Approach to patients with pseudo-Cushing’s states

Abstract

The distinction between pseudo-Cushing’s states (PCS) and Cushing’s syndrome (CS) poses a significant clinical challenge even for expert endocrinologists. A patient’s clinical history can sometimes help to distinguish between them (as in the case of alcoholic individuals), but the overlap in clinical and laboratory findings makes it difficult to arrive at a definitive diagnosis. We aim to describe the most common situations that can give rise to a condition resembling overt endogenous hypercortisolism and try to answer questions that physicians often face in clinical practice. It is important to know the relative prevalence of these different situations, bearing in mind that most of the conditions generating PCS are relatively common (such as metabolic syndrome and polycystic ovary syndrome), while CS is rare in the general population. Physicians should consider CS in the presence of additional features. Appropriate treatment of underlying conditions is essential as it can reverse the hormonal abnormalities associated with PCS. Close surveillance and a thorough assessment of a patient’s hormone status will ultimately orient the diagnosis and treatment options over time.

Stress as cause of signs and symptoms of pseudo‐Cushing’s syndrome in buffy‐tufted marmosets (Callithrix aurita)

“…Study findings are inconsistent and no consensus on the correct diagnosis has been reached yet. Appropriate treatment of underlying conditions is essential as it can reverse the hormonal abnormalities associated with PCS 21 …”

Cyclic Cushing’s Syndrome – A Diagnostic Challenge

“…If there are any doubts regarding the origin of observed abnormalities, initial testing for Cushing’s syndrome can be introduced. In obesity and PCOS the low-dose overnight DST and/or late-night serum cortisol are the tests of choice ( 30 , 31 ).…”

Ipercortisolismo funzionale e sue possibili conseguenze cliniche

“…Fino al 30% dei pazienti affetti da depressione maggiore (MD), prevalentemente di genere maschile, sviluppa FH [2].…”

“…L'iperattivazione del sistema limbico stimola la produzione di CRH che si autoamplifica a causa della desensitizzazione e down-regulation dei recettori per i glucocorticoidi situati nell'ippocampo dove, peraltro, citochine infiammatorie inducono modifiche neuroanatomiche e funzionali [1]. Ne risultano un'alterata pulsatilità dell'ormone adrenocorticotropo (ACTH) e un sovvertimento del ritmo circadiano del cortisolo (picchi mattutini più accentuati e mancato nadir serale), con riscontro morfologico di iperplasia surrenalica reversibile [1,2]. Concomita una maggior biodisponibilità tissutale del cortisolo per ridotta attività degli enzimi Fig.…”

“…Sebbene sostenuto da meccanismi fisiopatologici disturbo-specifici, l'FH può essere indistinguibile dalla Sindrome di Cushing (CS), con la quale condivide manifestazioni cliniche (Fig. 1), alterazioni biochimiche e problematiche di diagnostica differenziale, tanto da esser noto anche col nome di pseudoCushing [1,2]. Similmente a quanto accade nella CS, si ipotizza che sia l'azione deleteria tessuto-specifica del cortisolo la responsabile delle complicanze sistemiche (principalmente cardiovascolari e metaboliche) e dell'eccesso di mortalità osservabile anche nelle varie situazioni di FH [3].…”