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Journal of Clinical Endocrinology & Metabolism, doi:10.1210/jc.2008-0833
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The Journal of Clinical Endocrinology & Metabolism Vol. 93, No. 9 3515-3518
Copyright © 2008 by The Endocrine Society


BRIEF REPORT

Lipodystrophy in Patients with Acromegaly Receiving Pegvisomant

Vivien S. Bonert, Laurence Kennedy, Stephan Petersenn, Ariel Barkan, John Carmichael and Shlomo Melmed

Department of Medicine (V.S.B., J.C., S.M.), Cedars-Sinai Medical Center, David Geffen School of Medicine at University of California, Los Angeles, Los Angeles, California 90048; Department of Medicine (L.K.), University of Florida, Gainesville, Florida 32610; Division of Endocrinology (S.P.), Medical Center, University of Duisburg-Essen, 47048 Duisburg, Germany; and Department of Neurosurgery and Division of Metabolism, Endocrinology, and Diabetes (A.B.), University of Michigan Medical Center, Ann Arbor, Michigan 48105

Address all correspondence and requests for reprints to: Vivien Bonert, M.D., Cedars-Sinai Medical Center, 8700 Beverly Boulevard, Los Angeles, California 90048. E-mail: Vivian.Bonert{at}cshs.org.

Context: Pegvisomant, a GH receptor antagonist, suppresses serum IGF-I levels into the normal range in more than 95% of patients with acromegaly. Documented side effects in the initial registration studies included headache, injection-site reactions, flu-like syndrome, and reversible elevation of hepatic enzymes.

Objective: We report seven patients with acromegaly treated with pegvisomant who developed lipodystrophy at the site of injection (anterior abdominal wall, thigh, buttock, and upper arm). This side effect resulted in discontinuation of pegvisomant in four patients, with subsequent regression of lipohypertrophy.

Subjects: Six female and one male patient with acromegaly, aged 24–59 yr, are reported. All patients had undergone prior transsphenoidal surgery, and four received subsequent radiotherapy. Four patients had been treated with maximal doses of somatostatin analogs with partial suppression of IGF-I levels before initiation of pegvisomant therapy. Pegvisomant suppressed IGF-I levels into the normal range in five of seven subjects, before discontinuation of the drug. Two of seven patients received pegvisomant as first-line medical therapy, without prior somatostatin analog treatment, and one received combination therapy with a long-acting somatostatin analog and weekly pegvisomant injections. One patient experienced an erythematous superficial injection-site reaction that responded to application of steroid cream before the onset of lipohypertrophy.

Conclusions: We report seven patients with acromegaly who developed lipohypertrophy at the pegvisomant injection site. Pegvisomant was discontinued due to dissatisfaction with lipohypertrophy by four patients. Lipohypertrophy regressed in all patients when the medication was discontinued. Lipohypertrophy recurred when two patients were rechallenged with pegvisomant. Patients receiving pegvisomant should undergo frequent examination of injection sites for lipohypertrophy.







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Copyright © 2008 by The Endocrine Society