A Unique Growth Factor in Patients with Acromegaloidism*

Ashcraft, Michael W.; Hartzband, Pamela; Herle, André J. Van; Bersch, Noelle; Golde, David W.

doi:10.1210/jcem-57-2-272

Cited by 58 publications

(15 citation statements)

References 4 publications

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“…In a related group of adults with acromegaloidism (pseudoacromegaly) who clinically resemble patients with acromegaly, yet have normal basal and dynamic GH values, Ashcraft et al [22]reported significant GPA in the patients’ sera using the EPC assay. Analysis of serum fractions revealed that the GPA resided in molecular-weight fraction 70,000 daltons and had an approximate isoelectric point at pH 7.5.…”

Section: Discussionmentioning

confidence: 99%

Near-Normal Linear Growth in the Setting of Markedly Reduced Growth Hormone and IGF-1

Murashita

Tajima²,

Nakae³

et al. 1999

Horm Res Paediatr

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A 14.2-year-old prepubertal boy diagnosed with complete-type growth hormone deficiency and tertiary hypothyroidism, keeps growing in the height range between –1 and –2 SD. He has been treated with levothyroxine only. To understand the growth mechanism of this boy, we analyzed the serum growth hormone (GH) with a radioimmunoassay (RIA), serum GH bioactivity with Nb2 and erythroid progenitor cell bioassays, and growth hormone-binding protein (GHBP) with a ligand-mediated immunofunctional assay (LIFA). In addition, IGF-1 and free IGF-1 were analyzed by immunoradiometric assay (IRMA) and insulin-like growth factor-binding protein-3 (IGFBP-3) by Western immunoblot. Peak GH-RIA responses to insulin, arginine and GH-releasing factor, and nocturnal GH secretion, were low (0.5–2.3 ng/ml); bioactive GH was low (0.313 ng/ml), and GHBP was elevated (84 ng/ml). The serum levels of IGF-1 and free IGF-1 were continuously low, 17.1–39.3 and 0.17–0.26 ng/ml, respectively. Moreover, serum IGFBP-3 levels were low (1.68– 1.39 mg/l) and IGFBP-3 protease activity was negative. Prolactin and insulin were in the normal range. The result of the assay for growth-promoting activity showed that the patient’s serum stimulated normal erythroid progenitor cells twice as potently as did healthy thin adult control serum. These results suggest that GH and IGF-1 are not indispensable for maintaining physical growth in this boy. Thus, it appears that circulating GH and IGF-1 are not mandatory requirements for maintaining normal physical growth, and other, as yet uncharacterized, pathways or growth factors might be sufficiently compensatory under certain conditions.

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Section: Discussionmentioning

confidence: 99%

Near-Normal Linear Growth in the Setting of Markedly Reduced Growth Hormone and IGF-1

Murashita

Tajima²,

Nakae³

et al. 1999

Horm Res Paediatr

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“…The presence of an unidentified growth factor in the serum of patients with acromegaloidism has been suggested by Ashcraft et al [1]. A substance of approximate molecular weight of 70000 daltons was found in the sera of five subjects with acromegaloid features.…”

Section: Discussionmentioning

confidence: 78%

“…Acromegaloidism describes a highly heterogeneous group of disorders with a normal somatotropic axis. The aetiology of overgrowth of acromegaloidism is unclear but the presence of other growth factors different from IGF-1 or defective in IGF-1 binding has been demonstrated in serum of these patients [1].…”

Section: Introductionmentioning

confidence: 99%

Acromegaloidism with normal growth hormone secretion associated with X-Tetrasomy

Álvarez-Vázquez

Rivera²,

Figueroa

et al. 2006

Pituitary

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We reported a case of a 26-year-old female who was referred to our clinic with the diagnosis of possible acromegaly. She was born from a term pregnancy by forceps delivery. The patient was diagnosed as having hip luxation at one month and spoke her first word at 15 months. She had been diagnosed at the age of 9 years old as having perinatal encephalopathy with intellectual and motor affectation. Since this period of time she has undergone an insidious change in her appearance, mainly comprising progressive coarsening of the face. For this reason she was submitted to our clinic with presumed acromegaly. Dynamic tests of growth hormone secretion ruled out such a diagnosis. The Patient was considered as having "acromegaloidism", a term used for patients whom manifest clinical features of acromegaly but do not present a demonstrable growth hormone hypersecretion. Subsequently cytogenetic evaluation revealed an infrequent chromosome pattern: X-Tetrasomy. In the present article a differential diagnosis of acromegaloidism and the potential role of genes present on X-chromosome involved in human growth such as SHOX gene are discussed. Overdosification of SHOX gene might explain tall stature of girls with X-tetrasomy. Our observation suggested that X-tetrasomy should be considered in the differential diagnosis of acromegaloidism. Furthermore, this may lead to the identification of new genes in the X-chromosome that are important for growth of facial structures.

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“…Those patients may produce an erythroprogenitor growth factor. 8 Sometimes, pachydermoperiostosis may also mimic acromegaloidism. 9 Our patient had a confirmed pituitary adenoma, with no GH elevation.…”

Section: Discussionmentioning

confidence: 99%

Acromegaly with Normal Basal Growth Hormone Levels

Mohr

Chen²,

Schweitzer

1997

Can. j. neurol. sci.

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Background: The most common cause of acromegaly is excess of growth hormone (GH) secretion. Methods: We report a 42-year-old male patient, who had become acromegalic over the past 5 years. There were no visual changes or change in sexual function, no gynaecomastia or galactorrhoea. Both CT and MRI scans showed a large mass measuring 2.5 x 2.5 x 3.5 cm, originating from the sella turcica and extending into and totally filling up the sphenoid sinus with diffusely invasive features. Results: Basal serum GH level was within normal range, but insulin-like growth factor 1 (IGF-1) was elevated with slightly increased prolactin (PRL) and impaired GH secretory regulation as well. A pituitary adenoma was partially removed through transsphenoidal microsurgery. Pathology confirmed a mammo-somatotrophic adenoma but immunocytochemistry study of the tumour showed only positivity for PRL but not GH. Conclusions: When acromegaly occurs without GH level elevation, one should pay attention that: 1) IGF-1 might be the cause of the clinical feature of acromegaly; 2) The tumour might undergo morphological transformation; and 3) Hyperinsulinemia or GH receptor antibody formation could also be the cause of the acromegalic appearance. RESUME: Acromegalic avec niveau normal d'hormone de croissance: a propos d'un cas. Introduction: La cause la plus commune de l'acromfigalie est l'exces de secretion d'hormone de croissance (GH). Methodes: Nous rapportons le cas d'un patient de 42 ans qui etait devenu acromegale depuis les cinq dernieres ann6es. II n'y avait aucune modification de la vision ni des fonctions sexuelles, aucune gyn£comastie ni galactorrhea. La tomodensitometrie et l'imagerie par resonnance magnetique (IRM) ont montre une volumineuse masse a caracteres invasifs diffus, mesurant 2.5 x 2.5 x 3.5 cm, prenant origine au niveau de la selle turcique et remplissant completement le sinus sphenoidal. Resultats: Le niveau serique basal de GH etait normal, mais le niveau du factor de croissance 1 de genre insulinique (IGF-1) 6tait Sieve avec une legere elevation de la prolactine (PRL) et une alteration dans la regulation de la secretion de GH. Un ad6nome hypophysaire fut partiellement reseque par microchirurgie transspheWidale. L'examen anatomopathologique a confirme qu'il s'agiasait d'un adenome mammo-somatotrophe mais l'examen immunohistochimique de la tumeur n'a montre de positivit6 que pour la PRL, mais non pour la GH. Conclusions: Lorsqu'il y a symptomes d'acromegalie sans elevation de GH, on devrait se demander si: 1) l'IGF-1 peut etre la cause des signes d'acrom6galie; 2) la tumeur pourrait subir une transformation morphologique; et 3) une hyperinsulinemie ou la formation d'anticorps diriges contre le r6cepteur GH pourraient etre la cause des signes d'acromegalie.Can. J. Neurol. Sci. 1997; 24: 250-253 Acromegaly was first recognized as a distinct clinical syndrome by Marie in 1886.' The pituitary source of the disorder was confirmed in 1909 by Cushing.2 Now, it has been generally recognized as the result of an unrestra...

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A Unique Growth Factor in Patients with Acromegaloidism*

Cited by 58 publications

References 4 publications

Near-Normal Linear Growth in the Setting of Markedly Reduced Growth Hormone and IGF-1

Near-Normal Linear Growth in the Setting of Markedly Reduced Growth Hormone and IGF-1

Acromegaloidism with normal growth hormone secretion associated with X-Tetrasomy

Acromegaly with Normal Basal Growth Hormone Levels

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