Salisburydempsey4126

Finding the source of adrenocorticotropic hormone (ACTH)-independent cortisol-producing adenoma in the patients with subclinical Cushing syndrome (SCS) and bilateral adrenal nodules is sometimes challenging. Computed tomography (CT) and positron emission tomography are helpful, but adrenal venous sampling (AVS) is the gold standard approach. However, interpretation of AVS is important to improve the accuracy of decision-making for surgery. We report a case and review of the literature to assess the benefit of using adrenal vein cortisol to metanephrine ratio to determine the source of cortisol production in SCS and bilateral nodules.

Three authors searched PubMed for data on patients with SCS who had AVS procedure and measurements of cortisol and catecholamines.

A 51-year-old woman with SCS and hypertension crisis presented to our clinic. Paraclinical investigations revealed that she had an ACTH-independent cortisol-producing adenoma and her CT scan showed bilateral adrenal nodules. After AVS, cortisol (high to low) lateralization ratio could not determine the source of cortisol production but the cortisol to metanephrine ratio localized the source to the left side, which included the larger nodule according to CT measurements. Left adrenalectomy led to clinical and paraclinical improvement.

There is a possibility of co-secretion of other steroids accompanied with cortisol in the setting of ACTH-independent SCS. Moreover, cortisol measurement alone and interpretation of AVS results based on cortisol values may not help lateralizing the source of cortisol production with bilateral adrenal nodules. Therefore, we suggest applying cortisol to metanephrine ratio with the same gradient (gradient > 2.3, highest to lowest concentration) when the source of cortisol production cannot be determined by cortisol lateralization ratio.

2.3, highest to lowest concentration) when the source of cortisol production cannot be determined by cortisol lateralization ratio.

Polycystic ovary syndrome (PCOS) is common and associated with metabolic syndrome. In the general population, metabolic disease varies by race and ethnicity.

This work aimed to examine in depth the interaction of race and ethnicity with PCOS-related metabolic disease in adolescent youth.

A secondary analysis was conducted of data from girls (age 12-21 years) with overweight or obesity (> 90 body mass index [BMI] percentile) and PCOS. Measurements included fasting hormone and metabolic measures, a 2-hour oral glucose tolerance test (OGTT), and magnetic resonance imaging for hepatic fat. Groups were categorized by race or ethnicity.

Participants included 39 non-Hispanic White (NHW, age 15.7 ± 0.2 years; BMI 97.7 ± 0.2 percentile), 50 Hispanic (HW, 15.2 ± 0.3 years; 97.9 ± 0.3 percentile), and 12 non-Hispanic Black (NHB, 16.0 ± 0.6 years; 98.6 ± 0.4 percentile) adolescents. Hepatic markers of insulin resistance were worse in NHW, including lower sex hormone-binding globulin and higher triglycerides over high-density lipoprotein cholesterol (TGs/HDL-C) ratio (

 = .002 overall, HW vs NHB [

 = .009] vs NHW [

 = 0.020]), although homeostasis model assessment of estimated insulin resistance was worst in NHB (

 = .010 overall, NHW vs NHB

 = .014). learn more Fasting and 2-hour OGTT glucose were not different between groups, although glycated hemoglobin A

(HbA

) was lowest in NHW (overall

 < .001, NHW 5.2 ± 0.3 vs HW 5.5 ± 0.3

 < .001 vs 5.7 ± 0.4%,

 < .001). The frequency of hepatic steatosis (HW 62%, NHW 42%, NHB 25%,

 = .032); low HDL-C < 40 mg/dL (HW 82%, NHW 61%, NHB 50%,

 < .001) and prediabetes HbA

5.7% to 6.4% (NHB 50%, HW 36%, NHW 5%,

 < .001) were different between the groups.

Adolescents with PCOS appear to show similar racial and ethnic variation to the general population in terms of metabolic disease components.

Adolescents with PCOS appear to show similar racial and ethnic variation to the general population in terms of metabolic disease components.

Primary pigmented nodular adrenocortical disease (PPNAD) is a rare cause of ACTH-independent Cushing syndrome (CS) associated mostly with Carney complex (CNC), a rare autosomal dominant multiple neoplasia syndrome. More than two-thirds of familial cases and approximately one-third of sporadic cases of CNC harbor germline inactivating

defects. Increasingly sensitive technologies for the detection of genetic defects such as next-generation sequencing (NGS) have further highlighted the importance of mosaicism in human disease.

A 33-year-old woman was diagnosed with ACTH-independent CS with abdominal computed tomography showing bilateral micronodular adrenal hyperplasia with a left adrenal adenoma. She underwent left adrenalectomy with pathology demonstrating PPNAD with a 1.5-cm pigmented adenoma. DNA analysis by Sanger sequencing revealed 2 different

variants in the adenoma that were absent from DNA extracted from blood and saliva c.682C > T and c.974-2A > G. "Deep" NGS revealed that 0.31% of DNAhe first recorded case of a patient with PRKAR1A mosaicism, PPNAD, and an adenoma forming due to complete inactivation of PRKAR1A in adrenal tissue from a second, somatic-only, PRKAR1A coding sequence mutation.

In severe primary hypothyroidism (sPH), the serum thyrotropin (TSH) levels are elevated with an increased degree of sialylation. The circulating TSH comprises 2 different TSH glycoforms TSHdi with 2 and TSHtri with 3 N-glycans and methods have developed to determine their contents of anionic monosaccharides (AMS), that is, sialic acid (SA) and sulfonated N-acetylglactosamine (SU) residues.

Characterize N-glycosylation and glycan composition of circulating TSH molecules and determine the effects during levothyroxine treatment in patients with sPH.

Serum samples were obtained from 25 patients with sPH, from 159 euthyroid individuals, and from 12 women during treatment with levothyroxine for sPH. Degrees of N-glycosylation and concentrations of TSHdi and TSHtri as well as their contents of AMS, SA, and SU residues were determined.

The circulating TSH molecules in sPH patients had lower degrees of N-glycosylation, higher degrees of sialylation, and lower degrees of sulfonation than in euthyroid individuals.