Adductor tenotomy: its role in the management of sports-related chronic groin pain

Patients and methods  

Chronic adductor-related groin pain in athletes is debilitating and is often challenging to treat. Little is published on the surgical treatment when conservative measures fail. This single center study reviews the outcomes of 48 patients (68 groins) who underwent percutaneous adductor tenotomy for sports-related chronic groin pain. Questionnaire assessments were made preoperatively and at a minimum follow-up of 25 months.     

��-Cell Failure in Diet-Induced Obese Mice Stratified According to Body Weight Gain: Secretory Dysfunction and Altered Islet Lipid Metabolism Without Steatosis or Reduced ��-Cell Mass

OBJECTIVE

C57Bl/6 mice develop obesity and mild hyperglycemia when fed a high-fat diet (HFD). Although diet-induced obesity (DIO) is a widely studied model of type 2 diabetes, little is known about β-cell failure in these mice.

RESEARCH DESIGN AND METHODS

DIO mice were separated in two groups according to body weight gain: low- and high-HFD responders (LDR and HDR). We examined whether mild hyperglycemia in HDR mice is due to reduced β-cell mass or function and studied islet metabolism and signaling.

RESULTS

HDR mice were more obese, hyperinsulinemic, insulin resistant, and hyperglycemic and showed a more altered plasma lipid profile than LDR. LDR mice largely compensated insulin resistance, whereas HDR showed perturbed glucose homeostasis. Neither LDR nor HDR mice showed reduced β-cell mass, altered islet glucose metabolism, and triglyceride deposition. Insulin secretion in response to glucose, KCl, and arginine was impaired in LDR and almost abolished in HDR islets. Palmitate partially restored glucose- and KCl-stimulated secretion. The glucose-induced rise in ATP was reduced in both DIO groups, and the glucose-induced rise in Ca²⁺ was reduced in HDR islets relatively to LDR. Glucose-stimulated lipolysis was decreased in LDR and HDR islets, whereas fat oxidation was increased in HDR islets only. Fatty acid esterification processes were markedly diminished, and free cholesterol accumulated in HDR islets.

CONCLUSIONS

β-Cell failure in HDR mice is not due to reduced β-cell mass and glucose metabolism or steatosis but to a secretory dysfunction that is possibly due to altered ATP/Ca²⁺ and lipid signaling, as well as free cholesterol deposition.While insulin resistance is a common feature in most obese subjects, insulin secretion is increased to compensate for its reduced action and normoglycemia is maintained (1,2). In obese type 2 diabetes subjects, however, β-cell compensation fails due to marked impairment of glucose-stimulated insulin secretion (GSIS), often with reduced β-cell mass (2). The relationship between β-cell function and mass as causative factors in β-cell failure and diabetes progression is debated, with emphasis on the relevance of “functional β-cell mass” rather than total mass (2). Increased adiposity leads to elevated circulating free fatty acids (FFAs) and triglycerides, and in vitro and in vivo studies have indicated a causative role for dyslipidemia in insulin resistance (1,3). Although FFAs are necessary for the amplification of GSIS, their excess supply may also have a role in β-cell failure (4), as prolonged elevation of FFA levels both in vivo and in vitro cause β-cell dysfunction (5,6) and, at least in vitro, apoptosis (7).At least part of the β-cell compensation to insulin resistance is due to an increase in β-cell mass (4). Either long-term high-fat diet (HFD) (8) or a short-term lipid infusion (9) can result in increased β-cell mass without augmentation of GSIS, indicating that β-cell function and mass are not necessarily linked. Rodent studies have indicated that HFD leads to increased β-cell mass (8), which is also observed in normoglycemic obese individuals (10). Unclear at present is the dynamics between the factors driving compensatory increase in β-cell mass and function and those reducing them through the various stages of type 2 diabetes development, particularly as FFA may do both. Genetic islet susceptibility may be a critical determinant of these dynamics, both in humans and animal models (4,11,12).Even though studies employing genetically modified models (e.g., Zucker Diabetic Fatty rats, db/db mice) have helped in understanding some of these pathological processes (13–16), several of these models are of extreme nature, with rapid development of pronounced type 2 diabetes. These models, therefore, differ from human obesity-linked type 2 diabetes, which usually develops more gradually. In an attempt to gain insight into the basis of β-cell failure in a mild model of diabetes, we recently developed a new model of type 2 diabetes, the 60% pancreatectomized obese hyperlipidemic Zucker Fatty rat (14). In this model, severe β-cell dysfunction was found without any evidence of a falling β-cell mass or islet steatosis (14). More detailed examination of the pancreatectomized Zucker Fatty rat islets showed marked depletion of insulin stores and altered glycerolipid metabolism (14). The Zucker Fatty rat, as opposed to the Zucker Diabetic Fatty rat, however, does not have genetic predisposition to diabetes, as it maintains normoglycemia despite severe obesity-related insulin resistance (4). The diet-induced obese (DIO) C57BL/6 mouse gradually develops hyperglycemia (17). This suggests that DIO islets are unable to fully compensate for the obesity-related insulin resistance, as occurs in human type 2 diabetes.In the present study, we investigated β-cell dysfunction in DIO mice stratified into two groups according to the effect of HFD on body weight: the low responders to HFD (LDR) were less obese, developed intermediate severity of insulin resistance, and had only mild impairment in glycemia. The high responders to HFD (HDR) were more obese, insulin resistant, and hyperinsulinemic and were clearly hyperglycemic. Thus, the LDR and HDR groups allowed for analysis and comparison of islet β-cell mass and function in response to different levels of insulin resistance with corresponding very mild perturbation of glucose homeostasis and overt but mild hyperglycemia, respectively. When extended to obese humans, these two groups correspond to the pre-diabetes and early diabetes situations.     

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.     

Efficacy of the InVance male sling in men with stress urinary incontinence

OBJECTIVES: To evaluate the efficacy and safety of the InVance bulbourethral sling in male stress urinary incontinence. MATERIALS AND METHODS: Between June 2003 and April 2005, the InVance bulbourethral sling was implanted into 50 patients with urinary incontinence after prostate surgery in 49 cases and pelvic trauma in 1 case. The patients were monitored and evaluated in a prospective manner (continence, tolerance, and satisfaction). The treatment was considered to be successful if the patient stopped wearing any kind of continence pad (patient cured) or only one pad per day (patient improved), with no de novo urinary disorders and without significant postvoid residual urine. Patient satisfaction with the procedure was assessed. RESULTS: After a median follow-up of 6 mo, 50% of patients were dry, 26% had improved, and 24% suffered treatment failure. The success rates for the patients with severe incontinence and those who had undergone radiation therapy were 50% and 25%, respectively. All patients who were dry or had improved were satisfied and presented no obstructive or irritative de novo urinary disorders. The overall success rate for the 51 procedures conducted was 74.5%. Six cases of transitory acute urine retention and six cases of persistent perineal pain were reported. Explantation was necessary because of suppuration of the sling in three patients and of a de novo irritative urinary disorder in one patient. No cases of pubic osteitis or urethral erosion were reported. CONCLUSIONS: The InVance bulbourethral sling procedure makes it possible to treat stress urinary incontinence after prostate surgery with satisfactory and lasting short-term results. Severe incontinence and a past history of pelvic radiation therapy seem to be factors contributing to the failure of this procedure.     

Intramuscular Injection of Sevoflurane Detects Malignant Hyperthermia Predisposition in Susceptible Pigs

Background: The authors hypothesized that intramuscular sevoflurane injection allows diagnostic differentiation between malignant hyperthermia-susceptible (MHS) and -nonsusceptible (MHN) pigs by measurement of intramuscular lactate and carbon dioxide partial pressure (Pco2), and that dantrolene reduces the sevoflurane-induced Pco2 increase.

Methods: With approval of the local animal care committee, microdialysis probes with attached microtubing for sevoflurane injection were placed in the adductor muscles of nine MHS and six MHN pigs, and Pco2 probes with microtubing were positioned in the triceps muscle of eight MHS and six MHN pigs. After equilibration, sevoflurane boluses at different concentrations and a sevoflurane-dantrolene bolus were injected synchronously. Lactate, pyruvate, and glucose as well as Pco2 were measured spectrophotometrically, and the rate of Pco2 increase was calculated.

Results: Intramuscular sevoflurane injection increased local lactate and Pco2 dose dependently, and significantly higher in MHS than in MHN pigs. Measurement of the rate of Pco2 increase allowed a distinct differentiation between single MHS and MHN pigs. No significant increase in Pco2 was found with sevoflurane and dantrolene.     

Adrenergic Receptor Genotype but Not Perioperative Bisoprolol Therapy May Determine Cardiovascular Outcome in At-risk Patients Undergoing Surgery with Spinal Block: The Swiss Beta Blocker in Spinal Anesthesia (BBSA) Study: A Double-blinded, Placebo-controlled, Multicenter Trial with 1-Year Follow-up

Background: Neuraxial blockade is used as primary anesthetic technique in one third of surgical procedures. The authors tested whether bisoprolol would protect patients at risk for cardiovascular complications undergoing surgery with spinal block.

Methods: The authors performed a double-blinded, placebo-controlled, multicenter trial to compare the effect of bisoprolol with that of placebo on 1-yr composite outcome including cardiovascular mortality, nonfatal myocardial infarction, unstable angina, congestive heart failure, and cerebrovascular insult. Bisoprolol was given orally before and after surgery for a maximum of 10 days. Adrenergic receptor polymorphisms and safety outcome measures of bisoprolol therapy were also determined.

Results: A total of 224 patients were enrolled. Spinal block could not be established in 5 patients. One hundred ten patients were assigned to the bisoprolol group, and 109 patients were assigned to the placebo group. The mean duration of treatment was 4.9 days in the bisoprolol group and 5.1 days in the placebo group. Bisoprolol therapy reduced mean heart rate by 10 beats/min. The primary outcome was identical between treatment groups and occurred in 25 patients (22.7%) in the bisoprolol group and 24 patients (22.0%) in the placebo group during the 1-yr follow-up (hazard ratio, 0.97; 95% confidence interval, 0.55-1.69; P = 0.90). However, carriers of at least one Gly allele of the [beta]1-adrenergic receptor polymorphism Arg389Gly showed a higher number of adverse events than Arg homozygous (32.4% vs. 18.7%; hazard ratio, 1.87; 95% confidence interval, 1.04-3.35; P = 0.04).     

Cost reduction of perioperative coagulation management in cardiac surgery: value of ‘bedside’ thrombelastography (ROTEM)

Objective: Demographic changes and aggressive platelet inhibition have resulted in a marked increase in blood- and coagulation product expenditure and costs in cardiac surgery. We analyzed ‘bedside’ coagulation test (ROTEM) in order to verify clot forming quality for the purpose of finding a cost-effective treatment path. Methods: Annual treatment costs of all cardiosurgical patients were analyzed before (729 patients) and after (693 patients) implementation of ‘bedside’ ROTEM. Cumulative numbers and costs of platelet concentrates (PltC), fresh frozen plasma (FFP), red blood cell units (RBC), and coagulation factors: pooled coagulation concentrates (PCC), recombinant factor VIIa (rFVIIa), factor XIII (FXIII), and fibrinogen were assessed. Average monthly numbers and costs were compared. Number of resternotomies and early mortality was assessed and compared in both periods. Results: After ROMTEM implementation cumulative RBC expenditure showed 25% decrease while PltC exhibited 50% decrease. FFP expenditure remained unchanged. PCC, FXIII were markedly reduced (−80%) while rFVIIa were entirely omitted. Fibrinogen, however, increased two-fold. Cumulative average monthly costs of all blood products decreased from 66,000€ to 45,000€ (−32%). Coagulation factor average monthly costs decreased from 60,000€ to 30,000€ (−50%) yielding combined savings of 44%. In contrast, average monthly costs for ROTEM were 1.580€. Total number of resternotomies decreased from 6.6% to 5.5% while early mortality (5.9%; 6.0%) remained stable. Conclusion: Cumulative costs for treatment of perioperative coagulation disorders can be reduced by ‘bedside’ ROTEM analysis to achieve a selective substitution management. Saved costs for blood- and coagulation products clearly outweighed the expenses of ROTEM. Adequate differential coagulation management can therefore be cost-effective.     

Severity of vertebral fracture reflects deterioration of bone microarchitecture

Introduction Bone microarchitecture, a component of bone strength, is generally measured on transiliac bone biopsy samples. The objective of this study was to determine whether assessment of four grades of vertebral fracture severity could serve as a noninvasive surrogate marker for trabecular bone volume and microarchitecture. Methods Baseline vertebral fracture severity was determined by semiquantitative assessment of spine radiographs from 190 postmenopausal women with osteoporosis. Bone-structure indices were obtained by 2D histomorphometry and 3D microcomputed tomography (CT) analyses. Significance of differences was determined after adjusting for age, height, and lumbar spine bone mineral density. Results There were significant (P < 0.05) trends in decreasing bone volume, trabecular number, and connectivity, and increasing trabecular separation with greater vertebral fracture severity. Histomorphometric bone volume was 25 and 36% lower (P < 0.05) in women with moderate and severe fractures than in women with no fractures, respectively. Compared with women without fractures, women with mild, moderate, and severe fractures had lower (P < 0.05) microCT bone volume (23, 30, and 51%, respectively). Conclusions Microarchitectural deterioration was progressively worse in women with increasing severity of vertebral fractures. We conclude that assessment of vertebral fracture severity is an important clinical tool to evaluate the severity of postmenopausal osteoporosis.     

The comparative effects of bariatric surgery on weight and type 2 diabetes

Background: Epidemiological evidence confirms that risk of developing type 2 diabetes is related to weight gain. Weight reduction is beneficial as relative risk is reduced to 0.13 for weight loss >20 kg. This raises the question of effectiveness of bariatric surgery on 1) weight loss and 2) diabetes-related outcomes in morbidly obese patients. Methods: We reviewed the literature using Medline. Only 2 meta-analyses reporting on both outcomes were included, as well as 50 systematic reviews or primary studies. Results: Meta-analyses mainly based on case series data as well as controlled studies confirm that bariatric surgery is highly effective in obtaining weight reduction in morbidly obese patients up to 60% of the excess weight, along with resolution of preoperative diabetes in more than 75% of cases. Among bariatric surgery techniques, malabsorptive procedures (biliopancreatic diversion and gastric bypass) appear to be more effective on both outcomes than restrictive procedures (gastroplasty and gastric banding). Conclusion: Even if more studies are needed to confirm current evidence, bariatric surgery is effective for controlling diabetes. It appears as an efficient strategy from economic modeling due to savings from reduction in diabetes-related costs.