Diagnosis and Treatment > Investigation > Glucose suppression test
You are looking at 1 - 3 of 3 items
Search for other papers by Katia Regina Marchetti in
Google Scholar
PubMed
Search for other papers by Maria Adelaide Albergaria Pereira in
Google Scholar
PubMed
Search for other papers by Arnaldo Lichtenstein in
Google Scholar
PubMed
Search for other papers by Edison Ferreira Paiva in
Google Scholar
PubMed
Summary
Adrenacarcinomas are rare, and hypoglycemic syndrome resulting from the secretion of insulin-like growth factor II (IGF-II) by these tumors have been described infrequently. This study describes the case of a young woman with severe persistent hypoglycemia and a large adrenal tumor and discusses the physiopathological mechanisms involved in hypoglycemia. The case is described as a 21-year-old woman who presented with 8 months of general symptoms and, in the preceding 3 months, with episodes of mental confusion and visual blurring secondary to hypoglycemia. A functional assessment of the adrenal cortex revealed ACTH-independent hypercortisolism and hyperandrogenism. Hypoglycemia, hypoinsulinemia, low C-peptide and no ketones were also detected. An evaluation of the GH–IGF axis revealed GH blockade (0.03; reference: up to 4.4 ng/mL), greatly reduced IGF-I levels (9.0 ng/mL; reference: 180–780 ng/mL), slightly reduced IGF-II levels (197 ng/mL; reference: 267–616 ng/mL) and an elevated IGF-II/IGF-I ratio (21.9; reference: ~3). CT scan revealed a large expansive mass in the right adrenal gland and pulmonary and liver metastases. During hospitalization, the patient experienced frequent difficult-to-control hypoglycemia and hypokalemia episodes. Octreotide was ineffective in controlling hypoglycemia. Due to unresectability, chemotherapy was tried, but after 3 months, the patient’s condition worsened and progressed to death. In conclusion, our patient presented with a functional adrenal cortical carcinoma, with hyperandrogenism associated with hypoinsulinemic hypoglycemia and blockage of the GH–IGF-I axis. Patient’s data suggested a diagnosis of hypoglycemia induced by an IGF-II or a large IGF-II-producing tumor (low levels of GH, greatly decreased IGF-I, slightly decreased IGF-II and an elevated IGF-II/IGF-I ratio).
Learning points:
-
Hypoglycemyndrome resulting from the secretion of insulin-like growth factor II (IGF-II) by adrenal tumors is a rare condition.
-
Hypoinsulinemic hypoglycemia associated with hyperandrogenism and blockage of the GH–IGF-I axis suggests hypoglycemia induced by an IGF-II or a large IGF-II-producing tumor.
-
Hypoglycemia in cases of NICTH should be treated with glucocorticoids, glucagon, somatostatin analogs and hGH.
Search for other papers by Ekaterina Manuylova in
Google Scholar
PubMed
Search for other papers by Laura M Calvi in
Google Scholar
PubMed
Search for other papers by Catherine Hastings in
Google Scholar
PubMed
Search for other papers by G Edward Vates in
Google Scholar
PubMed
Search for other papers by Mahlon D Johnson in
Google Scholar
PubMed
Search for other papers by William T Cave Jr in
Google Scholar
PubMed
Search for other papers by Ismat Shafiq in
Google Scholar
PubMed
Summary
Co-secretion of growth hormone (GH) and prolactin (PRL) from a single pituitary adenoma is common. In fact, up to 25% of patients with acromegaly may have PRL co-secretion. The prevalence of acromegaly among patients with a newly diagnosed prolactinoma is unknown. Given the possibility of mixed GH and PRL co-secretion, the current recommendation is to obtain an insulin-like growth factor-1 (IGF-1) in patients with prolactinoma at the initial diagnosis. Long-term follow-up of IGF-1 is not routinely done. Here, we report two cases of well-controlled prolactinoma on dopamine agonists with the development of acromegaly 10–20 years after the initial diagnoses. In both patients, a mixed PRL/GH-cosecreting adenoma was confirmed on the pathology examination after transsphenoidal surgery (TSS). Therefore, periodic routine measurements of IGF-1 should be considered regardless of the duration and biochemical control of prolactinoma.
Learning points:
-
Acromegaly can develop in patients with well-controlled prolactinoma on dopamine agonists.
-
The interval between prolactinoma and acromegaly diagnoses can be several decades.
-
Periodic screening of patients with prolactinoma for growth hormone excess should be considered and can lead to an early diagnosis of acromegaly before the development of complications.
Search for other papers by Maryam Rahman in
Google Scholar
PubMed
Search for other papers by Ignacio Jusué-Torres in
Google Scholar
PubMed
Search for other papers by Abdulrahman Alkabbani in
Google Scholar
PubMed
Search for other papers by Roberto Salvatori in
Google Scholar
PubMed
Search for other papers by Fausto J Rodríguez in
Google Scholar
PubMed
Search for other papers by Alfredo Quinones-Hinojosa in
Google Scholar
PubMed
Summary
Pituitary adenomas are usually solitary lesions. Rarely, patients may present with two distinct pituitary tumors. We report a case of synchronous secretory pituitary adenomas in a woman who initially presented with elevated prolactin levels. She was initially treated with cabergoline, but, after many years, she began developing symptoms consistent with acromegaly. Imaging revealed two distinct tumors within the pituitary gland. Endocrinological investigation confirmed acromegaly. At the time of surgery, two separate tumors were identified and resected. Pathological analysis demonstrated one tumor as a prolactinoma, and the other tumor as a GH-secreting adenoma. Postoperatively, her GH and IGF1 levels normalized, while the prolactin level remained slightly above normal. This case highlights that GH and prolactin level elevation is not always from co-secretion by the same adenoma.
Learning points
-
Synchronous pituitary adenomas represent <0.5% of pituitary tumors requiring surgery.
-
In the setting of elevated GH and prolactin levels, one cannot assume that they are co-secreted by the same adenoma.
-
A careful study of hormonal workup and pre-operative imaging is necessary for synchronous pituitary adenomas to assure resection of both tumors.
