Adenoma de hipófisis como forma infrecuente de insuficiencia suprarrenal secundaria. Presentación de un caso

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Abstract

Los adenomas de hipófisis son tumores benignos originados en uno de los cinco tipos celulares de la hipófisis anterior. La insuficiencia suprarrenal secundaria ocurre cuando las glándulas adrenales no producen hormonas por la falta de hormona adenocorticotrópica hipofisaria o del factor liberador de corticotropina hipotalámico. Se presenta el caso de una paciente de 37 años de edad, que un año atrás comenzó con fasciculaciones musculares de piernas y brazos, debilidad muscular, cansancio fácil, dolores musculares, cefalea hemicránea derecha, intensa y pulsátil, entre otros síntomas. Se le realizaron varios estudios (dosificación de cortisol en sangre, hormona adenocorticotrópica, calcio y fósforo en sangre y orina, resonancia magnética de cráneo) que permitieron el diagnóstico de adenoma de hipófisis con déficit aislado de hormona adenocorticotrópica e insuficiencia suprarrenal secundaria. El tratamiento con esteroides y suplementos de calcio garantizaron la evolución favorable.

Translated abstract

Pituitary adenomas are benign tumors arising from one of the five cell types in the anterior pituitary. Secondary adrenal insufficiency occurs when the adrenal glands do not produce hormones due to the lack of pituary adrenocorticotropic hormone or hypothalamic corticotropin-releasing factor. The case of a 37-year-old female patient who started developing muscle twitching in legs and arms, muscular weakness, fatigue, muscle aches, severe and throbbing hemicrania on the right side, among other symptoms, a year ago is presented. Several tests were performed (cortisol level, adrenocorticotropic hormone, calcium and phosphorus in blood and urine, magnetic resonance imaging of the skull), leading to the diagnosis of pituitary adenoma with isolated adrenocorticotropic hormone deficiency and secondary adrenal insufficiency. Treatment with steroids and calcium supplements ensured a satisfactory recovery.

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Most cited references 21

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Hypothalamic pituitary adrenal function during critical illness: limitations of current assessment methods.

Baha M Arafah (2006)

Activation of the hypothalamic-pituitary-adrenal (HPA) axis represents one of several important responses to stressful events and critical illnesses. Despite a large volume of published data, several controversies continue to be debated, such as the definition of normal adrenal response, the concept of relative adrenal insufficiency, and the use of glucocorticoids in the setting of critical illness. The primary objective was to review some of the modulating factors and limitations of currently used methods of assessing HPA function during critical illness and provide alternative approaches in that setting. This was a critical review of relevant data from the literature with inclusion of previously published as well as unpublished observations by the author. Data on HPA function during three different forms of critical illnesses were reviewed: experimental endotoxemia in healthy volunteers, the response to major surgical procedures in patients with normal HPA, and the spontaneous acute to subacute critical illnesses observed in patients treated in intensive care units. The study was conducted at an academic medical center. Participants were critically ill subjects. There was no intervention. The main measure was to provide data on the superiority of measuring serum free cortisol during critical illness as contrasted to those of total cortisol measurements. Serum free cortisol measurement is the most reliable method to assess adrenal function in critically ill, hypoproteinemic patients. A random serum free cortisol is expected to be 1.8 microg/dl or more in most critically ill patients, irrespective of their serum binding proteins. Because the free cortisol assay is not currently available for routine clinical use, alternative approaches to estimate serum free cortisol can be used. These include calculated free cortisol (Coolens' method) and determining the free cortisol index (ratio of serum cortisol to transcortin concentrations). Preliminary data suggest that salivary cortisol measurements might be another alternative approach to estimating the free cortisol in the circulation. When serum binding proteins (albumin, transcortin) are near normal, measurements of total serum cortisol continue to provide reliable assessment of adrenal function in critically ill patients, in whom a random serum total cortisol would be expected to be 15 microg/dl or more in most patients. In hypoproteinemic critically ill subjects, a random serum total cortisol level is expected to be 9.5 microg/dl or more in most patients. Data on Cosyntropin-stimulated serum total and free cortisol levels should be interpreted with the understanding that the responses in critically ill subjects are higher than those of healthy ambulatory volunteers. The Cosyntropin-induced increment in serum total cortisol should not be used as a criterion for defining adrenal function, especially in critically ill patients. The routine use of glucocorticoids during critical illness is not justified except in patients in whom adrenal insufficiency was properly diagnosed or others who are hypotensive, septic, and unresponsive to standard therapy. When glucocorticoids are used, hydrocortisone should be the drug of choice and should be given at the lowest dose and for the shortest duration possible. The hydrocortisone dose (50 mg every 6 h) that is mistakenly labeled as low-dose hydrocortisone leads to excessive elevation in serum cortisol to values severalfold greater than those achieved in patients with documented normal adrenal function. The latter data should call into question the current practice of using such doses of hydrocortisone even in the adrenally insufficient subjects.

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The approach to the adult with newly diagnosed adrenal insufficiency.

Wiebke Arlt (2009)

Adrenal insufficiency, primarily presenting as an adrenal crisis, is a life-threatening emergency and requires prompt therapeutic management including fluid resuscitation and stress dose hydrocortisone administration. Primary adrenal insufficiency is most frequently caused by autoimmune adrenalitis, and hypothalamic-pituitary tumors represent the most frequent cause of secondary adrenal insufficiency. However, the exact underlying diagnosis needs to be confirmed by a stepwise diagnostic approach, with an open eye for other differential diagnostic possibilities. Chronic replacement therapy with glucocorticoids and, in primary adrenal insufficiency, mineralocorticoids requires careful monitoring. However, current replacement strategies still require optimization as evidenced by recent studies demonstrating significantly impaired subjective health status and increased mortality in patients with primary and secondary adrenal insufficiency. Future studies will have to explore the potential of dehydroepiandrosterone replacement and modified delayed-release hydrocortisone to improve the prospects of patients with adrenal insufficiency.

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Inadequacies of glucocorticoid replacement and improvements by physiological circadian therapy.

Andrew J. Ross, M Debono, John Newell (2009)

Patients with adrenal insufficiency need lifelong glucocorticoid replacement, but many suffer from poor quality of life, and overall there is increased mortality. Moreover, it appears that use of glucocorticoids at the higher end of the replacement dose range is associated with increased risk for cardiovascular and metabolic bone disease. These data highlight some of the inadequacies of current regimes. The cortisol production rate is estimated to be equivalent to 5.7-7.4 mg/m(2) per day, and a major difficulty for replacement regimes is the inability to match the distinct circadian rhythm of circulating cortisol levels, which are low at the time of sleep onset, rise between 0200 and 0400 h, peaking just after waking and then fall during the day. Another issue is that current dose equivalents of glucocorticoids used for replacement are based on anti-inflammatory potency, and few data exist as to doses needed for equivalent cardiovascular and bone effects. Weight-adjusted, thrice-daily dosing using hydrocortisone (HC) reduces glucocorticoid overexposure and represents the most refined regime for current oral therapy, but does not replicate the normal cortisol rhythm. Recently, proof-of-concept studies have shown that more physiological circadian glucocorticoid therapy using HC infusions and newly developed oral formulations of HC have the potential for better biochemical control in patients with adrenal insufficiency. Whether such physiological replacement will have an impact on the complications seen in patients with adrenal insufficiency will need to be analysed in future clinical trials.