2026-08-11 | Pituitary tumour shrinkage and diabetic remission in two cats with Cushing syndrome treated with cabergoline.
We describe two cats with diabetes mellitus and Cushing's syndrome. Diabetes mellitus was initially managed with insulin glargine (Lantus; Sanofi-Aventis, Paris, France), nutritional therapy and continuous glucose monitoring. Hypercortisolism was suspected based on severe hypertension (Case 1), and insulin resistance in combination with typical clinical features of Cushing's syndrome (Case 2). Endocrine testing revealed non-suppressible cortisol concentrations on low-dose-dexamethasone suppression test, elevated endogenous adenocorticotrophic hormone (ACTH) concentration and pituitary enlargement on computed tomography. Cabergoline (Holiday®, Holliday-Scott S.A., Buenos Aires, Argentina) was initiated at a dose of 10 μg/kg po every 48 hours targeting both the pituitary tumour and hypercortisolism. In Case 2, the cabergoline dosage was gradually increased to a final dose of 10 μg/kg po every 12 hours. Both cats achieved diabetic remission within 1 and 6 months of treatment, respectively. Serial monitoring demonstrated a decrease in endogenous ACTH concentrations and a reduction in pituitary volume of 29% of baseline (Case 1) and of 52% of baseline (Case 2) after 8 months of treatment. These findings suggest that cabergoline may be a potential medical treatment option in cats with pituitary-dependent hypercortisolism.
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2026-07-03 | Importance of Hypercortisolism in BP Control, Cardiovascular Risk and in Patients With Difficult-to-Control Hypertension: An Overview for Primary Care Physicians.
Hypertension remains one of the most prevalent and consequential modifiable cardiovascular risk factors worldwide, affecting approximately 1.28 billion adults globally and nearly half of the United States population. Despite the availability of effective therapies, optimal blood pressure control is achieved in fewer than one in four patients, contributing substantially to the burden of myocardial infarction, stroke, heart failure, chronic kidney disease and cognitive decline. Resistant hypertension, defined as blood pressure remaining above goal despite three maximally tolerated antihypertensive agents including a diuretic or requiring four or more agents to achieve control, affects a meaningful proportion of hypertensive patients and carries a disproportionately elevated risk of end-organ damage and adverse cardiovascular events. In this review, we sought to describe how hypercortisolism has historically been underrecognized and under screened as a secondary cause of resistant hypertension, in part due to the perception that overt Cushing's syndrome is rare. However, emerging evidence is challenging this assumption. The CATALYST study demonstrated a 24% prevalence of endogenous hypercortisolism amongst patients with difficult-to-control type 2 diabetes and a 37% prevalence in those requiring three or more antihypertensive medications. Treatment with the glucocorticoid receptor antagonist mifepristone resulted in improvements in glycemic control and body weight, providing hypothesis generating evidence that hypercortisolism may be a relevant, as opposed to an incidental, contributor to cardiometabolic dysregulation. The MOMENTUM registry prospectively evaluated the prevalence of endogenous hypercortisolism specifically in patients with resistant hypertension and found that hypercortisolism was present in 27.3% of this cohort of patients. Primary care providers occupy a central role in the recognition, initial workup and coordinated management of hypertension, including appropriate screening for secondary causes. Awareness of hypercortisolism as an underdiagnosed driver of treatment-resistant hypertension represents an important and potentially treatable opportunity to improve outcomes at the primary care level.
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2026-04-24 | Deterioration Of Blood Lipids During Early Postoperative Remission Of Cushing's Syndrome: A Longitudinal Cohort Study.
Cushing´s syndrome (CS) is associated with an unfavorable lipid profile. However, data on lipid alterations during early postoperative remission, a particularly cardiovascular vulnerable period, are lacking. Evaluation of lipid profiles during active CS and the early postoperative period. In this single-center cohort study at LMU Hospital Munich, we analyzed lipid profiles (Total cholesterol, LDL, HDL, ApoA1, ApoB, Lipoprotein (a), Triglycerides and Non-esterified fatty acids) and metabolic markers in 26 patients with endogenous CS before surgery and 1, 3, 6, 12 and 24 months (n=23) after curative surgery, and compared them with 26 age-, BMI-, and sex-matched controls without hypercortisolism at baseline. Paradoxically most lipid parameters postoperatively worsened. One month postoperatively, HDL (1mo postoperative 38 mg/dL [35-46] vs. active CS 49.5 mg/dL [45-61.3], p<0.0001) and ApoA1 concentrations (1mo postoperative 160 mg/dL [147-168] vs. active CS 193 mg/dL [169-211], p<0.0001) were significantly lower compared to preoperative levels. Similarly one month following surgery triglycerides concentrations (1mo postoperative 185 mg/dL [154-218] vs. active CS 129 mg/dL [89.3-186] preoperatively, p<0.0001) were higher. These changes remained evident until 6 months post-surgery. The triglyceride-glucose index increased during early remission and showed a positive correlation with inflammatory markers CRP and IL-6. Non-esterified fatty acids displayed three distinct postoperative trajectories depending on BMI at baseline. During the early remission phase following curative surgery, we observed a further deterioration in lipid parameters. This can affect cardiovascular health and provides the basis for targeted therapy.
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2026-04-09 | "Glucocorticoids, Cushing syndrome and cellular senescence: a mechanistic link to metabolic ageing".
Glucocorticoids are key regulators of immune, stress and inflammatory responses, as well as of multiple metabolic pathways throughout life, and they play an anabolic role in tissue and organ development. Chronic glucocorticoid excess, whether due to endogenous Cushing syndrome, long-term pharmacological treatment or persistent stress, induces tissue-specific alterations that closely resemble those seen during physiological ageing. These shared changes include loss of tissue regenerative capacity, altered body composition, impaired glucose and lipid homeostasis and increased cardiovascular and neuropsychiatric vulnerability. Emerging evidence indicates that glucocorticoid excess can promote cellular senescence, amplify proinflammatory signalling and disrupt interorgan communication, thereby accelerating a state of metabolic ageing. This review synthesises current clinical and experimental data linking glucocorticoid excess with cellular senescence in key metabolic organs and systems, including adipose tissue, skeletal muscle, liver, bone, the cardiovascular system and the brain. Particular emphasis is placed on chronic neoplastic hypercortisolism as a human model, while also considering prolonged pharmacological glucocorticoid exposure and sustained stress as more prevalent, subclinical sources of hormonal overload. By integrating these lines of evidence, we outline the emerging concept of glucocorticoid-driven metabolic ageing and highlight potential mechanistic targets along the glucocorticoid axis and within senescence pathways. A better understanding of these mechanisms may inform strategies to prevent or mitigate age-related metabolic and cardiovascular complications in patients with Cushing syndrome, in individuals exposed to long-term glucocorticoid therapy and in the broader ageing population.
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2026-04-03 | Small-cell carcinoma of the cervix with acute-onset psychotic symptoms associated with clinically diagnosed ectopic ACTH production: a case report.
Small-cell carcinoma of the cervix (SCCC) is a rare and highly aggressive histological subtype of cervical cancer, associated with poor prognosis. SCCC is histologically classified as a neuroendocrine tumor and has the potential to produce ectopic hormones, leading to various paraneoplastic syndromes. This report is a rare case of recurrent SCCC presenting with psychiatric symptoms due to endogenous Cushing's syndrome caused by ectopic adrenocorticotropic hormone (ACTH) production. The patient initially developed mood and behavioral disturbances as the disease progressed, leading to hospitalization under the suspicion of a primary psychiatric disorder. However, further evaluation, prompted by the discovery of severe hypokalemia, revealed Cushing's syndrome associated with clinically diagnosed ectopic ACTH production in the setting of recurrent disease. Her psychiatric symptoms rapidly remitted following the administration of a cortisol synthesis inhibitor. This case highlights the importance of considering endocrine disorders as potential causes of psychiatric manifestations in patients with cancer, particularly those with neuroendocrine tumors such as SCCC. Acute and marked elevation of endogenous cortisol can induce distinct psychiatric symptoms, such as manic features and grandiose delusions, that often respond better to endocrine treatment aimed at normalizing cortisol levels rather than to antipsychotic therapy alone. Clinicians should be aware of this rare but important clinical presentation as timely diagnosis and management can improve patient outcomes.
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