Adrenal suppression inhaled corticosteroids

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The clinical pathways are based upon publicly available medical evidence and/or a consensus of medical practitioners at The Children’s Hospital of Philadelphia (“CHOP”) and are current at the time of publication. These clinical pathways are intended to be a guide for practitioners and may need to be adapted for each specific patient based on the practitioner’s professional judgment, consideration of any unique circumstances, the needs of each patient and their family, and/or the availability of various resources at the health care institution where the patient is located.

Accordingly, these clinical pathways are not intended to constitute medical advice or treatment, or to create a doctor-patient relationship between/among The Children’s Hospital of Philadelphia (“CHOP”), its physicians and the individual patients in question. CHOP does not represent or warrant that the clinical pathways are in every respect accurate or complete, or that one or more of them apply to a particular patient or medical condition. CHOP is not responsible for any errors or omissions in the clinical pathways, or for any outcomes a patient might experience where a clinician consulted one or more such pathways in connection with providing care for that patient.

Untreated, adrenal insufficiency is fatal, and indeed this was invariably the case until the advent of synthetic cortisone in 1949. Treatment of Addison's disease is lifelong. The prognosis for any patient with adrenal insufficiency will depend on the underlying cause. In those patients in whom the prognosis is not affected by the underlying pathology, replacement therapy should result in a return to health. However, a Norwegian study found an excess of mortality in patients diagnosed with Addison's disease at a young age, associated with acute adrenal failure, infection and sudden death. [ 16 ]

Pheochromocytoma is a neoplasm composed of cells similar to the chromaffin cells of the mature adrenal medulla. Pheochromocytomas occur in patients of all ages, and may be sporadic, or associated with a hereditary cancer syndrome , such as multiple endocrine neoplasia (MEN) types IIA and IIB, neurofibromatosis type I, or von Hippel-Lindau syndrome . Only 10% of adrenal pheochromocytomas are malignant , while the rest are benign tumors . The most clinically important feature of pheochromocytomas is their tendency to produce large amounts of the catecholamine hormones epinephrine (adrenaline) and norepinephrine . This may lead to potentially life-threatening high blood pressure , or cardiac arrythmias , and numerous symptoms such as headache , palpitations , anxiety attacks , sweating , weight loss , and tremor . Diagnosis is most easily confirmed through urinary measurement of catecholamine metabolites such as VMA and metanephrines . Most pheochromocytomas are initially treated with anti-adrenergic drugs to protect against catecholamine overload, with surgery employed to remove the tumor once the patient is medically stable.

Combined pituitary hormone deficiency (including ACTH deficiency) due to genetic pituitary abnormalities is rare. ACTH and cortisol deficiency have been described in patients with multiple pituitary hormone deficiencies due to mutations in the PROP-1 (Prophet of Pit-1) gene, even though PROP-1 is not expressed in corticotropes. The onset of cortisol deficiency, which may be severe, ranges from childhood to late adulthood [ 2-5 ]. Mutations in other transcription factors involved in early pituitary development (HESX1, LHX4) also can result in variable degrees of hypopituitarism that include ACTH deficiency [ 6,7 ]. (See "Causes of hypopituitarism", section on 'Genetic diseases' .)

Dexamethasone suppression tests are used to assess the status of the hypothalamic-pituitary-adrenal (HPA) axis and for the differential diagnosis of adrenal hyperfunction. The low-dose dexamethasone suppression tests are used to assess nonsuppressible cortisol production by adrenal incidentalomas and to differentiate patients with Cushing's syndrome of any cause from patients who do not have Cushing's syndrome. The high-dose dexamethasone suppression tests help to distinguish patients with Cushing's disease (Cushing's syndrome caused by pituitary hypersecretion of corticotropin [ACTH]) from most patients with the ectopic ACTH syndrome (Cushing's syndrome caused by nonpituitary ACTH-secreting tumors).

Adrenal suppression inhaled corticosteroids

adrenal suppression inhaled corticosteroids

Combined pituitary hormone deficiency (including ACTH deficiency) due to genetic pituitary abnormalities is rare. ACTH and cortisol deficiency have been described in patients with multiple pituitary hormone deficiencies due to mutations in the PROP-1 (Prophet of Pit-1) gene, even though PROP-1 is not expressed in corticotropes. The onset of cortisol deficiency, which may be severe, ranges from childhood to late adulthood [ 2-5 ]. Mutations in other transcription factors involved in early pituitary development (HESX1, LHX4) also can result in variable degrees of hypopituitarism that include ACTH deficiency [ 6,7 ]. (See "Causes of hypopituitarism", section on 'Genetic diseases' .)

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