Project Title

ACROMEGALY TREATMENT AND RESOLUTION OF SLEEP APNEA

Authors' Affiliations

Sathvika Gaddam, Department of Internal Medicine, East Tennessee State University, Johnson city, TN. Ali Bokhari, Department of Internal Medicine, East Tennessee State University, Johnson city, TN. Deepika Nallala, Department of Endocrinology, East Tennessee State University, Johnson city, TN.

Location

Mt Mitchell

Start Date

4-12-2019 9:00 AM

End Date

4-12-2019 2:30 PM

Poster Number

147

Faculty Sponsor’s Department

Other - please list

Endocrinology

Name of Project's Faculty Sponsor

Dr. Deepika Nallala

Type

Poster: Competitive

Classification of First Author

Medical Resident or Clinical Fellow

Project's Category

Healthcare and Medicine, Endocrine System

Abstract Text

Introduction

Acromegaly is an endocrine disorder characterized by excessive growth hormone production.The most common cause is a benign pituitary adenoma, which can be an isolated tumor or part of a group of concomitant endocrine neoplasms. We present a case of a middle aged woman with sleep apnea and a newly diagnosed acromegaly secondary to a pituitary macroadenoma.

Case presentation

A 51-year-old woman was seen in the endocrinology clinic for evaluation of hyperparathyroidism and mild hypercalcemia. She had no symptoms related to hypercalcemia. However, she complained of enlargement of her fingers and toes. She also reported galactorrhea and breast engorgement. There was no hyperhidrosis or frontal bossing present and she denied headaches or vision symptoms. Past medical history was significant for obstructive sleep apnea. Insulin like growth factor level was 630 ng/ml (reference 53 - 190 ng/ml), prolactin level was 109 ng/ml (reference 1.9- 25 ng/ml), and Follicular stimulating hormone was 0.4mIU/ml (reference 1.2 - 21.0 mIU/ml). TSH, free T4, ACTH, and cortisol were normal. The labs were consistent with pituitary macroadenoma secreting growth hormone (GH) and prolactin. MRI pituitary showed a 1.9 cm macroadenoma with no evidence of optic nerve compression. Due to the coexisting diagnoses of hyperparathyroidism and pituitary adenoma, CT abdomen was done to evaluate for neuroendocrine tumor and to rule out Multiple Endocrine Neoplasia (MEN) Type 1. She then underwent transsphenoidal resection of the pituitary, with immunostaining reflecting diffuse prolactin and patchy GH expression. Post-surgery IGF, prolactin, thyroid function tests were normal. She was started on hydrocortisone replacement due to abnormal ACTH and cortisol. Her calcium levels normalized, and further genetic testing for MEN was abandoned. Her repeat sleep study also showed resolution of sleep apnea. She did not suffer from further symptoms of acromegaly and was scheduled for periodic surveillance for thyroid axis dysfunction.

Discussion

Dysregulated growth hormone production seen in acromegaly leads to increased GH and IGF-1 levels. It has many ramifications including debilitating arthritis from osteoarthropathy, glucose intolerance due to insulin resistance, higher propensity for GI neoplasms, and macroglossia with prognathism causing sleep apnea. Average lifespan is decreased by 30% due to cardiovascular and pulmonary dysfunction. Treatment is aimed at decreasing IGF levels and controlling any mass effect or metabolic abnormalities caused by the tumor. Treatment options include invasive procedures for good surgical candidates and medical therapy via somatostatin analogue for patients who are not. Residual or unresectable tumors can be treated with medical therapy or radiation therapy if there is no response to medication.

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Apr 12th, 9:00 AM Apr 12th, 2:30 PM

ACROMEGALY TREATMENT AND RESOLUTION OF SLEEP APNEA

Mt Mitchell

Introduction

Acromegaly is an endocrine disorder characterized by excessive growth hormone production.The most common cause is a benign pituitary adenoma, which can be an isolated tumor or part of a group of concomitant endocrine neoplasms. We present a case of a middle aged woman with sleep apnea and a newly diagnosed acromegaly secondary to a pituitary macroadenoma.

Case presentation

A 51-year-old woman was seen in the endocrinology clinic for evaluation of hyperparathyroidism and mild hypercalcemia. She had no symptoms related to hypercalcemia. However, she complained of enlargement of her fingers and toes. She also reported galactorrhea and breast engorgement. There was no hyperhidrosis or frontal bossing present and she denied headaches or vision symptoms. Past medical history was significant for obstructive sleep apnea. Insulin like growth factor level was 630 ng/ml (reference 53 - 190 ng/ml), prolactin level was 109 ng/ml (reference 1.9- 25 ng/ml), and Follicular stimulating hormone was 0.4mIU/ml (reference 1.2 - 21.0 mIU/ml). TSH, free T4, ACTH, and cortisol were normal. The labs were consistent with pituitary macroadenoma secreting growth hormone (GH) and prolactin. MRI pituitary showed a 1.9 cm macroadenoma with no evidence of optic nerve compression. Due to the coexisting diagnoses of hyperparathyroidism and pituitary adenoma, CT abdomen was done to evaluate for neuroendocrine tumor and to rule out Multiple Endocrine Neoplasia (MEN) Type 1. She then underwent transsphenoidal resection of the pituitary, with immunostaining reflecting diffuse prolactin and patchy GH expression. Post-surgery IGF, prolactin, thyroid function tests were normal. She was started on hydrocortisone replacement due to abnormal ACTH and cortisol. Her calcium levels normalized, and further genetic testing for MEN was abandoned. Her repeat sleep study also showed resolution of sleep apnea. She did not suffer from further symptoms of acromegaly and was scheduled for periodic surveillance for thyroid axis dysfunction.

Discussion

Dysregulated growth hormone production seen in acromegaly leads to increased GH and IGF-1 levels. It has many ramifications including debilitating arthritis from osteoarthropathy, glucose intolerance due to insulin resistance, higher propensity for GI neoplasms, and macroglossia with prognathism causing sleep apnea. Average lifespan is decreased by 30% due to cardiovascular and pulmonary dysfunction. Treatment is aimed at decreasing IGF levels and controlling any mass effect or metabolic abnormalities caused by the tumor. Treatment options include invasive procedures for good surgical candidates and medical therapy via somatostatin analogue for patients who are not. Residual or unresectable tumors can be treated with medical therapy or radiation therapy if there is no response to medication.