Abstract


The indications for Botox have evolved beyond cosmetic use to urinary incontinence and muscle spasms. With this popularity come more potential adverse effects, which are known to be short-lived and involve general or extremity weakness and pain. We present the first reported case of a potential severe adverse side effect affecting the pituitary gland and persisting over a year after the injection. view more

The indications for Botox have evolved beyond cosmetic use to urinary incontinence and muscle spasms. With this popularity come more potential adverse effects, which are known to be short-lived and involve general or extremity weakness and pain. We present the first reported case of a potential severe adverse side effect affecting the pituitary gland and persisting over a year after the injection.
A 70-year-old female with a no significant medical history who suffered a stroke was referred for endocrine evaluation. The stroke had been managed medically and she had completed several weeks of rehabilitation.  Two months later, she continued to suffer from right arm spasticity and Botox injections were recommended. She received 300 units of Botox to multiple muscle groups over her right upper extremity.  Four days later, she developed acute bilateral lower extremity pain and weakness making her unable to participate in her physical therapy sessions.  She was assured that these side effects were not unexpected and supportive care was recommended and statin was held. A week later, leg pain had improved but had not resolved. She resumed physical therapy at which time her blood pressure was low and she endorsed persistent fatigue. Laboratory tests revealed an undetectable cortisol, which led to her endocrine referral. On evaluation, she endorsed poor appetite, 10-12 lb. weight loss, and fatigue. Subsequent testing confirmed secondary adrenal insufficiency with a cortisol level of <1.2 mcg/dL (ref. range 3.09 -22.40 mcg/dL) and undetectable ACTH <5.0 pg/mL (ref. range: 9.0 – 50.0 pg/mL). Thyroid function tests, prolactin and insulin growth factor-1 were unremarkable. She was started on hydrocortisone 10/5mg daily and her symptoms improved quickly. Imaging from stroke ruled out pituitary masses albeit not done with pituitary protocol. Repeated testing of the hypothalamic-pituitary-adrenal axis over the next year showed continued suppression of ACTH and cortisol despite titrating hydrocortisone doses to lowest tolerable dose of 7.5/2.5mg.
Botulinum toxin inhibits neurotransmitter release by cleaving SNAP-25 and SNARE proteins. These proteins are necessary for vesicular exocytosis and have been implicated in the release of hormones from the anterior pituitary. This mechanism for GH and prolactin release has made Botox a targeted secretion inhibitor to treat prolactinomas and acromegaly. Similarly, Botox could have caused inhibition of ACTH release resulting in central adrenal insufficiency for our patient. Dysport1 and Botox2 have reported adverse effects of asthenia in areas away from the injection site hours to weeks after treatment but do not specifically endorse endocrine abnormalities. Central adrenal insufficiency is a severe but treatable condition. Being aware of this potential adverse event and further researching its mechanism can help diagnose and treat affected patients promptly.

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