Difficulties in diagnosing acromegaly, acromegaly with apparently normal GH: Micromegaly

INTRODUCTION: Acromegaly results from pathologically increased secretion of growth hormone (GH) from the pituitary somatotroph adenoma. If left untreated, it is associated with increased morbidity and mortality. We present a case of micromegaly, whose diagnosis is challenging for clinicians. CLINICAL CASE: A 40-year-old woman presented with complaints of enlarged facial features, hands and feet, and separation between teeth. She was using a salbutamol inhaler with the diagnosis of asthma. Her physical examination was unremarkable except for a body mass index of 28.7 kg/m2 and malocclusion. Insulin-like growth factor (IGF)-1 250 ng/mL (101–234) and GH 2.1 ng/mL was detected. 0, 1. and 2nd hour in oral glucose tolerance test (OGTT)-GH; hour GH/glucose values were 6.7/70, 1.5/98, 0.35 ng/ml /95 mg/dl, respectively. Sella magnetic resonance imaging (MRI) revealed an 8×5mm adenoma in the pituitary gland (Figure). Pseudoacromegaly causes such pachydermoperiostitis, severe insulin resistance, familial mandibular prognathism, use of phenytoin and minoxidil, and causes of false IGF-1 elevation such as pregnancy, puberty/adolescent period, thyrotoxicosis, glucocorticoid use were excluded. It was decided that the patient should be operated on. No adenoma was detected in the pathology tissue of the operated patient, but IGF-1 was detected at 201 ng/ml (101–234) and GH was 1,1 ng/ml in the 3rd postoperative month. The nadir GH was found to be 0.3 ng/ml in the OGTT-GH suppression test. Medical treatment was not started. The case has been followed for 2 years in remission. CONCLUSION: Micromegaly describes a subset of patients with clinically evident acromegaly and elevated IGF-1 with apparently normal basal GH and often <0.4 ng/mL glucose suppressed GH. This condition is relatively rare in patients with acromegaly. As in our case, micromegaly should be considered in diagnosing patients with “normal” GH but with clinical signs, or even patients without clinical signs but with pituitary tumors and elevated IGF-1. [Figure: see text] [Figure: see text]