnesses.

{beta}-Cell mass dynamics and islet cell plasticity in human type 2 diabetes.

Studies of long-standing type 2 diabetes (T2D) report a deficit in beta-cell mass due to increased apoptosis, whereas neogenesis and replication are unaffected. It is unclear whether these changes are a cause or a consequence of T2D. Moreover, whereas islet morphogenetic plasticity has been demonstrated in vitro, the in situ plasticity of islets, as well as the effect of T2D on endocrine differentiation, is unknown. We compared beta-cell volume, neogenesis, replication, and apoptosis in pancreata from lean and obese (body mass index > or = 27 kg/m(2)) diabetic (5 +/- 2 yr since diagnosis) and nondiabetic cadaveric donors. We also subjected isolated islets from diabetic (3 +/- 1 yr since diagnosis) and nondiabetic donors to an established in vitro model of islet plasticity. Differences in beta-cell volume between diabetic and nondiabetic donors were consistently less pronounced than those reported in long-standing T2D. A compensatory increase in beta-cell neogenesis appeared to mediate this effect. Studies of induced plasticity indicated that islets from diabetic donors were capable of epithelial dedifferentiation but did not demonstrate regenerative potential, as was seen in islets from nondiabetic donors. This deficiency was associated with the overexpression of Notch signaling molecules and a decreased neurogenin-3(+) cell frequency. One interpretation of these results would be that decreased beta-cell volume is a consequence, not a cause, of T2D, mediated by increased apoptosis and attenuated beta-cell (re)generation. However, other explanations are also possible. It remains to be seen whether the morphogenetic plasticity of human islets, deficient in vitro in islets from diabetic donors, is a component of normal beta-cell mass dynamics.