This Week in Endocrinology — Jul 28, 2026

Welcome to This Week in Endocrinology. This week we're covering 10 notable papers spanning adrenal disorders and mineralocorticoid excess, bone and mineral metabolism, and diabetes complications. Let's dive in.

We begin with new insights into the management and pathophysiology of adrenal disorders and Cushing's syndrome In a multicenter, retrospective phase four study published in The Journal of Clinical Endocrinology and Metabolism, Pivonello and colleagues evaluated the real-world effectiveness and safety of osilodrostat across eleven Italian endocrine referral centers involving one hundred patients with Cushing's syndrome, of whom seventy-four percent had pituitary disease, sixteen percent had adrenal disease, and ten percent had ectopic sources [1]. At the last observation, eighty-one percent of patients achieved normal urinary free cortisol levels, and ninety-two percent achieved normalization at least once during the study period [1]. Adverse events occurred in twenty-nine percent of patients and were mostly mild to moderate, with adrenal insufficiency being the most common, reported in twenty percent [1]. Treatment led to significant improvements in anthropometric parameters, blood pressure, glucose metabolism, and quality of life [1]. Complementing this real-world evidence, a study in the European Journal of Endocrinology by Parasiliti-Caprino and colleagues investigated the interpretation of the one-milligram overnight dexamethasone suppression test using liquid chromatography-tandem mass spectrometry compared to chemiluminescent immunoassay in six hundred thirty-six participants [9]. The authors found that very low post-test dexamethasone concentrations were uncommon, and that chemiluminescent immunoassay and liquid-chromatography tandem mass spectrometry cortisol measurements showed comparable diagnostic performance for detecting overt hypercortisolism, with area under the curve values around zero point nine seven [9]. The data indicate that dexamethasone suppression test interpretation remains reliable even when dexamethasone levels fall below conventional thresholds, supporting selective rather than routine dexamethasone measurement [9].

Shifting to primary aldosteronism and low-renin hypertension, three separate publications illuminate diagnostic and therapeutic challenges In a longitudinal nationwide study published in the European Journal of Endocrinology, Tsai and colleagues analyzed data from seven point eight million hypertensive individuals in Taiwan between 2001 and 2022 to evaluate screening and diagnosis trends for primary aldosteronism [6]. Over the two-decade study period, only four point four percent of hypertensive patients received primary aldosteronism screening, and by 2022, screening rates remained critically low at just one percent in resistant hypertension, three point two percent in early-onset hypertension, and three point six percent in hypokalemia, demonstrating a profound implementation gap between international guidelines and clinical practice [6]. Once screening is completed, subtype differentiation relies heavily on adrenal vein sampling. In a ten-year single-centre retrospective study in Clinical Endocrinology, Zibar Tomsic and colleagues evaluated two hundred fifty-one patients with primary aldosteronism who underwent two hundred sixty-eight adrenal vein sampling procedures [5]. Overall procedural success was seventy-nine percent, but success rates increased significantly from seventy percent in the first three years to eighty-seven point five percent in the subsequent seven years, highlighting a clear radiologist learning curve [5]. Furthermore, computed tomography showed a concordance of only sixty-one percent with adrenal vein sampling, exhibiting a sensitivity of sixty-nine percent and specificity of fifty-five percent for correct subtype classification, confirming that imaging alone is an unreliable surrogate and reinforcing the need to centralize adrenal vein sampling in experienced centers [5]. Expanding on this phenotypic spectrum, a review in The Journal of Clinical Endocrinology and Metabolism by Shah and colleagues highlights low-renin hypertension as a distinct clinical phenotype that encompasses primary aldosteronism, mineralocorticoid mimics, and renal tubular sodium transport disorders [10]. The authors emphasize that patients with low-renin hypertension respond more favorably to therapies targeting sodium retention—such as mineralocorticoid receptor antagonists, epithelial sodium channel inhibitors, or thiazide diuretics—than to agents directed primarily at vasoconstriction [10].

Congenital adrenal hyperplasia and thyroid eye disease represent another major theme, with breakthroughs in targeted therapies and natural history In a prospective case series published in The Journal of Clinical Endocrinology and Metabolism, Tschaidse and colleagues evaluated eight women with classic congenital adrenal hyperplasia and menstrual irregularities or unfulfilled pregnancy desires who were switched from conventional glucocorticoid therapy to modified-release hydrocortisone [4]. Following the switch, regular menstrual cycles were restored in all patients, and all five women actively seeking pregnancy conceived within a median of nine point six months, alongside six healthy live births and one early miscarriage, all achieved with a lower median hydrocortisone dose equivalent [4]. In a parallel study published in the same journal, Adriaansen and colleagues investigated the natural history of untreated classic and non-classic twenty-one-hydroxylase deficiency in a multicenter retrospective cohort [7]. Remarkably, forty-eight percent of patients with classic congenital adrenal hyperplasia had never received glucocorticoid treatment, and seventy-one percent of these untreated patients experienced no adrenal crises during the untreated period, even during illness or surgical interventions, providing crucial insights into disease variability and glucocorticoid independence [7]. Finally, targeting the pathophysiology of thyroid eye disease, Roztocil and colleagues published a study in The Journal of Clinical Endocrinology and Metabolism evaluating lonigutamab, a next-generation anti-insulin-like growth factor one receptor monoclonal antibody [8]. Using orbital fibroblasts from patients with thyroid eye disease, the authors demonstrated that lonigutamab significantly reduced both basal and insulin-like growth factor one-induced hyaluronan production by promoting receptor internalization and subsequent degradation through proteasomal and lysosomal pathways, supporting its therapeutic potential [8].

Bone and mineral metabolism disorders round out our coverage this week In a large-scale retrospective cohort study published in The Journal of Clinical Endocrinology and Metabolism, Ghaleb and colleagues evaluated one hundred seventeen thousand three hundred ninety-five United States adults with sarcoidosis from the TriNetX network [2]. The authors discovered that primary hyperparathyroidism was markedly underdiagnosed, with seventy-five percent of biochemically defined cases carrying no corresponding international classification of diseases code, and parathyroidectomy being associated with a four-point-two-fold reduction in three-year mortality [2]. Routine parathyroid hormone measurement in sarcoidosis patients presenting with hypercalcemia is therefore essential to prevent anchoring bias [2]. In another major bone metabolism study, published in Diabetes Care, Feodoroff and colleagues utilized data from the Finnish Diabetic Nephropathy Study and controls to quantify fracture risks in type 1 diabetes [3]. The standardized incidence ratio for any fracture in type 1 diabetes was two point fifteen, rising to two point sixty for major osteoporotic fractures and five point twenty-four for hip fractures, with hip fracture risk peaking dramatically in individuals aged forty to forty-nine years at eight point thirteen [3]. Furthermore, fracture risk increased progressively across stages of diabetic kidney disease, reaching a standardized incidence ratio of five point zero eight for any fracture in patients with kidney failure, indicating that fracture risk assessment should begin much earlier in patients with diabetic kidney disease [3].

If you only have time for one paper this week, make it the study by Tschaidse and colleagues in The Journal of Clinical Endocrinology and Metabolism on modified-release hydrocortisone for female fertility in congenital adrenal hyperplasia [4]. This prospective case series provides actionable evidence that circadian optimization of glucocorticoid therapy can restore menstrual cyclicity and enable high rates of spontaneous conception in women previously struggling with infertility [4].

Here are the key takeaways from this week in Endocrinology: - Osilodrostat demonstrates robust real-world effectiveness and safety in Cushing's syndrome, achieving high rates of urinary free cortisol normalization and metabolic improvement [1]. - Primary hyperparathyroidism is profoundly underdiagnosed in patients with sarcoidosis, and parathyroidectomy is associated with significantly reduced mortality, highlighting the need for routine parathyroid hormone assessment [2]. - Type 1 diabetes carries a markedly increased fracture risk, which escalates steeply with advancing stages of diabetic kidney disease and requires earlier clinical evaluation [3]. - Modified-release hydrocortisone successfully restores normal menstrual cycles and high spontaneous conception rates in women with classic congenital adrenal hyperplasia using lower glucocorticoid doses [4]. - Adrenal vein sampling for primary aldosteronism demonstrates a clear radiologist learning curve and superior diagnostic accuracy compared to computed tomography, which shows poor subtype concordance [5].

That's your roundup for This Week in Endocrinology. The full transcript and references are available on the episode page in your AudioScholar library. This is an AI-curated summary—for clinical decisions, always consult primary sources and current guidelines. See you next week.

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