Elbow luxation in a patient with congenital dislocation of the radial head.

Elbow dislocations are commonly seen and can occur after trauma or be congenital. The literature on congenital dislocations is scarce. No cases of an additional luxation of a pre-existing congenital radial head dislocation with a traumatic ulnohumeral dislocation have been described. This case involves a young man with no prior history who presented after trauma of the right elbow. He presented with pain, and his radial head was palpable behind the olecranon, and on imaging it appeared to be more proximal. After additional imaging, the dislocation of the radial head turned out to be congenital combined with an additional luxation of the ulna. This finding influenced our diagnostic approach and reposition method, which, instead of only traction-countertraction, also included pronation and supination.This case highlights the clinical importance of identifying and recognising a patient with a congenital dislocation of the radial head and an additional luxation of the elbow.

Postprandial lipid and apolipoprotein responses following three consecutive meals associate with liver fat content in type 2 diabetes and the metabolic syndrome.

OBJECTIVE: Liver fat is associated with dyslipidemia following a fat load. Previous studies demonstrated that alimentary fat is temporarily retained within enterocytes and mobilized by subsequently ingested nutrients. As this potentially contributes to cumulative postprandial hyperlipidemia, we assessed postprandial lipoprotein changes and their association with liver fat following 3 consecutive meals during a 24 h period in males with type 2 diabetes, and men with the metabolic syndrome (MetS). METHODS: Plasma lipids were measured in 14 type 2 diabetic, 14 MetS and 14 healthy age-matched males, following a standardized breakfast (t=0 h), lunch (t=4 h) and diner (t=8 h). Blood samples were collected before and at t=2, 4, 6, 8, 12, 16, 20 and 24 h following breakfast. Liver fat was measured by proton magnetic resonance spectroscopy. RESULTS: Type 2 diabetic (mean age 55 (4.2) years; HbA1c 7.2 (1.1)%) and MetS men had similar BMI, waist, blood pressure and triglycerides. 24 h-AUC triglycerides, ApoB, and cholesterol-rich-remnants, but not ApoB-48, differed significantly among groups (calculated by ANOVA, all P<0.05). Liver fat was independently associated with 24 h-AUC triglycerides, ApoB and cholesterol-rich-remnants (r=0.57, P<0.001, r=0.38, P=0.017; r=0.48, P=0.002, respectively), but not with 24 h-AUC ApoB-48 (r=0.22, P=0.18). CONCLUSIONS: In type 2 diabetes and the MetS exposure to 3 consecutive meals produced exaggerated 24 h triglyceride, ApoB and cholesterol-rich-remnant concentrations, which were closely associated with liver fat. Instead, ApoB-48 peak was delayed in type 2 diabetes, but not related to liver fat. In addition to liver fat, other mechanisms, including local intestinal processes, determine atherogenic postprandial lipoprotein changes following 3 consecutive meals during 24 h.

Lack of association of liver fat with model parameters of beta-cell function in men with impaired glucose tolerance and type 2 diabetes.

OBJECTIVE: Hepatic steatosis and obesity are components of the metabolic syndrome and risk factors for developing type 2 diabetes (T2DM). We studied how liver fat and body fat distribution relate to various aspects of beta-cell function. METHODS: In 12 men with T2DM, 10 men with impaired glucose tolerance (IGT), and 14 age- and body mass index-matched controls, we measured body fat distribution and liver fat by magnetic resonance imaging and spectroscopy. An oral glucose tolerance test was performed to calculate insulin secretory rate (ISR) by C-peptide deconvolution, and beta-cell function using a mathematical model that describes ISR as a function of absolute glucose levels (insulin secretory tone and glucose sensitivity), the glucose rate of change (rate sensitivity), and a potentiation factor. RESULTS: Waist circumference and the various body fat compartments did not differ among groups. IGT had the highest total and late phase insulin secretion (P<0.001), whereas patients had the lowest insulinogenic index adjusted for insulin resistance (P=0.006). In spite of the hypersecretion, IGT had beta-cell glucose sensitivity, rate sensitivity, and potentiation similar to controls. Liver fat content was highest in diabetic patients (P=0.004) and showed the strongest association with total and late phase of insulin secretion in the IGT group (r=0.657, P=0.039 and r=0.732, P=0.016 respectively). Model beta-cell function variables showed no association with liver fat or body fat compartments. CONCLUSIONS: These data suggest that, in spite of the association of central adiposity and liver fat with T2DM risk, additional, hitherto unknown factors may contribute to beta-cell dysfunction in susceptible humans.

Pancreatic fat content and beta-cell function in men with and without type 2 diabetes.

OBJECTIVE: Insulin resistance, associated with increased lipolysis, results in a high exposure of nonadipose tissue to lipids. Experimental data indicate that fatty infiltration of pancreatic islets may also contribute to beta-cell dysfunction, but whether this occurs in humans in vivo is unknown. RESEARCH DESIGN AND METHODS: Using proton magnetic resonance spectroscopy and oral glucose tolerance tests, we studied the association of pancreatic lipid accumulation in vivo and various aspects of beta-cell function in 12 insulin-naive type 2 diabetic and 24 age- and BMI-matched nondiabetic men. RESULTS: Patients versus control subjects had higher A1C, fasting plasma glucose, and insulin and triglyceride levels and lower HDL cholesterol, but similar waist circumference. Median (interquartile range) pancreatic fat content in patients and control subjects was 20.4% (13.4-43.6) and 9.7% (7.0-20.2), respectively (P = 0.032). Pancreatic fat correlated negatively with beta-cell function parameters, including the insulinogenic index adjusted for insulin resistance, early glucose-stimulated insulin secretion, beta-cell glucose sensitivity, and rate sensitivity (all P < 0.05), but not potentiation. However, these associations were significantly affected by the diabetic state, such that a significant association of pancreatic fat with beta-cell dysfunction was only present in the nondiabetic group (all P < 0.01), suggesting that once diabetes occurs, factors additional to pancreatic fat account for further beta-cell function decline. In control subjects, the association of pancreatic fat and beta-cell function remained significant after correction for BMI, fasting plasma glucose, and triglycerides (P = 0.006). CONCLUSIONS: These findings indicate that pancreatic lipid content may contribute to beta-cell dysfunction and possibly to the subsequent development of type 2 diabetes in susceptible humans.