Rarely in less than 5 of cases it is due to an excess of GHRH from a

Rarely in less than 5 of cases it is due to an excess

This preview shows page 1 - 2 out of 2 pages.

Rarely, in less than 5% of cases, it is due to an excess of GHRH from a hypothalamic tumor or a neuroendocrine tumor (usually from lung or pancreas origin). More rarely an ectopic source of GH related to abdominal or hematopoietic tumor may be the etiology of acromegaly [4,5]. In some cases, the source of excess of GH became a challenge when the investigations failed to identify the etiology of acromegaly. There is a lack of a standard guidelines in management of such form of acromegaly with unidentifiable source of GH. Case Report A 60-year-old woman was referred to our hospital on clinical suspicion of acromegaly. She had a history of progressive change in facial appearance, with coarse facial features, and progressive enlargement of hands and feet. Acromegaly was confirmed by a lack of growth hormone level after 75 g glucose challenge test. by oral glucose tolerance test (OGTT) showing and elevated level of Insulin-like growth factor-1 (IGF-1). Other pituitary hormones are summarized in Table 1. Pituitary MRI with was normal (Figures 1 and 2). Search for an ectopic tumor included chest, abdomen computed tomography didn’t reveal any abnormality. Octreoscan did not show any ectopic uptake. Measurement of serum GHRH was normal: 0.78 ng/ml (0-10 ng/ml). In the absence of standard practice guidelines for the management of acromegaly with unidentifiable source of GH excess, we give the patient the option to undergo a surgical exploration of the pituitary gland, but she refused it. Our patient accepted medical treatment with Somatostatin receptor ligands (SRLs), as an alternative approach. Therefore, she was treated with somatostatin analogue. After one year of the treatment we achieve a biochemical remission with normal (IGF-1). Biochemical tests Results Basal serum GH μg/L 4.74 GH nadir during OGTT μg/L 3.45 IGF-1: (117-329 μg/L) 548.6 TSH: (0.3-5.5 mIU/L) 0.72 FT4: (5,1-19,5 ng/l) 12.28 FSH: (1.5-12.4 mIU/L) 46.71 LH: (1.6-8.5 mIU/L) 15.86 Table 1: Hormonal analysis of patient. Figure 1: T1 weighted sagitatl MRI pre-contrast. Figure 2: T1 weighted sagitatl MRI post-contrast.
Image of page 1
Citation: Jemel M (2017) Challenge of Dealing with Acromegalic Patient with Non-Culprit Lesion. J Clin Case Rep 7: 1050. doi: 10.4172/2165- 7920.10001050 Page 2 of 2 Volume 7 • Issue 11 • 10001050 J Clin Case Rep, an open access journal ISSN: 2165-7920 Discussion In view of the laboratory investigations that included measurement of serum insulin-like growth factor 1 (IGF1) and lack of suppression of GH to <1 µg/l during OGTT test. Once the biochemical diagnosis of acromegaly is made, current guidelines recommend contrast-enhanced pituitary MRI as the first line imaging modality [6]. Pituitary computed tomography should be performed If MRI is contraindicated or unavailable. At diagnosis, macroadenomas are detected in 73% of patients sometimes with extrasellar extension [1]. In rare case, acromegaly can be caused by GH secreting pituitary adenoma that are not evident on conventional MRI but discovered at surgical transsphenoidal pituitary exploration.
Image of page 2

You've reached the end of your free preview.

Want to read both pages?

  • Fall '19
  • Pituitary adenoma

  • Left Quote Icon

    Student Picture

  • Left Quote Icon

    Student Picture

  • Left Quote Icon

    Student Picture