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OBJECTIVE An increase in maternal use of licit or illicit substances, alcohol, and tobacco has resulted in an increased incidence of neonatal abstinence syndrome (NAS). In recent years, NAS management has shifted to initiating an Eat, Sleep, Console (ESC) approach prior to pharmacologic treatment. The objective of this study was to evaluate the impact of ESC in combination with pharmacologic treatment in the management of NAS for infants exposed to substance use in utero. METHODS This single system, multisite, retrospective cohort study evaluated infants with known exposure to substance or polysubstance use in utero or those who had signs and symptoms of withdrawal with a positive toxicology screen. The primary outcome of rate of pharmacologic therapy initiated was evaluated pre and post implementation of ESC. Secondary outcomes included hospital length of stay, day of life that pharmacologic therapy was initiated, and an evaluation of the ESC guideline. A subgroup analysis with similar outcomes was also performed for patients with maternal polysubstance use. RESULTS A total of 2843 patients were screened, and 50 patients were randomly selected for inclusion in both pre- and post-groups. The rate of pharmacologic therapy initiated post implementation of ESC decreased from 58% to 30% (p < 0.01). In the post-group, there was a decrease in the number of patients requiring scheduled morphine (33%, p < 0.01) and duration of pharmacologic therapy (14.6 days vs 6.47 days, p < 0.01). CONCLUSIONS Implementing an ESC guideline decreased the length of stay and rate of pharmacologic intervention needed for infants with NAS at our institution. [ABSTRACT FROM AUTHOR]

This document is a letter to the editor disputing the recommendations from the 2023 International Evidence-based Guideline for the Assessment and Management of Polycystic Ovary Syndrome (PCOS). The authors argue that the guideline's definition of hirsutism and its association with PCOS are inconsistent with previous international recommendations. They state that the majority of hirsutism is due to androgen excess, usually caused by PCOS, but some cases are idiopathic hirsutism and would be incorrectly diagnosed as PCOS according to the 2023 guidelines. The authors recommend maintaining the standard definition of hirsutism as an FG score of 8 or greater and treating women with lower scores who have other clinical evidence of PCOS. [Extracted from the article]

Objective: The extent to which weight loss contributes to increases in insulin sensitivity (IS) and β-cell function after surgical or medical intervention has not been directly compared in individuals with impaired glucose tolerance or newly diagnosed type 2 diabetes.Methods: The Restoring Insulin Secretion (RISE) Study included adults in the Beta-Cell Restoration Through Fat Mitigation Study (n = 88 randomized to laparoscopic gastric banding or metformin [MET]) and the Adult Medication Study (n = 267 randomized to placebo, MET, insulin glargine/MET, or liraglutide + MET [L + M]). IS and β-cell responses were measured at baseline and after 12 months by modeling of oral glucose tolerance tests and during arginine-stimulated hyperglycemic clamps. Linear regression models assessed differences between and within treatments over time.Results: BMI decreased in all treatment groups, except placebo, at 12 months. IS increased in all arms except placebo and was inversely correlated with changes in BMI. L + M was the only treatment arm that enhanced multiple measures of β-cell function independent of weight loss. Insulin secretion decreased in the laparoscopic gastric banding arm proportional to increases in IS, with no net benefit on β-cell function.Conclusions: Reducing demand on the β-cell by improving IS through weight loss does not reverse β-cell dysfunction. L + M was the only treatment that enhanced β-cell function. [ABSTRACT FROM AUTHOR]

The polycystic ovary syndrome could be diagnosed after the exclusion of other medical conditions that cause irregular menstrual cycles and androgen excess and the determination that oligoovulation and polycystic ovaries defined by ultrasonography are present. These criteria acknowledge that polycystic ovaries need not be present to make a diagnosis of the polycystic ovary syndrome and conversely, their presence alone does not establish the diagnosis.

Deterioration in glucose tolerance occurs rapidly in women with polycystic ovary syndrone (PCOS), suggesting that pancreatic [beta]-cell dysfunction may supervene early. To determine whether the compensatory insulin secretory response to an increase in insulin resistance induced by the glucocorticoid dexamethasone differs in women with PCOS and control subjects, we studied 10 PCOS and 6 control subjects with normal glucose tolerance. An oral glucose tolerance test (OGTT) and a graded glucose infusion protocol were performed at baseline and after subjects took 2.0 mg of dexamethasone orally. Basal ([[PHI].sub.b]), static ([[PHI].sub.s]) dynamic ([[PHI].sub.d]), and global ([PHI]) indexes of [beta]-cell sensitivity to glucose were derived. Insulin sensitivity [S.sub.i]) was calculated using the minimal model; a disposition index (DI) was calculated as the product of [S.sub.i] and [PHI]. PCOS and control subjects had nearly identical fasting and 2-h glucose levels at baseline. [[PHI].sub.b] was higher, although not significantly so, in the PCOS subjects. The [[PHI].sub.d], [[PHI].sub.s] and [PHI] indexes were 28, 19, and 20% higher, respectively, in PCOS subjects. The DI was significantly lower in PCOS (30.01 [+ or -] 5.33 vs. 59.24 [+ or -] 7.59) at baseline. After dexamethasone, control subjects averaged a 9% increase (to 131 [+ or -] 12 mg/dl) in 2-h glucose levels; women with PCOS had a significantly greater 26% increase to 155 [+ or -] 6 mg/dl. The C-peptide-to-glucose ratios on OGTF increased by 44% in control subjects and by only 15% in PCOS subjects. The accelerated deterioration in glucose tolerance in PCOS may result, in part, from a relative attenuation in the response of the [beta]-cell to the demand placed on it by factors exacerbating insulin resistance. insulin resistance; insulin secretion; type 2 diabetes

Objective: To determine whether metformin or lifestyle modification can lower rates of all-cause and cause-specific mortality in the Diabetes Prevention Program and Diabetes Prevention Program Outcomes Study.Research Design and Methods: From 1996 to 1999, 3,234 adults at high risk for type 2 diabetes were randomized to an intensive lifestyle intervention, masked metformin, or placebo. Placebo and lifestyle interventions stopped in 2001, and a modified lifestyle program was offered to everyone, but unmasked study metformin continued in those originally randomized. Causes of deaths through 31 December 2018 were adjudicated by blinded reviews. All-cause and cause-specific mortality hazard ratios (HRs) were estimated from Cox proportional hazards regression models and Fine-Gray models, respectively.Results: Over a median of 21 years (interquartile range 20-21), 453 participants died. Cancer was the leading cause of death (n = 170), followed by cardiovascular disease (n = 131). Compared with placebo, metformin did not influence mortality from all causes (HR 0.99 [95% CI 0.79, 1.25]), cancer (HR 1.04 [95% CI 0.72, 1.52]), or cardiovascular disease (HR 1.08 [95% CI 0.70, 1.66]). Similarly, lifestyle modification did not impact all-cause (HR 1.02 [95% CI 0.81, 1.28]), cancer (HR 1.07 [95% CI 0.74, 1.55]), or cardiovascular disease (HR 1.18 [95% CI 0.77, 1.81]) mortality. Analyses adjusted for diabetes status and duration, BMI, cumulative glycemic exposure, and cardiovascular risks yielded results similar to those for all-cause mortality.Conclusions: Cancer was the leading cause of mortality among adults at high risk for type 2 diabetes. Although metformin and lifestyle modification prevented diabetes, neither strategy reduced all-cause, cancer, or cardiovascular mortality rates. [ABSTRACT FROM AUTHOR]