ABSTRACT
Isolated adrenocorticotropic hormone (ACTH) deficiency is an uncommon disorder for which the pathogenetic mechanism has not yet been identified. It has been reported that isolated ACTH deficiency (ICD) may be accompanied by deficiencies in other pituitary hormones; impaired growth hormone (GH) secretion was noted in 20 to 30% of ICD patients. Here, we describe a female patient with isolated ACTH deficiency accompanied by empty sella syndrome presenting as hypoglycemia, which was confirmed via various endocrine tests and magnetic resonance imaging (MRI) of the sella turcica. The patient's symptoms improved rapidly with prednisolone therapy and, during follow-up, her previously impaired GH response to provocative stimuli and high TSH levels were corrected by glucocorticoid replacement alone. However, treatment failed to normalize plasma IGF-1 levels, suggesting that physiological cortisol levels are necessary for a normal plasma GH response to provocative stimuli.
Subject(s)
Female , Humans , Adrenal Insufficiency , Adrenocorticotropic Hormone , Empty Sella Syndrome , Follow-Up Studies , Growth Hormone , Hydrocortisone , Hypoglycemia , Insulin-Like Growth Factor I , Magnetic Resonance Imaging , Plasma , Prednisolone , Sella TurcicaABSTRACT
Myasthenia gravis and autoimmune thyroid disorders often overlap. It is known that hyperthyroidism occurs in 2~17.5% of patients with myasthenia gravis. Thyrotoxicosis may influence the clinical course of myasthenia gravis. Overlapping clinical features may cause diagnostic confusion when Graves' disease and myasthenia gravis co-exist. Thus, various tests may be needed to distinguish these two diseases. It is clinically important to screen patients with myasthenia gravis for the co-existence of autoimmune thyroid disorders and vice versa. We cared for a patient with Graves' disease associated with ocular myasthenia gravis who presented with fluctuating double vision and ptosis. Ocular myasthenia gravis was diagnosed by electrophysiologic study and presence of acetylcholine receptor antibody. The patient had a favorable clinical and laboratory response to treatment with an anticholinesterase (pyridostigmine) and an antithyroid drug (propylthiouracil), and he had minimal symptoms at the 9-month follow-up examination.