Predictive Value of the International Classification of Diseases, 9th Revision Codes for Identifying Ocular Oncology Diagnoses.

Introduction: The aim of this study was to determine the predictive value of International Classification of Diseases, 9th Revision (ICD-9) billing codes for identifying ocular oncology diagnoses. Methods: Population-based retrospective cohort study of all Olmsted County, Minnesota residents with any ocular neoplasm-related ICD-9 code from January 1, 2006 to October 1, 2015. All medical records were reviewed for confirmation of ocular neoplasm. Diagnoses with ≥5 cases confirmed via a medical record review were compared to corresponding ICD-9 codes. Main outcome measures included positive predictive value (PPV), negative predictive value (NPV), sensitivity, and specificity of ICD-9 codes. Results: Among 3,932 subjects with ≥1 ocular neoplasm-related ICD-9 code, 21 diagnoses met study criteria. The most frequent intraocular, extraocular/orbital, and ocular surface diagnoses were choroidal nevus (n = 824), epidermal inclusion cyst (n = 263), and conjunctival nevus (n = 74), respectively. PPVs ranged from 1.2% to 73.8%, NPVs from 96.9% to 100%, sensitivity from 0% to 100%, and specificity from 85.7% to 100%. Among malignant neoplasms, PPV ranged from 0% to 73.8%: ocular surface squamous neoplasia (PPV: 0%), choroidal melanoma (PPV: 25.0%), eyelid squamous cell carcinoma (PPV: 46.7%), and eyelid basal cell carcinoma (PPV: 73.8%). Among benign neoplasms, PPV ranged from 1.2% (dermoid cyst) to 61.6% (choroidal nevus). Conclusion: There was a wide variation in a predictive value of ocular neoplasm-related ICD-9 billing codes, which suggests that ocular oncology-related claims data alone may overestimate the true number of ocular oncology diagnoses.

Incidence and clinical characteristics of pediatric ocular tumors in a Midwestern US population.

PURPOSE: To investigate the incidence and clinical characteristics of pediatric ocular tumors in a US Midwestern county population. METHODS: Retrospective population-based cohort study of all Olmsted County, Minnesota, pediatric patients (<18 years old) diagnosed with any ocular neoplasm from January 1, 2006, to December 31, 2015. Subjects were identified via the Rochester Epidemiology Project, a record-linkage system that captures virtually all medical care provided in this county. Medical records were reviewed to confirm diagnoses. Age- and sex-adjusted incidence rates were calculated and adjusted to the 2010 Olmsted County, Minnesota, pediatric population. RESULTS: There were 87 incident pediatric ocular tumor diagnoses, yielding an overall age- and sex-adjusted incidence rate of 24.0 per 100,000 per year (95% CI, 19.0-29.1). Females accounted for 46 cases (53%) cases, and 62 (85%) were White. Incidence rate for ocular tumors overall did not differ by patient age (P = 0.08) or sex (P = 0.47). All tumors were benign lesions. The most frequent adnexal/orbital, ocular surface, and intraocular tumors were epidermal inclusion cyst in 18 (21%) cases, conjunctival nevus in 10 (12%), and choroidal nevus in 18 (21%), respectively. The mean follow-up duration was 25.5 months (range, 7 days to 138.6 months), and benign tumor growth occurred in one conjunctival nevus. There were no cases of malignant transformation. CONCLUSIONS: Pediatric ocular tumors were rare with an estimated incidence of approximately 1 in 4,200 pediatric patients in Olmsted County, Minnesota. All lesions were benign, with benign growth in only 1% of cases, and no tumors underwent malignant transformation.

Insulin-stimulated endoproteolytic TUG cleavage links energy expenditure with glucose uptake.

TUG tethering proteins bind and sequester GLUT4 glucose transporters intracellularly, and insulin stimulates TUG cleavage to translocate GLUT4 to the cell surface and increase glucose uptake. This effect of insulin is independent of phosphatidylinositol 3-kinase, and its physiological relevance remains uncertain. Here we show that this TUG cleavage pathway regulates both insulin-stimulated glucose uptake in muscle and organism-level energy expenditure. Using mice with muscle-specific Tug (Aspscr1)-knockout and muscle-specific constitutive TUG cleavage, we show that, after GLUT4 release, the TUG C-terminal cleavage product enters the nucleus, binds peroxisome proliferator-activated receptor (PPAR)γ and its coactivator PGC-1α and regulates gene expression to promote lipid oxidation and thermogenesis. This pathway acts in muscle and adipose cells to upregulate sarcolipin and uncoupling protein 1 (UCP1), respectively. The PPARγ2 Pro12Ala polymorphism, which reduces diabetes risk, enhances TUG binding. The ATE1 arginyltransferase, which mediates a specific protein degradation pathway and controls thermogenesis, regulates the stability of the TUG product. We conclude that insulin-stimulated TUG cleavage coordinates whole-body energy expenditure with glucose uptake, that this mechanism might contribute to the thermic effect of food and that its attenuation could promote obesity.