Effect of surgery on the long-term use of opioids in patients with degenerative back disorders: a retrospective register-based study.

PURPOSE: This study based exclusively on register-data provides a scientific basis for further research on the use of opioids in patients with degenerative back disorder. The main objective of this study is to investigate whether surgically treated back pain patients have the same risk of being long-term opioid users as back pain patients who did not have surgery. METHODS: We performed a retrospective register-based cohort study based on all patients diagnosed with a degenerative back disorder at the Spine Center of Southern Denmark from 2011 to 2017. The primary outcome of the study was the use of opioids two years after the patient's first hospital contact with a degenerative back condition. Fisher exact tests were used for descriptive analyses. The effect of the surgery was estimated using adjusted logistic regression analyses. RESULTS: For patients who used opioids before the first hospital contact, the ratio for long-term opioid use for surgically treated patients is significantly lower than for non-surgically treated patients (OR = 0.75, 95%CI (0.66; 0.86)). For patients who did not use opioids before, the ratio for long-term opioid use for surgically treated patients does not differ from that of non-surgically treated patients (OR = 1.01, 95%CI (0.84; 1.22)). CONCLUSIONS: Patients with a degenerative back disorder who used opioids before their first visit to a specialized spine center have a lower risk of becoming long-term opioid users if they were surgically treated. Whereas for patients who did not use opioids before the first visit, surgical treatment does not influence the risk of becoming long-term opioid users.

Common variation in oxidative phosphorylation genes is not a major cause of insulin resistance or type 2 diabetes.

AIMS/HYPOTHESIS: There is substantial evidence that mitochondrial dysfunction is linked to insulin resistance and is present in several tissues relevant to the pathogenesis of type 2 diabetes. Here, we examined whether common variation in genes involved in oxidative phosphorylation (OxPhos) contributes to type 2 diabetes susceptibility or influences diabetes-related metabolic traits. METHODS: OxPhos gene variants (n = 10) that had been nominally associated (p < 0.01) with type 2 diabetes in a recent genome-wide meta-analysis (n = 10,108) were selected for follow-up in 3,599 type 2 diabetic and 4,956 glucose-tolerant Danish individuals. A meta-analysis of these variants was performed in 11,729 type 2 diabetic patients and 43,943 non-diabetic individuals. The impact on OGTT-derived metabolic traits was evaluated in 5,869 treatment-naive individuals from the Danish Inter99 study. RESULTS: The minor alleles of COX10 rs9915302 (p = 0.02) and COX5B rs1466100 (p = 0.005) showed nominal association with type 2 diabetes in our Danish cohort. However, in the meta-analysis, none of the investigated variants showed a robust association with type 2 diabetes after correction for multiple testing. Among the alleles potentially associated with type 2 diabetes, none negatively influenced surrogate markers of insulin sensitivity in non-diabetic participants, while the minor alleles of UQCRC1 rs2228561 and COX10 rs10521253 showed a weak (p < 0.01 to p < 0.05) negative influence on indices of glucose-stimulated insulin secretion. CONCLUSIONS/INTERPRETATION: We cannot rule out the possibility that common variants in or near OxPhos genes may influence beta cell function in non-diabetic individuals. However, our quantitative trait studies and a sufficiently large meta-analysis indicate that common variation in proximity to the examined OxPhos genes is not a major cause of insulin resistance or type 2 diabetes.