{"title":"Octreotide-LAR as primary therapy for acromegaly: a retrospective serial case","authors":"R. Batista","doi":"10.15406/jdmdc.2018.05.00144","DOIUrl":null,"url":null,"abstract":"Acromegaly is a chronic disease with signs and symptoms resulting from the excess of circulating growth hormone (GH).1–3 More than 95% of the cases are related to the presence of a GHsecreting adenoma. This hormone stimulates hepatic synthesis of the insulin-like growth factor type I (IGF-I), which is responsible for the GH-related somatic effects.1,4 The incidence of acromegaly is approximately 3-4 cases per million population, while prevalence is around 60 cases per million population per year. This condition occurs with equal frequency in males and females, more commonly in the fourth and fifth decades.5‒7 Because of the insidious progression of acromegaly and failure to recognize its clinical manifestations, diagnosis is delayed in around 8 to 10 years after the onset of the disease.4,8 Continued exposure to excess GH and IGF-I is related to high morbidity and mortality due to cardiovascular, respiratory, neoplastic and metabolic complications, in addition to severe functional impairment as a result of skeletal complications.3,4,8,9 Recent evidence shows a mortality rate for acromegalic patients 1.7 times higher than that of the general population. The reverse proportion is true when GH levels are reduced to values below 2.5mcg/L, regardless of the therapy instituted.10–12 The treatment of acromegaly aims to reduce symptoms, control tumor growth, inhibit GH hypersecretion and normalize IGF-I serum concentrations, thereby reducing acromegalyrelated morbidity and mortality. Three treatment options are available: surgery, drug therapy and radiotherapy.13 Transsphenoidal surgery (TSS) is the first-line treatment for acromegaly, since the complete resection of the adenoma regulates hormone levels and improves the alterations that compromise tissues and organs. The success of TSS depends on the neurosurgeon ́s experience and skills, the size and extension of the tumor and preoperative GH levels. In patients with a microadenoma, normalization of IGF-I occurs after TSS in 75-95% of the cases. Normalization is less frequent with macroadenomas, and is found in approximately 50% of cases.14–16 Medical treatment is often required, especially when no surgical cure is achieved and for patients at an advanced age and/or when severe comorbidity is present that contraindicates the surgery. Preoperative use of somatostatin analogs can be beneficial, as they promote tumor shrinkage and this facilitates surgical resection and attenuates the perioperative complications deriving from GH excess.17 The medical treatment options currently available are somatostatin analogs (octreotide, lanreotide (LAN) and pasireotide); dopamine agonists (bromocriptine and cabergoline), and GH-receptor antagonist pegvisomant.4","PeriodicalId":92240,"journal":{"name":"Journal of diabetes, metabolic disorders & control","volume":"106 1","pages":""},"PeriodicalIF":0.0000,"publicationDate":"2018-05-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"1","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of diabetes, metabolic disorders & control","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.15406/jdmdc.2018.05.00144","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 1
Abstract
Acromegaly is a chronic disease with signs and symptoms resulting from the excess of circulating growth hormone (GH).1–3 More than 95% of the cases are related to the presence of a GHsecreting adenoma. This hormone stimulates hepatic synthesis of the insulin-like growth factor type I (IGF-I), which is responsible for the GH-related somatic effects.1,4 The incidence of acromegaly is approximately 3-4 cases per million population, while prevalence is around 60 cases per million population per year. This condition occurs with equal frequency in males and females, more commonly in the fourth and fifth decades.5‒7 Because of the insidious progression of acromegaly and failure to recognize its clinical manifestations, diagnosis is delayed in around 8 to 10 years after the onset of the disease.4,8 Continued exposure to excess GH and IGF-I is related to high morbidity and mortality due to cardiovascular, respiratory, neoplastic and metabolic complications, in addition to severe functional impairment as a result of skeletal complications.3,4,8,9 Recent evidence shows a mortality rate for acromegalic patients 1.7 times higher than that of the general population. The reverse proportion is true when GH levels are reduced to values below 2.5mcg/L, regardless of the therapy instituted.10–12 The treatment of acromegaly aims to reduce symptoms, control tumor growth, inhibit GH hypersecretion and normalize IGF-I serum concentrations, thereby reducing acromegalyrelated morbidity and mortality. Three treatment options are available: surgery, drug therapy and radiotherapy.13 Transsphenoidal surgery (TSS) is the first-line treatment for acromegaly, since the complete resection of the adenoma regulates hormone levels and improves the alterations that compromise tissues and organs. The success of TSS depends on the neurosurgeon ́s experience and skills, the size and extension of the tumor and preoperative GH levels. In patients with a microadenoma, normalization of IGF-I occurs after TSS in 75-95% of the cases. Normalization is less frequent with macroadenomas, and is found in approximately 50% of cases.14–16 Medical treatment is often required, especially when no surgical cure is achieved and for patients at an advanced age and/or when severe comorbidity is present that contraindicates the surgery. Preoperative use of somatostatin analogs can be beneficial, as they promote tumor shrinkage and this facilitates surgical resection and attenuates the perioperative complications deriving from GH excess.17 The medical treatment options currently available are somatostatin analogs (octreotide, lanreotide (LAN) and pasireotide); dopamine agonists (bromocriptine and cabergoline), and GH-receptor antagonist pegvisomant.4