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Endocrine Abstracts (2016) 41 EP271 | DOI: 10.1530/endoabs.41.EP271

1Ankara Yildirim Beyazit University School of Medicine, Department of Endocrinology and Metabolism, Ankara, Turkey; 2Ankara Yildirim Beyazit University School of Medicine, Department of Haematology, Ankara, Turkey.


Introduction: Acromegaly patients are known to have an increased risk of malignancies. This may be as a result of the effect of insulin-like growth factor I (IGF-I) on cellular proliferation and apoptosis inhibition. Although there are various reports related with hematological malignancies in children who treated with growth hormone (GH), few data are available about hematological malignancies in acromegaly patients. Here, we report a patient with acromegaly who has been developed chronic lypmhocytic leukemia (CLL) in the follow-up period.

Case: A 30-year-old woman who was at 25th weeks gestation were consulted for gestational diabetes mellitus 9 years ago. Physical examination, random GH, IGF-I levels and glucose suppression test results were consistent with acromegaly. She reached full term without treatment and had a caesarian section and delivered a 4200-gr-baby boy with Apgar score of 9. After 1 year delivery transsphenoidal surgery was performed and 3 months after the operation long-acting somatostatin analog treatment was begun. Since she had residual adenoma and biochemical remission was not achieved with medical treatment, she had underwent second operation after 1 year later the first surgery. Since the remission was not achieved despite the medical treatment, after 1 year later the second operation gamma-knife therapy has been performed. After 5 years later the radiotherapy, GH and IGF-I levels were decreased gradually, somatostatin therapy was lowered and finally discontinued. However, the patient had progressive leukocytosis with 90% lymphocytes. Flowcytometric analysis of the peripheral blood was consisted with CD5+, CD19+, CD20+, CD22+, CD79b+, CD43+, CD200+ lymphocytes with surface anti-kappa monoclonality. Fluorescent in situ hybridization analysis of bone marrow aspiration revealed 20% deletion 17p13.1(TP53). Her findings were consistent with CLL-stage II.

Conclusion: Occurrence of CLL in the course of acromegaly may have been caused by excessive endogenous GH or may be a coincidental situation.

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