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In the USA, nearly 40% of adults ≥ 20 years have a body mass index (BMI) ≥ 30, and 11% of households are reported as food insecure. In adults, evidence shows women are more likely than men to be food insecure. Among adults with food insecurity, differences in BMI exist between men and women with women reporting higher BMI. Factors associated with this difference in BMI between genders are less understood.The aim of this study was to assess gender differences in the relationship between food insecurity and BMI.Hierarchical models were analyzed using a general linear model by entering covariates sequentially in blocks (demographics, lifestyle behaviors, comorbidities, and dietary variables) and stratified by gender.The sample included 25,567 adults in the USA from the National Health and Nutrition Examination Survey (NHANES), 2005-2014.The dependent variable was BMI, and food insecurity was the primary predictor.Approximately 51% of the sample was women. Food insecure women were significantly more likely to have higher BMI compared to food secure women in the fully adjusted model after controlling for demographics (β = 1.79; 95% CI 1.17, 2.41); demographic and lifestyle factors (β = 1.79; 95% CI 1.19, 2.38); demographic, lifestyle, and comorbidities (β = 1.21; 95% CI 0.65, 1.77); and demographic, lifestyle, comorbidities, and dietary variables (β = 1.23; 95% CI 0.67, 1.79). There were no significant associations between food insecure and food secure men in the fully adjusted model variables (β = 0.36; 95% CI - 0.26, 0.98).In this sample of adults, food insecurity was significantly associated with higher BMI among women after adjusting for demographics, lifestyle factors, comorbidities, and dietary variables. This difference was not observed among men. More research is necessary to understand this relationship among women.

Purpose To assess whether 6-mm OCT scans, which image the macula, can distinguish complete from partial posterior vitreous detachment (PVD) in comparison with 16.5-mm OCT scans, which image the macula, optic nerve, and mid periphery. Design Retrospective cross-sectional study. Participants We compared 6-mm and 16.5-mm scans in 157 eyes of 157 retina clinic patients (mean age, 50 years; range, 10–64 years) with diabetic retinopathy (36%), no retinal disease (19%), and various retinal conditions (45%). We also analyzed 16.5-mm scans in 35 healthy eyes (asymptomatic fellow eyes of patients with unilateral retinal conditions; mean age, 46 years; range, 9–63 years). Methods Each participant underwent Heidelberg Spectralis imaging with the standard lens (6-mm scan) and/or the 55° lens (16.5-mm scan). On 6-mm scans, we classified eyes as stage 3 partial PVD when the posterior vitreous cortex was visualized without visible attachment. On 16.5-mm scans, we classified eyes as stage 3 when the vitreous was attached at the optic nerve and separated from the macula. On both scan types, we classified eyes as stage 4 when neither the premacular bursa nor the posterior vitreous cortex were visualized. We assessed the accuracy of this system for detecting complete PVD on 6-mm scans by calculating test characteristics using 16.5-mm scans as a reference standard. Main Outcome Measure Posterior vitreous detachment stage (0–4). Results Posterior vitreous detachment stage was identical in 6-mm and 16.5-mm scans in 88% of eyes. Compared with 16.5-mm scans, 6-mm scans detected complete PVD (vs. earlier stages 0–3) with 91% sensitivity and 99% specificity. Seven eyes were classified as no PVD on 6-mm scans and were classified as partial PVD on 16.5-mm scans because vitreoretinal separation was localized to the mid periphery. All 16.5-mm scans showed some degree of PVD, including scans from 9 participants between 9 and 20 years of age. Conclusions Six-millimeter scans distinguished complete from partial PVD with good sensitivity and specificity but missed the earliest stages of PVD, which occur in the mid periphery. Posterior vitreous detachment may begin as early as the second decade of life.

BACKGROUND: Older patients with acute myeloid leukemia (AML) have a dismal prognosis, even after treatment with a hypomethylating agent. Azacitidine added to venetoclax had promising efficacy in a previous phase 1b study. METHODS: We randomly assigned previously untreated patients with confirmed AML who were ineligible for standard induction therapy because of coexisting conditions, because they were 75 years of age or older, or both to azacitidine plus either venetoclax or placebo. All patients received a standard dose of azacitidine (75 mg per square meter of body-surface area subcutaneously or intravenously on days 1 through 7 every 28-day cycle); venetoclax (target dose, 400 mg) or matching placebo was administered orally, once daily, in 28-day cycles. The primary end point was overall survival. RESULTS: The intention-to-treat population included 431 patients (286 in the azacitidine-venetoclax group and 145 in the azacitidine-placebo [control] group). The median age was 76 years in both groups (range, 49 to 91). At a median follow-up of 20.5 months, the median overall survival was 14.7 months in the azacitidine-venetoclax group and 9.6 months in the control group (hazard ratio for death, 0.66; 95% confidence interval, 0.52 to 0.85; P

Medicare is keenly aware of the secular changes in weight gain and of the nearly parallel increases in both the incidence and prevalence of type 2 diabetes throughout the U.S. population. The Medicare population, however, differs from the population at large because of its advanced age and frequency of comorbid conditions and/or disability. These factors affect life span as well as participation in and potential benefit from lifestyle modification and risk-factor reduction activities. Further, macrovascular disease is the greatest burden for older beneficiaries with diabetes, and its risks may antedate the appearance of hyperglycemia. Both diabetes prevention and treatment must be considered in this context. Medicare benefits focus on reduction of cardiovascular risk and mitigation of more temporally immediate complications of weight gain and glucose elevation. These preventive services and interventions are described.

Pediatric hypertension is rare, and an underlying cardiac, renal, or endocrine etiology should be considered. We report an adopted 26-year-old white man with asymptomatic hypertension identified at age 14 during a sports examination. His medical history was notable for ulcerative colitis. The physical examination revealed hypertension despite a body mass index of 20.3 kg/m2. A left adrenal mass enhanced on T2-weighted magnetic resonance imaging. The presumptive diagnosis was pheochromocytoma. A 7.0 × 6.0 × 3.5-cm lesion was resected without complication, and the hypertension resolved. Over the next 3 years, he developed thyroid nodules, a presumptive osteochondroma, and benign fibrous lesions. By age 15, his colitis symptoms worsened and multiple polyps were observed. Polyps were identified later in the duodenum and stomach as well. A desmoid tumor involved the superior mesenteric vasculature. Sequential surgical resections left only residual small bowel. Review of adrenal gland histology revealed sheets and nests of lipid-poor epithelioid cells with vesicular nuclei and variably prominent nucleoli. Pseudoglandular architecture and degenerative hemorrhagic “angiomatoid” change was present. Findings were diagnostic of adrenal cortical adenoma, but not pheochromocytoma. The clinical presentation is consistent with Gardner syndrome. The location and nature of mutations in the adenomatous polyposis coli tumor-suppressor gene often determine the presence of extraintestinal disease and disease severity. Seven percent to 13% of patients with Gardner syndrome have adrenal lesions. Most are nonfunctional. Functional lesions typically secrete cortisol. Although such lesions may not come to the attention of endocrinologists because of their nonsecretory status, endocrinologists should be aware of the syndrome and its diverse manifestations.

Study Objective. To explore the clinical characteristics of hyperglycemia in patients treated with risperidone. Design. Pharmacovigilance survey of spontaneously reported adverse events in risperidone-treated patients, with reports of haloperidol-associated hyperglycemia used as a control. Setting. Government-affiliated drug evaluation center. Intervention. The Food and Drug Administration MedWatch surveillance program was queried (risperidone, 1993-February 2002; haloperidol, late 1970s-February 2002) and results pooled with published cases. Measurements and Main Results. We identified 131 reports of risperidone-associated hyperglycemia in addition to seven reports of patients with hyperglycemia who received combined risperidone-haloperidol therapy and six reports of acidosis that occurred in the absence of hyperglycemia. We found 13 reports of haloperidol-associated hyperglycemia and 11 reports of acidosis without hyperglycemia. Of the reports of risperidone-associated hyperglycemia (monotherapy), 78 patients had newly diagnosed hyperglycemia, 46 had exacerbated preexisting diabetes, and 7 could not be classified. Mean ± SD age was 39.8 ± 17.4 years (range 8–96 yrs). Patients with new-onset diabetes (mean ± SD age 34.8 ± 15.7 yrs) were younger than those with preexisting diabetes (mean ± SD age 48.8 ± 17.5 yrs). The overall male:female ratio was 1.5. In most patients, hyperglycemia appeared within 3 months of the start of risperidone therapy. Severity of disease ranged from mild glucose intolerance to diabetic ketoacidosis or hyperosmolar coma. Twenty-six patients with acidosis or ketosis were reported. Four patients died. Conclusion. Atypical antipsychotic treatment may unmask or precipitate hyperglycemia. Although such cases attributed to clozapine or olanzapine are more numerous than those associated with risperidone, the number for risperidone-associated hyperglycemia is relatively higher than that observed with the conventional neuroleptic haloperidol.

Purpose Clozapine is a potent antipsychotic agent that has been marketed since 1990. Several published reports of diabetes mellitus occurring with clozapine therapy have appeared during the past 5 years. Because the risk and characteristics of clozapine-associated diabetes mellitus remain unclear, we conducted a descriptive epidemiologic study of spontaneous adverse event reports of hyperglycemia occurring in clozapine-treated patients. Material and methods The Food and Drug Administration MedWatch surveillance program was queried (January 1990 through February 2001), and the results were pooled with published cases. Parameters assessed included documentation of diabetes, clinical severity, new-onset diabetes versus exacerbation of preexisting disease, demographic characteristics of patients, time to onset of hyperglycemia, and effect of drug discontinuation and rechallenge. Results We identified 384 reports. Of these, new-onset diabetes was diagnosed definitively in 242 patients, and 54 patients had exacerbation of preexisting disease. The mean (± SD) age was 40 ± 12 years (range, 13 to 77). The male:female ratio was 2:0. Most cases appeared within 6 months of initiating clozapine therapy. One patient developed diabetes following a single 500-mg dose. There were 80 cases of metabolic acidosis or ketosis. Twenty-five patients died during hyperglycemic episodes. Forty-six patients had improved glycemic control after discontinuation or dose reduction of the drug. Conclusions A causal relationship between clozapine and diabetes is suggested by the number of reports, the temporal relation to clozapine initiation, the relatively young age of the affected patients, and the prompt reversibility on withdrawal of the drug in some patients. The severity of reported cases ranged from mild glucose intolerance to diabetic ketoacidosis or hyperosmolar coma.

Cutaneous metastases from thyroid cancers are rare. We report the case of an otherwise asymptomatic 81-year-old woman with an enlarging scalp lesion. Her solitary skin metastasis was the presenting feature of thyroid carcinoma. Routine histopathology of the lesion was notable for an atypical clear cell neoplasm. Immunohistochemistry was positive for thyroglobulin. Subsequent resection of the thyroid gland identified separate foci (< 1 cm) for both papillary and follicular carcinoma. Although such immunohistochemical staining has been used previously, it has never been reported to provide the definitive diagnosis for a solitary cutaneous metastasis from the thyroid. Previous tumors had anatomic features in a clinical context that permitted identification by routine light microscopy. Clear cell features found in the follicular focus of carcinoma in the thyroid suggest that it is the primary. A worldwide literature review reveals that follicular carcinoma has a greater preponderance than papillary carcinoma for cutaneous metastasis and that the majority of skin metastases from either papillary or follicular thyroid cancer are localized to the head and neck.

Objective To describe a patient with a potential harbinger of Zollinger-Ellison syndrome. Methods We present a case of a 29-year-old woman with persistent galactorrhea and gastric distress, who was a member of an extensive multiple endocrine neoplasia (MEN) I kindred. Both clinical and laboratory findings are reviewed. Results Laboratory studies were notable for persistent hypercalcemia and increased levels of parathyroid hormone and fasting pancreatic polypeptide. Because of nonspecific upper gastrointestinal distress, which was sometimes responsive to antacids, the patient underwent further diagnostic evaluation. Baseline gastrin levels were normal. A secretin challenge test yielded normal results. At upper endoscopy, visual findings in the stomach and duodenum were unremarkable. A raised nodule (4 by 2 by 2 mm) was removed from an otherwise normal-appearing duodenum as a routine biopsy procedure. The acinar architecture, the inconspicuous nucleoli, and the granular, eosinophilic cytoplasm of the cells were diagnostic of a neuroendocrine tumor. Histologic immunohistochemical staining was positive for gastrin but negative for pancreatic polypeptide. RNA studies were not technically possible. Subsequently, serum pancreatic polypeptide levels normalized. The patient ultimately had hyperplastic parathyroid glands resected. Conclusion The duodenal lesion may be a very early gastrinoma, a preclinical manifestation of the Zollinger- Ellison syndrome. The role of early resection of such lesions remains to be determined. (Endocr Pract. 1997; 3:353-356)

The association between pharmacologic doses of corticosteroids and the development of aseptic bone necrosis has been well documented. Recent reports have described the corticosteroid activity of megestrol acetate. A retrospective review of adverse events reported to the U.S. Food and Drug Administration identified three human immunodeficiency virus (HIV) seropositive patients who developed avascular necrosis of the femoral head during treatment with megestrol acetate. All were males, ages 34, 36, and 55 years, and were on therapy for 6, 1.5, and 18 months, respectively, when symptoms of aseptic necrosis occurred in the absence of antecedent trauma. Megestrol acetate doses were 640, 320, and 600-1200 mg/d, respectively. Two patients had no history of corticosteroid use whereas the third had taken an undisclosed dose and duration of corticosteroids concurrent with pentamidine administration. Notably, despite the predominant use of megestrol in women for hormone sensitive malignancies, none of the reports of aseptic necrosis occurred in this population. Megestrol acetate may be associated with the development of avascular necrosis via its glucocorticoid-like effects. Cachectic acquired immunodeficiency syndrome (AIDS) patients may have additional risk factors that predispose them to aseptic necrosis when receiving megestrol acetate.