Adrenal glands and pregnancy

The relationship between the adrenal glands and pregnancy represents one of the most complex areas of clinical endocrinology because gestation profoundly alters both the hypothalamic-pituitary-adrenal axis and mineralocorticoid and catecholaminergic homeostasis, while incorporating the placental and fetal compartments into endocrine regulation. Pregnancy does not merely increase the circulating concentrations of certain hormones; it reorganises the entire maternal steroidogenic system through increased corticosteroid-binding globulin, placental production of CRH and ACTH-like peptides, activation of the renin-angiotensin-aldosterone system and continuous interaction with the fetoplacental unit. Consequently, adrenal parameters interpreted according to criteria used outside pregnancy may become misleading, particularly when attempting to distinguish physiological adaptation from endocrine disease.

From a clinical perspective, adrenal disorders during pregnancy are less common than thyroid dysfunction, but when present they may have a potentially severe impact on maternal and fetal outcomes. Adrenal insufficiency increases the risk of adrenal crisis, hypotension, electrolyte disturbances and impaired uteroplacental perfusion; hypercortisolism increases the risk of hypertension, gestational diabetes, pre-eclampsia, preterm delivery and fetal growth restriction; pheochromocytoma and paraganglioma may mimic obstetric hypertension but carry a much greater haemodynamic risk; congenital disorders and adrenal tumours also require therapeutic decisions that must simultaneously take into account the mother, the fetus and gestational timing. In this setting, appropriate management depends on early recognition of a profoundly altered physiology and on the ability to adapt diagnosis, treatment and monitoring to the specific characteristics of pregnancy.

Pregnancy induces progressive remodelling of maternal adrenal function, involving both the cortex and, indirectly but in a clinically relevant manner, the medulla. The first factor to consider is the oestrogen-dependent increase in corticosteroid-binding globulin (CBG), which raises circulating total cortisol concentrations. At the same time, the placenta produces increasing amounts of CRH and peptides with ACTH-like activity, contributing to genuine activation of the maternal hypothalamic-pituitary-adrenal axis. The result is a state of physiological “gestational hypercortisolism” in which both total and, to some extent, free cortisol concentrations increase, while maintaining a biological balance that differs from pathological hypercortisolism.

This new endocrine state is not static. Cortisol begins to increase as early as the first trimester and continues to rise until the end of pregnancy, with values becoming progressively less comparable with those of non-pregnant women. An important feature is that the circadian rhythm of cortisol tends to be preserved, but at a higher “set point”. This detail has major diagnostic implications because simply demonstrating an elevated cortisol concentration loses significance, whereas loss of the physiological rhythm, clinical severity and the cautious use of tests interpreted according to pregnancy-specific ranges become central.

The mineralocorticoid compartment also undergoes profound changes. During pregnancy, the renin-angiotensin-aldosterone system is activated, with increased renin and aldosterone supporting plasma volume expansion and sodium retention required to maintain the uteroplacental circulation. However, the sodium-retaining effect of aldosterone is partly counterbalanced by the antimineralocorticoid effect of progesterone. This explains why pregnancy is simultaneously a state of physiological hyperaldosteronism and relative peripheral “resistance” to aldosterone, making it more difficult to distinguish physiological changes from primary aldosteronism.

The maternal adrenal environment cannot be separated from fetoplacental physiology. The placenta and fetal adrenal gland form an integrated steroidogenic unit in which the placenta uses fetal steroid precursors for oestrogen synthesis and participates in controlling fetal exposure to active glucocorticoids. Placental enzymes such as 11β-HSD2 inactivate a substantial proportion of maternal cortisol, limiting excessive fetal exposure. This “glucocorticoid barrier” is not absolute, but it plays a crucial role in protecting the fetus from inappropriate concentrations of active hormones and in modulating tissue and neuroendocrine development.

Adrenal physiology during pregnancy also has major haemodynamic and metabolic significance. Cortisol contributes to energy substrate availability, vascular responsiveness and stress tolerance, whereas aldosterone and the renin-angiotensin system support plasma volume expansion. Clinical interpretation of symptoms such as fatigue, nausea, mild orthostatic hypotension or changes in blood glucose therefore becomes difficult because many signs potentially compatible with adrenal disease may also occur during normal pregnancy. The challenge is not merely to recognise a biochemical abnormality, but to determine when a physiological response is disproportionate or maladaptive.

The adrenal medulla also contributes indirectly to this setting. Normal pregnancy does not cause a pathological increase in plasma metanephrines, which is clinically useful because it preserves the reliability of testing for pheochromocytoma or paraganglioma when suspicion is justified. However, gestational cardiovascular physiology, with relative tachycardia, blood pressure changes and greater symptom variability, may make catecholaminergic syndromes more difficult to recognise in their early stages.

These considerations show that pregnancy transforms adrenal assessment into a dynamic process. It is not sufficient to understand normal adult adrenal physiology; clinicians must recognise the new endocrine balance created by pregnancy, understand the role of the placenta and interpret hormonal findings in relation to trimester, laboratory method, clinical history and any pre-existing endocrine disorder. Without this framework, there is a dual risk: interpreting physiological findings as pathological, or attributing manifestations to pregnancy that are actually the first signs of a potentially serious adrenal disorder.

The first practical problem when assessing adrenal function during pregnancy is that almost all major biochemical axes change. Total cortisol increases because of increased CBG, urinary free cortisol tends to rise particularly in later trimesters, renin and aldosterone are physiologically elevated, and the clinical picture may be obscured by symptoms common to pregnancy. Consequently, interpretation of a single isolated parameter is often insufficient. During pregnancy more than ever, laboratory findings must be interpreted in the context of gestational physiology, symptoms, blood pressure, electrolytes and changes over time.

When adrenal insufficiency is suspected, basal cortisol measurement loses some of its discriminatory value because pregnancy raises baseline concentrations. A value that appears “not low” may therefore still be inappropriate for the trimester and clinical context. The presence of hypotension, unexplained hyponatraemia, persistent vomiting, disproportionately severe fatigue, hypoglycaemia or weight loss should lower the threshold for suspicion. The ACTH stimulation test may be used, but its interpretation requires expertise because traditional cut-offs are not always directly applicable to pregnant women and because, in suggestive clinical scenarios, the risk of delaying treatment may outweigh the benefit of awaiting perfect confirmation.

When hypercortisolism is suspected, pregnancy makes many tools routinely used outside gestation unreliable. The dexamethasone suppression test is particularly problematic because pregnancy-related changes in the hypothalamic-pituitary-adrenal axis reduce its discriminatory value. Urinary free cortisol may also be elevated during physiological pregnancy, especially from the second trimester onwards. Diagnostic reasoning must therefore focus on less non-specific clinical features, such as marked skin fragility, easy bruising, proximal myopathy, early severe hypertension, hypokalaemia, difficult-to-control diabetes and rapid metabolic deterioration, incorporating late-night salivary measurements and repeated assessments over time whenever possible.

Assessment of the renin-aldosterone system is another critical issue. During pregnancy, both renin and aldosterone increase physiologically, and the aldosterone-to-renin ratio may appear falsely reassuring, creating a risk of underdiagnosing primary aldosteronism. Suspicion therefore cannot rely on mechanical biochemical screening alone. In patients with resistant hypertension, spontaneous hypokalaemia, pre-existing hypertension or an early and severe obstetric presentation, clinical reasoning must precede laboratory interpretation. Confirmatory tests commonly used outside pregnancy may also be difficult or inappropriate during gestation, and the diagnostic pathway should be individualised in experienced centres.

By contrast, biochemical diagnosis of pheochromocytoma and paraganglioma retains relative reliability because plasma metanephrines generally remain stable during physiological pregnancy. When suspicion is justified, measurement of plasma free metanephrines or fractionated urinary metanephrines remains central. The main challenge is not hormonal interpretation but clinical recognition, because many patients are initially considered to have gestational hypertension or pre-eclampsia, whereas features such as paroxysmal hypertensive crises, severe headache, sweating, palpitations and marked blood pressure variability should suggest a catecholamine-secreting disorder.

Imaging must be used according to different criteria than in non-pregnant women. Ultrasound may have an initial role but is limited for adrenal assessment. Magnetic resonance imaging without gadolinium is the preferred technique when an adrenal mass or catecholamine-secreting tumour must be localised, whereas CT and nuclear medicine procedures are avoided except in exceptional circumstances because of fetal radiation exposure or lack of appropriateness during pregnancy. This places even greater decision-making weight on the integration of clinical and laboratory data.

The modern assessment strategy should therefore be organised in stages. The first level is clinical and is based on history, blood pressure, weight changes, electrolytes, blood glucose, skin findings and cardiovascular signs. The second level is biochemical, using tests selected specifically according to the clinical question. The third level is morphological, with targeted imaging when pre-test probability is sufficient. During pregnancy, this sequence is essential because it reduces errors caused by indiscriminate testing, which may otherwise produce false-positive results, false-negative results or diagnostic delays that are more dangerous than the initial uncertainty itself.

Finally, assessment requires methodological discipline. It is useful to use the same laboratory, the same analytical method and, whenever possible, the same sampling time. Repeating tests after clinical or therapeutic changes is often more informative than a single result. In adrenal disorders during pregnancy, laboratory testing is not an isolated verdict but one component of progressive clinical reasoning, in which the priority is always to identify conditions that threaten the mother and fetus and require prompt treatment, even when biochemical confirmation is not perfect or immediate.

Adrenal insufficiency during pregnancy is rare but clinically significant because the inability to increase glucocorticoid availability adequately and, in primary forms, mineralocorticoid availability may impair maternal adaptation to gestational stress. Disorders known before conception mainly create challenges related to monitoring and treatment adjustment; newly diagnosed cases are particularly insidious because early symptoms may overlap with common manifestations of pregnancy, delaying recognition until the condition becomes more severe or progresses to adrenal crisis.

Clinical suspicion should arise when nausea, vomiting, fatigue, weight loss, dizziness, orthostatic hypotension, hyponatraemia, hypoglycaemia or hyperkalaemia are disproportionate to normal pregnancy or cannot be convincingly explained by other causes. In primary autoimmune forms, other autoimmune endocrinopathies may coexist, whereas in secondary or tertiary forms a history of pituitary disease, chronic corticosteroid therapy or recent glucocorticoid withdrawal is highly relevant. During pregnancy, the main diagnostic trap is to regard symptoms as “normal” when they are actually manifestations of progressive hormonal deficiency.

In women with known adrenal insufficiency, pregnancy does not automatically require an immediate increase in treatment, but it does require close clinical monitoring. The need to increase hydrocortisone and, in primary adrenal insufficiency, fludrocortisone tends to become more apparent during the third trimester, when physiological adaptations in cortisol and aldosterone are more pronounced. Adjustment is not based on a single numerical value but on symptoms, orthostatic blood pressure, serum sodium and clinical tolerance. Excess treatment may promote hyperglycaemia, weight gain and hypertension; inadequate treatment increases the risk of adrenal crisis, reduced uteroplacental perfusion and haemodynamic decompensation.

Practical management centres on prevention of adrenal crisis. The patient must understand sick-day rules, have access to emergency parenteral hydrocortisone and be aware that persistent vomiting, fever, trauma, infection and hyperemesis gravidarum require an immediate increase in glucocorticoid coverage. Hyperemesis is particularly critical because it prevents oral administration and may rapidly precipitate hypovolaemia, hypotension and crisis. In these cases, hospital management with parenteral hydrocortisone, intravenous fluids and electrolyte monitoring is not excessive caution but an integral component of maternal and fetal safety.

Delivery represents a major stress and requires stress-dose steroid coverage according to dedicated protocols, regardless of whether labour is spontaneous or delivery occurs by caesarean section. The immediate postpartum period must also be managed as a phase of physiological stress, with temporary continuation of increased doses followed by gradual return to the usual regimen. This transition is important because risk does not end with birth: pain, blood loss, puerperal infection and difficulty taking oral medication may maintain increased requirements for several hours or days.

A crucial point is that hydrocortisone and fludrocortisone, when indicated as replacement therapy, must not be discontinued or reduced because of concern about fetal harm. The aim is to reproduce adequate physiology as closely as possible, not to expose the fetus to inappropriate pharmacological doses. The real threat to the fetus is not correct replacement therapy but inadequate maternal coverage. Pregnancy in a woman with adrenal insufficiency should therefore be planned, followed by a multidisciplinary team and supported by explicit counselling on treatment, vomiting, stress, delivery and postpartum dose reassessment.

Endogenous hypercortisolism during pregnancy is rare, but when present it creates one of the most difficult situations in endocrine and obstetric medicine. The difficulty arises because normal pregnancy is already characterised by a physiological increase in cortisol, whereas Cushing syndrome causes a pathological excess that may initially be masked by gestational physiology. In addition, many common features of pregnancy, including weight gain, striae, fatigue and mild glucose intolerance, may overlap with manifestations of hypercortisolism, delaying diagnosis until more severe and less non-specific signs appear.

Clinical suspicion should be high when early or severe hypertension, disproportionate gestational diabetes, hypokalaemia, marked skin fragility, easy bruising, proximal myopathy, osteoporosis, rapid metabolic deterioration or signs of hyperandrogenism are present. During pregnancy, a substantial proportion of cases are adrenal in origin, more often than outside gestation. This has both pathogenetic and practical relevance because ACTH-independent forms may be more compatible with conception than severe pituitary forms, which are more frequently associated with marked anovulation.

Diagnosis is complex. The dexamethasone suppression test is poorly reliable, while urinary free cortisol may be physiologically elevated, particularly from the second trimester onwards. Measurement of late-night salivary cortisol using trimester-specific ranges may be helpful, but clinical integration remains essential. The objective is not merely to document elevated cortisol, but to demonstrate loss of normal regulation and inappropriate production in relation to the gestational context. Localisation also requires caution and is generally based on magnetic resonance imaging and specialist assessment, avoiding unnecessary procedures or radiation exposure.

Maternal complications include hypertension, pre-eclampsia, heart failure, infections, fractures, metabolic decompensation and increased thrombotic risk; fetal complications include growth restriction, prematurity, pregnancy loss and fetal death. Hypercortisolism during pregnancy is therefore not exclusively an endocrine disorder but a systemic disease that alters maternal haemodynamics, placentation and fetal development. The severity of outcomes depends greatly on the promptness of recognition and the ability to reduce pathological cortisol exposure during pregnancy.

Treatment depends on aetiology, severity and gestational timing. When the cause is a secreting adrenal lesion and the clinical picture is significant, surgery during the second trimester may represent the most effective solution because it treats the source of hypersecretion at a relatively safer stage for the mother and fetus. When surgery cannot be performed promptly, medical therapy may be required in expert centres, with extremely cautious assessment of the risk-benefit balance of pharmacological treatment during pregnancy.

The postpartum period also requires attention because the end of pregnancy does not automatically produce endocrine stabilisation. If the patient has undergone surgical or medical treatment, adrenal function, possible suppression of the contralateral adrenal gland or pituitary axis and the risk of post-treatment adrenal insufficiency must be reassessed. If diagnosis was deferred until after delivery, the puerperium becomes the period in which the diagnostic work-up can be completed and treatment realigned with standard protocols, while still considering the impact that the disease has already had on the pregnancy and newborn.

Pheochromocytoma and paraganglioma are among the most dangerous endocrine disorders during pregnancy, not because of their frequency but because of the sudden haemodynamic risk they create. The main diagnostic problem is that they may mimic much more common obstetric disorders, particularly gestational hypertension and pre-eclampsia. However, whereas these disorders have placental or vascular pathophysiology, catecholamine-secreting tumours expose the patient to adrenergic surges causing severe vasoconstriction, hypertensive crises, arrhythmias, pulmonary oedema, ischaemia and a marked reduction in uteroplacental perfusion.

Suspicion should arise in the presence of paroxysmal or labile hypertension, severe headache, palpitations, sweating, pallor, tremor, abdominal or chest pain, and episodes triggered by postural changes, urination, anaesthesia, abdominal manipulation or labour. In some patients, the presentation is less typical and may consist mainly of resistant hypertension before the twentieth week or extremely unstable blood pressure. Antepartum diagnosis is the factor that most reduces maternal and fetal mortality, whereas cases recognised only during or after delivery have the poorest outcomes.

From a laboratory perspective, measurement of plasma free metanephrines or fractionated urinary metanephrines is the cornerstone of diagnosis because these markers are not substantially altered during physiological pregnancy. Once catecholamine secretion has been demonstrated, localisation is preferably performed using magnetic resonance imaging without gadolinium. It is essential to remember that, compared with other endocrine disorders, pregnancy does not so much reduce the reliability of the marker as make clinicians less likely to consider the diagnosis at the appropriate time.

Treatment begins with careful medical preparation based on alpha-adrenergic blockade, plasma volume expansion and the subsequent possible addition of a beta-blocker only after adequate alpha control has been achieved. The rationale is to avoid unopposed vasoconstriction, which could precipitate a crisis. Management must take place in centres with endocrine, anaesthetic, obstetric and surgical expertise because every phase, from stabilisation to delivery, requires extremely rigorous haemodynamic control.

Surgery is indicated in selected cases, and timing depends mainly on the gestational age at diagnosis and the degree of clinical control. If the tumour is identified sufficiently early and the patient has been stabilised, adrenalectomy during the second trimester may be considered. If diagnosis occurs later, the safest strategy is often medical control until a planned delivery in a protected setting, followed by surgery at the time of delivery or afterwards, depending on the specific characteristics of the case. The decision is not automatic and requires individualised assessment of maternal and fetal risk.

Delivery itself is a period of extremely high risk if the diagnosis has not been recognised or adrenergic blockade is inadequate. Contractions, pain, tumour compression, anaesthesia and haemodynamic fluctuations may trigger major catecholamine crises. The delivery plan must therefore be formalised in advance, defining timing, setting, invasive monitoring when required and the presence of a prepared team. Even after treatment, genetic and oncological follow-up remains necessary because many PPGLs are syndromic or associated with germline variants, and their implications extend beyond the individual pregnancy.

Primary aldosteronism during pregnancy is probably underdiagnosed rather than truly exceptional. The reason is pathophysiological: normal pregnancy already increases renin and aldosterone, reduces the usefulness of the aldosterone-to-renin ratio and introduces physiological antagonism by progesterone that may mask the classic phenotype. Consequently, many patients are classified generically as hypertensive or as having a hypertensive disorder of pregnancy, whereas a selected proportion actually have clinically significant autonomous adrenal secretion.

Suspicion becomes stronger in the presence of pre-existing hypertension, spontaneous hypokalaemia, a history of an adrenal nodule, resistant hypertension, very early pre-eclampsia or disproportionate obstetric complications. Formal diagnosis is difficult because screening and confirmatory tests are less robust than outside pregnancy and some procedures are inappropriate. In practice, management is often based on a combination of clinical suspicion, a compatible biochemical pattern, safe imaging and therapeutic response rather than on a rigid standardised algorithm.

Adrenal masses discovered during pregnancy require an orderly assessment because the main issue is not morphology alone but whether the lesion is functioning. When an incidentaloma is found, the priority is to exclude catecholamine secretion, clinically relevant hypercortisolism and, when suggested by the blood pressure profile, mineralocorticoid excess. At the same time, oncological risk must be estimated using ultrasound and particularly magnetic resonance imaging, assessing size, radiological characteristics, growth rate and the presence of compressive symptoms.

Many benign non-functioning lesions can be monitored until after delivery without worsening maternal prognosis. By contrast, a secreting mass or a lesion suspicious for adrenocortical carcinoma requires rapid multidisciplinary discussion because the risk is not only oncological but also endocrine and obstetric. In particular, adrenocortical carcinomas may be associated with hypercortisolism and hyperandrogenism, worsening the maternal metabolic and vascular profile and creating an unfavourable fetal environment.

Surgery may be indicated when the mass is suspicious, functioning or symptomatic, with the second trimester generally representing the most favourable window when intervention cannot be deferred. When the lesion appears stable, non-secreting and compatible with benignity, surveillance until the postpartum period is often the most reasonable option. This approach avoids excessive aggressiveness during a period in which pregnancy alters both the significance of some findings and procedural risk, but it must not become therapeutic inertia when warning signs are present.

An essential element is risk communication. Discovery of an adrenal mass during pregnancy often creates anxiety that exceeds the actual risk, whereas false reassurance in other cases may delay necessary investigations. The best management clearly separates immediate endocrine risk, oncological risk and obstetric timing, defining which decisions must be made immediately and which may safely wait until after delivery. Pregnancy does not invalidate the principles of adrenal pathology, but it changes their operational priorities.

Treatment of adrenal disorders during pregnancy must achieve a particularly narrow balance between maternal efficacy and fetal safety. Hydrocortisone is the preferred replacement glucocorticoid in adrenal insufficiency because it most closely reproduces normal physiology, allows flexible adjustment and is extensively inactivated by the placenta. Fludrocortisone also remains essential in primary adrenal insufficiency, with adjustments based on symptoms, blood pressure and sodium rather than renin alone, because renin loses some of its interpretative value during pregnancy.

The use of medication becomes more complex when treating hypercortisolism or secreting tumours. Some steroidogenesis inhibitors may be used only in selected cases and in highly specialised centres when the expected benefit outweighs the potential risk. There are no shortcuts during pregnancy: every pharmacological choice must address a specific clinical question, with the awareness that failure to treat severe adrenal disease may be more dangerous than controlled exposure to necessary therapy.

A specific issue concerns patients with congenital adrenal hyperplasia. In women with classic forms already receiving treatment, pregnancy generally requires continuation of hydrocortisone or prednisolone and, when necessary, fludrocortisone, with reassessment particularly during the second and third trimesters. Glucocorticoids that cross the placenta, such as dexamethasone, should not be used routinely as maternal treatment during pregnancy. Prenatal treatment of a fetus at risk of virilisation remains non-standard and should be considered only within ethically and scientifically controlled protocols.

In non-classic congenital adrenal hyperplasia, pregnancy is intertwined with issues of fertility, miscarriage risk, androgen status and genetic counselling. Management should ideally begin before conception, optimising endocrine control, clarifying the couple’s genetic risk and selecting the most appropriate glucocorticoid. During pregnancy, treatment should aim for maternal stability while avoiding both undertreatment, with androgen reactivation or risk of insufficiency, and overtreatment, with iatrogenic glucocorticoid excess.

In pheochromocytoma and paraganglioma, alpha-blocking agents are the cornerstone of preparation and control. Pregnancy does not alter the underlying pathophysiological principle: catecholamine-induced vasoconstriction is controlled first, followed by management of tachycardia and surgical timing. The key point is that medication is not prescribed merely to “normalise a number”, but to reduce the risk of maternal crisis and uteroplacental compromise. Haemodynamic monitoring is therefore as important as the choice of drug.

Finally, pharmacological management should be planned in phases. The first trimester is the period of greatest embryonic vulnerability and the most difficult symptom interpretation. The second trimester is often the time for surgical decisions when required. The third trimester mainly requires stabilisation, crisis prevention and delivery planning. The postpartum period requires dose reassessment because the end of pregnancy rapidly changes endocrine requirements. Quality of care depends on the continuity of this sequence, not merely on the correctness of a single prescription.

Fetal surveillance in adrenal disorders is not uniform because it depends on the type of maternal disease and the mechanism through which it may affect the fetus. In well-compensated adrenal insufficiency, risk mainly arises from episodes of maternal hypotension, adrenal crisis or electrolyte imbalance, which may reduce uteroplacental perfusion. In hypercortisolism, by contrast, the main problem is the maternal metabolic and vascular environment, which may lead to growth restriction, prematurity and increased obstetric morbidity.

In catecholaminergic syndromes, fetal risk is more directly haemodynamic. Catecholamine surges cause maternal and uteroplacental vasoconstriction, with possible acute impairment of fetal well-being. In these pregnancies, obstetric monitoring must be more intensive and integrated with maternal haemodynamic status because maternal blood pressure stability is itself part of fetal protection. Similarly, in primary aldosteronism or severe endocrine hypertension, fetal injury is often mediated by maternal vascular consequences rather than by the hormone itself.

Ultrasound surveillance of fetal growth therefore assumes particular importance in pregnancies complicated by clinically significant adrenal disease. Abnormalities of growth, amniotic fluid or placental perfusion are non-specific, but they become meaningful when occurring in the context of active endocrine disease, severe hypertension, hypokalaemia or complex treatment. The aim is not to medicalise every pregnancy complicated by endocrine disease, but to identify those in which the maternal disorder genuinely changes fetal risk.

In congenital adrenal hyperplasia, neonatal considerations have specific importance. When there is a genetic risk of the classic form, prenatal counselling should prepare the couple for possible diagnosis and endocrine assessment of the newborn. This does not mean automatically transferring the maternal problem to the fetus, but recognising that pregnancy may be the period in which a diagnostic and care pathway is established that will continue after birth. In patients receiving appropriate maternal glucocorticoid therapy, the objective remains maternal control with minimal unnecessary fetal exposure.

The neonatal phase also requires continuity of information. When pregnancy has been complicated by pheochromocytoma, severe hypercortisolism, unstable adrenal insufficiency or specialist treatment, the neonatal team should be informed before delivery. The newborn will not necessarily have endocrine dysfunction, but awareness of the maternal history allows better interpretation of any metabolic, growth or adaptation abnormalities and helps determine whether targeted investigations are necessary. Effective surveillance begins with a clear clinical handover, not with random interventions after birth.

In summary, fetal and neonatal surveillance in pregnancies at adrenal risk should be proportional to the mechanism involved: reduced perfusion in adrenal insufficiency and crises, metabolic and vascular injury in hypercortisolism, haemodynamic instability in catecholaminergic syndromes and genetic implications in congenital adrenal hyperplasia. Pregnancy complicated by adrenal disease does not automatically require exceptional protocols, but it always requires translation of endocrine risk into a concrete, documented and shared obstetric and neonatal plan.

The postpartum period represents a phase of rapid endocrine readjustment for the adrenal system. The end of pregnancy removes the placental contribution of CRH and the oestrogen-driven increase in CBG, altering total cortisol concentrations and the treatment requirements of patients with known adrenal disease over a relatively short period. The regimen achieved during pregnancy cannot therefore simply be maintained without reassessment. The puerperium is a transitional period with a high risk of error from either overtreatment or undertreatment.

In women with adrenal insufficiency, delivery requires stress-dose coverage, and the immediate postpartum period requires temporary continuation of increased doses followed by gradual return to the usual regimen. If hydrocortisone or fludrocortisone was increased during pregnancy, reduction should be guided by symptoms, blood pressure, electrolyte balance and clinical tolerance. If reduction is too rapid, there is a risk of under-replacement; if too slow, the patient may be unnecessarily exposed to excessive glucocorticoids at a time when physiological requirements are decreasing.

In women with pheochromocytoma or paraganglioma who have not yet undergone surgery, the postpartum period may provide the opportunity to complete definitive treatment if pregnancy was managed with medical stabilisation. In patients who underwent surgery during pregnancy or at delivery, follow-up must reassess catecholamine status, genetic findings, possible recurrence risk and planning for future pregnancies. In this group, delivery is not the end of the problem but often the transition to a new phase of specialist management.

In patients with hypercortisolism or known adrenal masses, the postpartum period requires realignment of the diagnostic and therapeutic pathway with standard non-pregnancy protocols. Gestational physiology no longer interferes with tests to the same extent, making it possible to complete hormonal and radiological investigations more accurately. This is particularly important when a conservative or temporary approach was chosen during pregnancy. The puerperium provides an opportunity to clarify what had merely been stabilised during gestation.

Breastfeeding is generally compatible with appropriate replacement therapy for adrenal insufficiency and, in most cases, with properly managed treatment of other adrenal disorders, provided that the medications used are selected and monitored by specialists. Pharmacological compatibility, however, is not the only issue: fatigue, sleep deprivation, puerperal infections, feeding difficulties and physical stress may increase the risk of decompensation in a woman with absent or reduced adrenal reserve. Counselling should therefore include treatment instructions, warning signs and an emergency plan.

Finally, the postpartum period is the time to plan the patient’s reproductive future. A woman who has undergone pregnancy with adrenal disease should leave the puerperium with a defined strategy: endocrine follow-up, genetic counselling when appropriate, treatment optimisation, guidance for future pregnancies and, in syndromic or neoplastic conditions, long-term follow-up. Quality of care is measured not only by a successful delivery, but by the ability to transform a complex pregnancy into a structured care pathway for the years that follow.