Vitamins and HormonesPub Date : 2026-01-01Epub Date: 2026-02-23DOI: 10.1016/bs.vh.2026.01.002
Luís Miguel Cardoso, Gabriela Silva, Bárbara Jesus, Alice Monsanto, João Vinagre, Leonor Gomes
{"title":"Acromegaly: Biochemical diagnosis.","authors":"Luís Miguel Cardoso, Gabriela Silva, Bárbara Jesus, Alice Monsanto, João Vinagre, Leonor Gomes","doi":"10.1016/bs.vh.2026.01.002","DOIUrl":"10.1016/bs.vh.2026.01.002","url":null,"abstract":"<p><p>The biochemical diagnosis of acromegaly presents significant challenges due to the dynamic nature of growth hormone (GH) secretion, assay variability, and the influence of both physiological and pathological factors. Measurement of serum insulin-like growth factor 1 (IGF-1) remains the cornerstone for diagnosis and disease monitoring, as it provides a stable indication of integrated GH secretion. However, discordance between GH and IGF-1 levels can occur in up to 30 percent of cases, complicating clinical decision-making and requiring an assay-aware, and context-sensitive approach. The oral glucose tolerance test (OGTT) serves as a critical adjunct in ambiguous cases. Analytical variability, physiological pulsatility, comorbidities, such as obesity, diabetes, hepatic and renal dysfunction, and methodological interferences can all contribute to discordant results. Advanced analytical techniques, including mass spectrometry-based IGF-1 assays, hold promise for improving diagnostic accuracy. Future directions emphasise assay standardisation and integration of multimodal biomarkers to enhance clinical decision-making. A multidisciplinary, patient-centred approach, that combines clinical expertise, robust biochemical evaluation, and innovative technologies is essential for optimising outcomes in acromegaly.</p>","PeriodicalId":51209,"journal":{"name":"Vitamins and Hormones","volume":"131 ","pages":"103-151"},"PeriodicalIF":0.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147583009","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Vitamins and HormonesPub Date : 2026-01-01Epub Date: 2026-04-24DOI: 10.1016/bs.vh.2026.02.003
Valentina Morelli, Antonio Musolino
{"title":"Ectopic Cushing's syndrome: Clinical presentation and diagnosis.","authors":"Valentina Morelli, Antonio Musolino","doi":"10.1016/bs.vh.2026.02.003","DOIUrl":"10.1016/bs.vh.2026.02.003","url":null,"abstract":"<p><p>ectopic Cushing syndrome (ECS) is a rare endocrinological disease caused by neuroendocrine tumors capable of secreting ATCH or POMC derived immature peptides. It accounts for 10-20 percent of Cushing syndrome cases. ACTH secretion usually leads to clinically severe hypercortisolism with a predominance of glucocorticoids catabolic effects on clinical presentation. It has been suggested that ECS should be divided into two phenotypes, aggressive and indolent. The first one is characterized by classical Cushingoid features, like weight gain, purple striae and so on. The latter is characterized by underlying tumor progression with more pronounced glucocorticoid catabolic effect on muscles, bones and skin tissues. Time from symptoms onset to diagnosis and survival can be reduced in ECS compared to other Cushing syndrome (CS) etiologies. ECS diagnosis can be challenging and is based on four points: clinical suspicion, hypercortisolism confirmation, differential diagnosis with pituitary Cushing (Cushing disease; CD) and tumor localization. All available screening tools for hypercortisolism are used in ECS with good sensitivity and specificity. Between the most used dynamic tests there are: CRH stimulation test, desmopressin test and high dose dexamethasone suppression test (HDDST); inferior petrosal sinus sampling (IPSS) is considered the gold standard for differential diagnosis. CT scan, MRI and functional imaging using radionuclide labelled tracers can help in localizing the responsible tumor even if smaller tumors can become radiologically evident only during follow-up. Circulating Mi-RNAs sequencing and machine learning algorithms may also help in the future for differential diagnosis and therapy personalization.</p>","PeriodicalId":51209,"journal":{"name":"Vitamins and Hormones","volume":"132 ","pages":"201-233"},"PeriodicalIF":0.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148158683","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Vitamins and HormonesPub Date : 2026-01-01Epub Date: 2026-05-04DOI: 10.1016/bs.vh.2026.02.002
Víctor Navas-Moreno, Carolina Sager-La Ganga, María Sara Tapia-Sanchiz, Marta Araujo-Castro, Mónica Marazuela
{"title":"Bilateral macronodular and micronodular hyperplasia: Biochemical, radiological and genetic diagnosis.","authors":"Víctor Navas-Moreno, Carolina Sager-La Ganga, María Sara Tapia-Sanchiz, Marta Araujo-Castro, Mónica Marazuela","doi":"10.1016/bs.vh.2026.02.002","DOIUrl":"10.1016/bs.vh.2026.02.002","url":null,"abstract":"<p><p>Adrenal-origin Cushing's syndrome (CS) accounts for up to 30 percent of cases, with approximately 10 percent attributable to bilateral adrenal disease. The fifth edition of the WHO classification has redefined the terminology previously referred to as bilateral macronodular and micronodular hyperplasia, now recognising these lesions as independent neoplastic entities and grouping them under the broader concept of \"adrenal cortical nodular disease\", which includes macronodular (BMACD) and micronodular (miBACD) forms. BMACD is predominantly diagnosed in adults over 50 years of age, typically presenting as an adrenal incidentaloma, although its true prevalence is likely underestimated. In contrast, miBACD presents earlier in life, with a female predominance in primary pigmented nodular adrenocortical disease (PPNAD) and constitutes an infrequent but important cause of ACTH-independent CS, particularly in paediatric and young adult populations. Both entities share a pathogenic mechanism driven by constitutive activation of the cAMP/PKA pathway, although their genetic backgrounds differ. ARMC5 is the most frequently implicated gene in BMACD (up to 80 percent of familial cases), whereas PRKAR1A mutations predominate in miBACD associated with Carney complex. PDE11A and PDE8B may act as modifier genes, particularly in iMAD. Clinical presentation ranges from autonomous cortisol secretion (ACS) to overt CS, with BMACD showing a progressive course and miBACD demonstrating greater variability, including cyclic CS. Diagnosis requires integration of biochemical, imaging and, when indicated, genetic assessments. Early recognition is crucial due to phenotypic heterogeneity and potential association with hereditary syndromes.</p>","PeriodicalId":51209,"journal":{"name":"Vitamins and Hormones","volume":"132 ","pages":"93-126"},"PeriodicalIF":0.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148158963","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Vitamins and HormonesPub Date : 2026-01-01Epub Date: 2025-12-15DOI: 10.1016/bs.vh.2025.08.007
Paolo Mulatero, Silvia Monticone, Jessica Goi
{"title":"Low-renin hypertension.","authors":"Paolo Mulatero, Silvia Monticone, Jessica Goi","doi":"10.1016/bs.vh.2025.08.007","DOIUrl":"10.1016/bs.vh.2025.08.007","url":null,"abstract":"<p><p>Low-renin hypertension (LRH) affects approximately 30 percent of patients with arterial hypertension and represents a spectrum of heterogeneous disorders characterized by low renin levels, increased sodium reabsorption, and expanded circulating volume. LRH includes monogenic and acquired secondary forms; however, the majority of the patients-particularly older individuals and those of African descent-present essential hypertension. Primary aldosteronism is the most frequent secondary cause, marked by excessive and autonomous aldosterone secretion. Other monogenic forms, such as Liddle syndrome, apparent mineralocorticoid excess and familial hyperkalaemic hypertension, are distinguished by specific biochemical and genetic profiles. Acquired causes of LRH include high dietary sodium intake, renal diseases, drugs inhibiting the renin-angiotensin-aldosterone system, and exogenous or endogenous factors like high consumption of mineralocorticoid-like substances (i.e. licorice) or cortisol excess. Careful clinical evaluation, including family history, and measurement of renin, aldosterone, and potassium levels are essential for accurate diagnosis and tailored treatment. Mineralocorticoid receptor activation and/or increased sodium reabsorption are a common mechanism in the pathogenesis of LRH, with a continuum between essential and secondary forms. Recognizing these subtypes has significant therapeutic implications, as targeted treatments can improve long-term outcomes and reduce cardiovascular events. This chapter describes the differential diagnosis and underlying mechanisms of the most common conditions presenting with a LRH phenotype, with a focus on diagnostic and therapeutic approaches.</p>","PeriodicalId":51209,"journal":{"name":"Vitamins and Hormones","volume":"130 ","pages":"217-253"},"PeriodicalIF":0.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146120740","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Vitamins and HormonesPub Date : 2026-01-01Epub Date: 2025-11-13DOI: 10.1016/bs.vh.2025.10.007
Gabriela A Caballero, Teresa Ribalta, Iban Aldecoa
{"title":"Acromegaly and histopathology.","authors":"Gabriela A Caballero, Teresa Ribalta, Iban Aldecoa","doi":"10.1016/bs.vh.2025.10.007","DOIUrl":"10.1016/bs.vh.2025.10.007","url":null,"abstract":"<p><p>Acromegaly is a chronic disorder caused by sustained excess of growth hormone (GH) and insulin-like growth factor-1 (IGF-1), most commonly due to GH-secreting pituitary neuroendocrine tumors (PitNETs), mainly limited to Pit-1 expressing lineages. Histopathology remains central to diagnosis, prognosis, and treatment planning. Among GH-secreting or somatotroph neoplasms, densely and sparsely granulated are the most relevant clinicopathological subgroups, as they show distinct morphological, radiological, and clinical profiles. Risk assessment is refined by combining routine histology with immunohistochemistry (IHC), including lineage factors, proliferative markers, and somatostatin receptor (SSTR) subtypes, as well as selected molecular tests. Some assays, such as standardized evaluation of SSTR expression, still require further validation. Radiological signs of invasion complement tissue findings and contribute to practical grading systems. Optimal care requires a multidisciplinary approach that integrates endocrine evaluation, high-quality MRI, and expert neuropathology, essential not only for routine care but also for recognizing atypical presentations of acromegaly, such as pituitary hyperplasia, or ectopic growth hormone-releasing hormone (GHRH) or GH secretion. The integration of clinical, pathological, and molecular information provides the foundation for accurate diagnosis and personalized therapy in acromegaly.</p>","PeriodicalId":51209,"journal":{"name":"Vitamins and Hormones","volume":"131 ","pages":"293-334"},"PeriodicalIF":0.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147583044","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Vitamins and HormonesPub Date : 2026-01-01Epub Date: 2026-01-20DOI: 10.1016/bs.vh.2025.10.004
Rocío Villar-Taibo, Eva Fernández-Rodríguez, Ignacio Bernabéu
{"title":"Acromegaly and clinical manifestations.","authors":"Rocío Villar-Taibo, Eva Fernández-Rodríguez, Ignacio Bernabéu","doi":"10.1016/bs.vh.2025.10.004","DOIUrl":"10.1016/bs.vh.2025.10.004","url":null,"abstract":"<p><p>Acromegaly is a chronic multisystem disorder driven by persistent hypersecretion of growth hormone (GH) and consequent elevation of insulin-like growth factor 1 (IGF-1). Beyond its hallmark acral and craniofacial alterations, it manifests with a broad spectrum of systemic complications that substantially contribute to morbidity and mortality. Skeletal and soft tissue overgrowth cause characteristic disfigurement, while musculoskeletal involvement-including degenerative arthropathy, vertebral fractures, myopathy, and neuropathies-remains a major determinant of long-term disability despite biochemical remission. Cutaneous changes such as skin thickening, hyperhidrosis, seborrhea, and acanthosis nigricans are common and may partially regress after treatment. Cardiovascular sequelae, particularly hypertension, cardiomyopathy, valvular disease, and arrhythmias, represent leading causes of morbidity and mortality. Respiratory involvement, especially obstructive sleep apnea, is frequent and often persists after disease control. Metabolic disturbances, including impaired glucose tolerance, diabetes, and dyslipidemia, are highly prevalent and significantly raise cardiovascular risk. Gastrointestinal manifestations include motility disorders, hepatobiliary involvement, and increased incidence of colonic polyps and colorectal cancer, with emerging evidence of elevated risk for other malignancies. Additional endocrine and neuropsychiatric complications, such as hypopituitarism, thyroid abnormalities, cognitive dysfunction, and depression, further aggravate disease burden and impair quality of life. Despite advances in surgery, medical therapy, and radiotherapy, residual morbidity and irreversible sequelae frequently persist. Early diagnosis and multidisciplinary care are crucial not only for achieving biochemical remission but also for mitigating comorbidities, improving quality of life, and enhancing survival outcomes in acromegaly.</p>","PeriodicalId":51209,"journal":{"name":"Vitamins and Hormones","volume":"131 ","pages":"153-193"},"PeriodicalIF":0.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147583053","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Vitamins and HormonesPub Date : 2026-01-01Epub Date: 2025-10-01DOI: 10.1016/bs.vh.2025.08.001
Jorge Gabriel Ruiz-Sanchez
{"title":"Prevalence of primary aldosteronism and screening indications.","authors":"Jorge Gabriel Ruiz-Sanchez","doi":"10.1016/bs.vh.2025.08.001","DOIUrl":"10.1016/bs.vh.2025.08.001","url":null,"abstract":"<p><strong>Introduction: </strong>Primary aldosteronism (PA) is a common yet underrecognized cause of secondary hypertension. Once identified as Conn's syndrome with hypokalemia and adrenal tumors, PA now includes broader forms with inappropriate aldosterone secretion and low renin. Despite its link to cardiovascular risk, under 15 percent of eligible patients are screened, leading to underestimated prevalence and missed treatment chances. Main Section: Improved assays and awareness reveal PA is more frequent than believed, often without hypokalemia and even in normotensive patients. Meta-analyses show PA prevalence of 6.8-10 percent in hypertensive groups, rising over 50 percent in resistant hypertension. Diagnostic and population differences cause varied detection, highlighting the need for standard screening. PA rates might increase in patients with higher reno-cardiometabolic compromise. Aldosterone excess promotes cardiovascular remodeling and arrhythmias, so early PA diagnosis in these groups can improve outcomes. Although current guidelines recommend broad screening for PA, particularly in high-risk patients, there is a growing trend toward universal screening in all individuals with hypertension. PA also occurs in mild or normotensive individuals (>10 percent prevalence), so many hypertensives qualify for screening. Adhering to guidelines supports screening nearly all hypertensives for timely diagnosis and treatment.</p><p><strong>Conclusions: </strong>PA is a common, clinically important yet often missed cause of hypertension, affecting resistant, mild, and normotensive cases. It is prevalent among those patients with cardiovascular complications. Guidelines, though recommending targeted screening, effectively endorse broad testing to enhance detection. Expanding screening and standardizing diagnostics are crucial to optimize diagnosis, enable tailored therapy, reduce cardiovascular risk, and improve outcomes.</p>","PeriodicalId":51209,"journal":{"name":"Vitamins and Hormones","volume":"130 ","pages":"43-67"},"PeriodicalIF":0.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146120867","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Vitamins and HormonesPub Date : 2026-01-01Epub Date: 2025-12-16DOI: 10.1016/bs.vh.2025.11.001
Elías Álvarez-García, Marta Bello-Rego
{"title":"Aldosterone: Synthesis and regulation.","authors":"Elías Álvarez-García, Marta Bello-Rego","doi":"10.1016/bs.vh.2025.11.001","DOIUrl":"10.1016/bs.vh.2025.11.001","url":null,"abstract":"<p><p>Aldosterone, the principal mineralocorticoid, is exclusively synthesized in the glomerular zone of the adrenal cortex. Its primary function is to maintain water and electrolyte balance and regulate blood pressure. The synthesis of aldosterone begins with the transport of cholesterol to the mitochondria, a process that is mediated by the StAR protein. This is followed by a sequence of reactions that are catalyzed by specific enzymes. CYP11A1, 3β-HSD2, CYP21A2, and finally CYP11B2. The regulation of its production is classified as acute, dependent on the rapid activation of StAR, and chronic, involving the sustained transcription of CYP11B2.The regulation of this process is influenced by three physiological stimuli: angiotensin II, which is produced through the renin-angiotensin system, increased extracellular potassium, and ACTH. Angiotensin II and potassium have been shown to activate intracellular signals that increase cytoplasmic calcium, thereby promoting both StAR activation and CYP11B2 expression. ACTH stimulates synthesis via the cAMP/PKA pathway, although its effect is brief.Other modulators of significance include natriuretic peptides, dopamine, serotonin, inflammatory cytokines, microRNAs, and sex hormones such as testosterone and progesterone. Comprehension of these mechanisms is imperative for the effective management of pathologies, including primary hyperaldosteronism, a condition that is associated with secondary hypertension and progressive organ damage.</p>","PeriodicalId":51209,"journal":{"name":"Vitamins and Hormones","volume":"130 ","pages":"1-26"},"PeriodicalIF":0.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146120445","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Vitamins and HormonesPub Date : 2026-01-01Epub Date: 2025-07-18DOI: 10.1016/bs.vh.2025.06.001
Ana Maria Garcia Cano, Laura Caja Guayerbas, Marta Rosillo Coronado
{"title":"Diagnosis of primary aldosteronism: Confirmatory test.","authors":"Ana Maria Garcia Cano, Laura Caja Guayerbas, Marta Rosillo Coronado","doi":"10.1016/bs.vh.2025.06.001","DOIUrl":"10.1016/bs.vh.2025.06.001","url":null,"abstract":"<p><p>The diagnosis of primary aldosteronism (PA) requires an Aldosterone-Renin-Ratio (ARR) to demonstrate a low or undetectable renin level and plasma aldosterone concentration that is inappropriately high for salt and volume status. The confirmatory tests are mandatory by the Endocrine Society Guideline for a definitive diagnosis of PA except if the patient presents spontaneous hypokalemia and Plasmatic Aldosterone Concentration (PAC) above 20 ng/dl plus Plasmatic Renin Activity (PRA) or Direct Renin Concentration (DRC) below assay detection limits. Then, the Endocrine Society Guideline recommends at least confirmatory test for confirmation or exclusion of the diagnosis of PA. Thanks to these confirmatory tests, the patients with negative confirmatory tests do not require unnecessarily invasive procedures such as adrenal vein sampling (AVS) or surgery. These tests are based on the premise that in PA the aldosterone secretion is at least partially autonomous from renin and therefore angiotensin release. Currently, there is no enough evidence to recommend one test over the others. The most employed suppression tests are saline infusion (intravenous infusion or orally), fludrocortisone (FST) or a captopril challenge (CCT) test. Several studies have compared the performance of these tests, but there is wide variability between them, the choice of confirmatory test and in threshold values between referral centers, because of differences in laboratory methodologies and patients' characteristics.</p>","PeriodicalId":51209,"journal":{"name":"Vitamins and Hormones","volume":"130 ","pages":"141-150"},"PeriodicalIF":0.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146120492","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Vitamins and HormonesPub Date : 2026-01-01Epub Date: 2026-04-29DOI: 10.1016/bs.vh.2026.03.001
Queralt Asla, Eulàlia Urgell, Sílvia Terzan, Rebeca Marín, Alicia Santos, Susan M Webb, Anna Aulinas
{"title":"Biochemical diagnosis of hypercortisolism: When and how?","authors":"Queralt Asla, Eulàlia Urgell, Sílvia Terzan, Rebeca Marín, Alicia Santos, Susan M Webb, Anna Aulinas","doi":"10.1016/bs.vh.2026.03.001","DOIUrl":"10.1016/bs.vh.2026.03.001","url":null,"abstract":"<p><p>Hypercortisolism constitutes several symptoms and signs due to inappropriately high and prolonged exposure to excess glucocorticoids (GCs), known as Cushing's syndrome (CS). While iatrogenic corticosteroid administration is the most frequent cause of CS, pituitary corticotroph adenoma, is the most common cause of endogenous excessive GC secretion. Since chronic exposure to high GC levels has been associated with an increased multisystemic morbidity and mortality, prompt identification and treatment are mandatory to minimize long-term complications. The main abnormalities and diagnostic biochemical tests to evaluate cortisol secretion include loss of the normal circadian rhythm assessed by late night salivary cortisol, reduced GC feedback assessed by overnight 1mg dexamethasone suppression test and elevated levels of biologically active cortisol measured by 24-h urinary free cortisol. This chapter addresses the biochemical diagnosis of hypercortisolism. It outlines when to suspect the condition, which biochemical tests are recommended and how they should be performed, providing tools and recommendations for the initial biochemical evaluation. It also discusses challenges, potential pitfalls, and accuracy of each test to aid interpretation and optimize their clinical use.</p>","PeriodicalId":51209,"journal":{"name":"Vitamins and Hormones","volume":"132 ","pages":"57-77"},"PeriodicalIF":0.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148158896","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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