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The pathogenesis of acromegaly

Clinical and immunocytochemical analysis in 75 patients

Edward R. Laws Jr., Bernd W. Scheithauer, Sandra Carpenter, Raymond V. Randall and Charles F. Abboud

T he pathogenesis of acromegaly was a matter of controversy for many years after the syndrome was first described by Pierre Marie in 1886. 20 Many authors, including Harvey Cushing, 7, 8 initially thought that the enlargement of the pituitary gland might merely be part of a generalized hypertrophic process affecting many endocrine glands and other organs. It was not until 1905 to 1910 that the intrasellar abnormality was generally recognized as a neoplasm actually responsible for the entire clinical syndrome. 18 Currently, acromegaly is one of the clearest

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Nancy Epstein, Margaret Whelan and Vallo Benjamin

S pinal stenosis is occasionally associated with acromegaly as a result of hypertrophy of the bones and ligaments. We present the case of a 54-year-old acromegalic man with a 30-year history of low-back pain, recent progressive paraparesis, and bilateral lumbosacral radiculopathy secondary to spinal stenosis. Despite earlier conventional surgery and radiation therapy directed at the pituitary tumor, the growth hormone (HGH) had remained elevated between 16 and 22 ng/ml, and was apparently the cause of this clinical state. Following an extensive laminectomy

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Familial acromegaly with pituitary adenoma

Report of three affected siblings

Kazem Abbassioun, Vahab Fatourehchi, Abbass Amirjamshidi and Nemotallah Aghai Meibodi

F amilial occurrence of pituitary adenomas with or without clinical acromegaly in association with other endocrine-related tumors (multiple endocrine adenomatosis) is a well recognized entity. 6, 8 However, familial cases of isolated acromegaly with pituitary adenoma are extremely rare, 2 and most reports lack biochemical and histological documentation. Recently, hypersomatotropism and acanthosis nigricans were reported in two brothers with pituitary tumors 4 and in uni-ovular twin brothers. 3 We are reporting the cases of three acromegalic brothers with

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Atul Goel, Abhidha H. Shah and Ram Menon

O steoarticular involvement is a feature of acromegaly that leads to arthropathy, which is a major cause of morbidity. The spine is noticeably affected by chronic GH excess and demonstrates widened intervertebral spaces, vertebral enlargement, and osteophyte formation, which are caused by endochondral, marginal, and subligamentous growth of vertebral bone. 10 Symptomatic atlas facet hypertrophy in relationship with acromegaly has not previously been reported in the literature. We report such a case, analyze the treatment, and review the literature on the

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Kenneth R. Feingold, Ira D. Goldfine and Philip R. Weinstein

T he signs and symptoms of acromegaly are almost always the result of a pituitary adenoma producing elevated serum levels of growth hormone (HGH). 8 Rarely, acromegalic patients have normal or nearly normal basal levels of HGH, and their acromegaly results from abnormal HGH secretory patterns. 19 We have recently had the opportunity to study a patient with acromegaly, elevated somatomedin levels, and an enlarged sella turcica, whose basal HGH values were within the normal range. This patient had evidence of abnormal HGH secretory dynamics, but at pituitary

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Sunil Manjila, Osmond C. Wu, Fahd R. Khan, Mehreen M. Khan, Baha M. Arafah, and Warren R. Selman

A cromegaly is a chronic disorder characterized by elevated GH secretion with a resultant increase in serum IGF-I level. A pituitary adenoma is the most common cause of the disorder. Persistently elevated levels of GH and IGF-I lead to significant morbidity and mortality. Complications of acromegaly include, but are not limited to, acral growth, cardiovascular disease, insulin resistance and diabetes, arthritis, hypertension, and sleep apnea. All of these adverse complications individually and collectively lead to a shortened life span. With GH

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Hélène Long, Hugues Beauregard, Maurice Somma, Ronald Comtois, Omar Serri and Jules Hardy

T ranssphenoidal selective adenomectomy is the most widely used primary treatment for acromegaly, and its efficacy and relative safety are now well established. 7, 10, 12, 18, 27–29 Overall, approximately 60% of patients achieve a postoperative basal growth hormone (GH) level of less than 5 µg/L with a complication rate of 7%. 27 Management of patients who are not cured or in whom disease recurs after surgery is still a matter of controversy. Options are radiotherapy, reoperation, and medical therapy with dopamine agonists and/or, more recently, with the

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Mark D. Krieger, William T. Couldwell and Martin H. Weiss

-line treatment modality for acromegaly. 1, 2, 4, 10, 14, 18, 20, 25, 32, 35, 39, 46, 48, 49, 51, 52 Radiation therapy and pharmacotherapy with the somatostatin analog octreotide are useful nonsurgical options or adjuncts. 41, 42 The determination of a cure in the postoperative period is used to direct subsequent management and follow-up regimens that are costly and may require additional biochemical testing, imaging, and initiation of pharmacotherapy. The generally accepted criteria for predictive assessment of long-term remission of acromegaly are in evolution. 3, 6, 11

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Tak Lap Poon, Samuel Cheong Lun Leung, Christopher Yee Fat Poon and Chung Ping Yu

stereotactic modality, delivers focal and precise radiation to the target in a single session and minimizes exposure of surrounding normal brain tissues to radiation. 6 , 11 In this article, we evaluate our experience in using GKS as adjuvant therapy in patients with acromegaly and analyze factors related to biochemical remission. Methods We retrospectively reviewed data spanning the period 1997–2008 in the Gamma Knife statistics database at our hospital. All patients with active acromegaly who underwent GKS were included. Tumor sizes and hormone levels before and

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Antonios Mammis, Jean Anderson Eloy and James K. Liu

1835, French dermatologist Jean-Louis-Marc Alibert described “Geant scrofuleux” in his monograph on dermatological disorders. 1 In 1857, W. O. Chalk described a case of pathological dislocation of the jaw secondary to macroglossia in a patient with acromegaly. 9 In 1864, the Italian neurologist Andre Verga described “prosopectasia” (widening of the face), while in 1868, Lombroso described “macrosomia.” 25 , 26 , 45 These were followed by case descriptions by Friedreich in 1868 and Henrot in 1877, the latter including an autopsy report in which a 45 × 30–mm tumor