Slow-release lanreotide and octreotide LAR in the medical therapy of acromegaly

Giusti, Massimo; Sessarego, Paola; Timossi, G; Bocca, Liliana

doi:10.1530/eje.0.1420697

Cited by 6 publications

(4 citation statements)

References 5 publications

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“…OCT-LAR successfully suppresses IGF-I levels (16 -22, 32) and some authors have found that it is more effective than lanreotide (17)(18)(19)(20). The results of the present study not only confirm that 12 months' treatment with OCT-LAR reduces the thickness of both weight-bearing and non-weight-bearing joints in de novo patients with active acromegaly (as has previously been observed with lanreotide) but also show that the patients in whom disease was controlled experienced a greater reduction in joint thickening at all of the investigated sites.…”

Section: Discussionmentioning

confidence: 99%

Twelve months of treatment with octreotide-LAR reduces joint thickness in acromegaly

Colao¹,

Cannavò

Marzullo³

et al. 2003

European Journal of Endocrinology

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Objective: To evaluate the role of age, gender, duration and control of acromegaly on the reversibility of arthropathy. Patients and design: 30 de novo patients with active acromegaly, 30 cured patients and 30 healthy subjects were studied in a tranverse and an open longitudinal study design. Methods: Shoulder, wrist and knee thickening was measured by ultrasonography at study entry in all 90 subjects and after 12 months of treatment with octreotide-LAR (OCT-LAR) at a dose of 10-40 mg every 28 days in the 30 de novo patients.Results: Thickness at all joint sites was greater in the active than in the cured patients and controls ðP , 0:001Þ; and was greater in the cured patients than in the controls ðP , 0:001Þ: There was no gender difference, but joint thickness was less in the patients with disease duration . 10 years. Age significantly correlated with wrist ðr ¼ 20:55; P , 0:001Þ; right knee ðr ¼ 20:45; P ¼ 0:01Þ; and left knee thickness ðr ¼ 20:42; P ¼ 0:02Þ in patients with active disease, and with wrist thickness ðr ¼ 0:88; P , 0:0001Þ in controls. Twelve months of OCT-LAR treatment led to disease control in 18 patients (60%). There was a decrease in the thickness of the shoulder ð15:1^3:2%Þ; wrist ð20:53 :1%Þ; right knee ð22:2^3:4%Þ and left knee ð18:2^2:8%Þ in all patients but the reduction in joint thickness at all sites was greater in the patients with controlled disease after OCT-LAR treatment than in the uncontrolled patients ðP , 0:01Þ: Shoulder and right knee thickening normalized in respectively 11 (61.1%) and 16 (88.9%) well-controlled patients. Conclusions: Growth hormone and insulin-like growth factor-I (IGF-I) suppression by 12 months' OCT-LAR treatment is accompanied by a significant decrease in the thickness of both weight-bearing and non-weight-bearing joints (mainly in patients whose disease is controlled) regardless of disease duration. These findings suggest that tissue hypertrophy in the context of the acromegalic arthropathy can be improved by suppressing IGF-I levels.

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Section: Discussionmentioning

confidence: 99%

Twelve months of treatment with octreotide-LAR reduces joint thickness in acromegaly

Colao¹,

Cannavò

Marzullo³

et al. 2003

European Journal of Endocrinology

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“…Control of IGF1 and GH by somatostatin agonists has been shown to reduce joint thickness in acromegaly by ultrasonography (10,11). High levels and long duration of excess growth mediators alone have not been shown to correlate with greater joint damage (1,3,12).…”

Section: Introductionmentioning

confidence: 99%

Impact of musculoskeletal disease on quality of life in long-standing acromegaly

Miller¹,

Doll²,

David³

et al. 2008

European Journal of Endocrinology

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Objective: To provide rheumatological assessment of patients with long-standing acromegaly and investigate the impact of musculoskeletal disease on quality of life. Design: Cross-sectional observational study. Methods: Fifty-eight patients diagnosed with acromegaly at least 5 years previously were interviewed and examined by a rheumatologist. Each patient completed the short form-36 (SF-36), arthritis impact measurement scales 2 (AIMS2) and acromegaly quality of life questionnaires (AcroQol). Results: Fifty-two out of 58 (90%) reported musculoskeletal pain, with 29 (50%) reporting neck pain. Hip osteoarthritis was present in 49 (84%) and knee osteoarthritis in 20 (34%). Half the patients (52%) reported sleep disturbance, but only 2 (3.5%) had fibromyalgia. Ten (17.2%) had previously undergone carpal tunnel decompression. Fifty-one (88%) patients had consulted their general practioner and 31 (54%) complementary therapists. SF-36, AIMS2 and AcroQol scores were lower in patients with musculoskeletal pain. Conclusions: This study of musculoskeletal problems in patients with acromegaly reports systematic rheumatological examination, use of medical services and quality of life scores. Musculoskeletal problems should be routinely addressed in acromegaly by both endocrinologist and rheumatologist and a multidisciplinary approach taken to management.European Journal of Endocrinology 158 587-593

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“…[66][67][68] SST analogs significantly reduce GH secretion and IGF-1 levels in patients with acromegaly. 35,36,39,41,42,53,75,[77][78][79][80][81][82][83][84][85][86][87][88]89 Their use is indicated in patients with a macroadenoma who have persistent disease after transsphenoidal surgery, as interim treatment in patients awaiting the full effects of external irradiation, and as preoperative treatment for 2 to 3 months to improve the medical condition of patients with severe disease. It can also be offered as primary therapy in patients who refuse surgery or those with severe medical problems that preclude surgery.…”

Section: Medical Managementmentioning

confidence: 99%

“…[73][74][75][76] Recently, long-acting slow-release formulations of both Sandostatin LAR and a second octapeptide analog Somatulin have become available. 35,36,39,41,42,53,75,[77][78][79][80][81][82][83] LAR is administered as a once-a-month intramuscular depo injection. Lanreotide is available only as the slow-release formulation, but because of its shorter duration of action (10 to 14 days), it needs to be injected two to three times a month.…”

Section: Medical Managementmentioning

confidence: 99%

Management of Growth Hormone-Secreting Adenomas: An Update

Oyesiku¹

2002

Seminars in Neurosurgery

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Acromegaly is a chronic, debilitating condition caused by excessive secretion of growth hormone (GH). The average incidence of acromegaly is approximately 3.3 per million each year with a prevalence of approximately 60 per million. 1,2 GH-secreting adenomas account for 20% of functional adenomas; 75% of GH adenomas are macroadenomas. In the majority of cases, the condition results from benign pituitary adenomas or, rarely, from ectopic production of GH-releasing hormone (GHRH). Ectopic production of GHRH may be from carcinoid, islet cell, and other tumors and may be identified histologically by hyperplasia of somatotrophs or biochemically by elevated circulating levels of GHRH. Excessive GH results in phenotypic changes including acral enlargement, soft tissue swelling, and facial coarsening. Other features include sweating, menstrual irregularity, headache, arthritis, carpal tunnel syndrome, diabetes, hypertension, cardiac dysfunction, loss of libido, galactorrhea, visual field defects, obstructive sleep apnea, and colonic neoplasia. 1,3-7 The mortality for acromegalic patients is two to three times higher than that of the general population, but with appropriate reduction of GH hypersecretion, it tends to shift into the normal range. 8 Treatment is directed to normalizing GH secretion, eradicating or stabilizing the pituitary tumor, preserving normal pituitary function, and managing any associated complications of GH hypersecretion. The treatment modalities available include transsphenoidal surgery, pharmacotherapy, and radiation or combination therapy. This article provides an update of the pathophysiology of GH hypersecretion in acromegaly, the newly defined diagnostic criteria and the end point for a cure for acromegaly, and new developments in pharmacotherapy and radiotherapy.Objectives: Upon completion of this article, the reader will have been updated on the pathophysiology of growth hormone hypersecretion in acromegaly, the newly defined diagnostic criteria and the end point for a cure for acromegaly, and new developments in pharmacotherapy and radiotherapy.hypothalamus to the anterior pituitary gland where they bind and activate specific G protein coupled membrane receptors. Under the influence of GHRH and SST, GH is released from pituitary somatotrophs in a pulsatile manner and acts on the liver and other peripheral targets to stimulate the production of insulin-like growth GROWTH HORMONE PHYSIOLOGY Normal secretion of growth hormone (GH) is regulated by a complex interaction of stimulatory and inhibitory hypothalamic influences, mediated by GH-releasing hormone (GHRH) and somatostatin (SST), respectively. 9-15 These two hormones are transported from the

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Slow-release lanreotide and octreotide LAR in the medical therapy of acromegaly

Cited by 6 publications

References 5 publications

Twelve months of treatment with octreotide-LAR reduces joint thickness in acromegaly

Twelve months of treatment with octreotide-LAR reduces joint thickness in acromegaly

Impact of musculoskeletal disease on quality of life in long-standing acromegaly

Management of Growth Hormone-Secreting Adenomas: An Update

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