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Update in Pituitary Disease--Cedars Sinaii Publication (UPDATE WITH FULL ARTICLE)


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I don't have the full article, but will try to get it!

 

Update in Pituitary Disease

Shlomo Melmed

Cedars-Sinai Medical Center, Los Angeles, California 90048

 

Address all correspondence and requests for reprints to: Shlomo Melmed, Cedars-Sinai Medical Center-David Geffen UCLA School of Medicine, Los Angeles, California 90048.

 

The pituitary gland secretes vital trophic hormones that maintain homeostatic regulation of the metabolic milieu. Not surprisingly, several thousand papers relevant to the pituitary gland were published this past year, including publication of important transforming advances in our understanding of the pathogenesis, diagnosis, and treatment of pituitary disorders. In an attempt to focus on outstanding key articles reporting highlights of the year, quality inclusion criteria were applied. High-quality articles were selected for their translational impact, scientific advances, enrichment of new knowledge, influence on how we understand pituitary disorders, transformation of therapeutic principles, and opening up new research vistas. Using these selection criteria, highlighted papers within the following categorical topics were further selected for analysis and review: advances in understanding subcellular mechanisms subserving the pathogenesis of pituitary disorders including pituitary tumors and pituitary failure; new challenges facing the physician treating patients harboring prolactinomas with dopamine agonists; and the appearance of new publications reporting the efficacy of long-term prospective medical treatment of acromegaly that now provide more rigorous patient outcome information.

 

Selected papers categorized by these topics all serve to significantly impact how the endocrinologist views disease pathogenesis, diagnosis, and treatment outcomes of patients with pituitary disease in 2007. The results of these publications have transformed our understanding of important principles underlying normal and abnormal pituitary function, as well as our approach to the management of pituitary disorders. Notably, they open up new vistas for creative scholarship in unraveling the challenges of pituitary medicine.

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Quote: "High-quality articles were selected for their translational impact, scientific advances, enrichment of new knowledge, influence on how we understand pituitary disorders, transformation of therapeutic principles, and opening up new research vistas. Using these selection criteria, highlighted papers within the following categorical topics were further selected for analysis and review: advances in understanding subcellular mechanisms subserving the pathogenesis of pituitary disorders including pituitary tumors and pituitary failure; new challenges facing the physician treating patients harboring prolactinomas with dopamine agonists; and the appearance of new publications reporting the efficacy of long-term prospective medical treatment of acromegaly that now provide more rigorous patient outcome information."

 

Sounds like they're coordinating, cooperating and focusing on good stuff!

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  • 2 weeks later...

You may read the full article here: http://home.comcast.net/~staticnrg/Cushing...ePitDisease.pdf

 

Judy and others with more than one family member with Cushing's, these stood out:

 

"A recent paper (8), for the first time, proposed the aryl hydrocarbon receptor interacting protein (AIP) gene as predisposing to pituitary adenoma......Drouin and colleagues (3) discovered that glucocorticoid resistance of ACTH-secreting tumors can be attributed to loss of Brg1 or histone deacetylase (HDAC)-2 nuclear expression. This transrepression of the POMC gene in corticotrophs could therefore be a mechanism underlying the formation of ACTH-secreting tumors (3)."

 

"A large body of work was published relating to the genetic analysis of pituitary tumors. A comprehensive study from Belgium (6) characterized familial isolated pituitary adenomas. These very rarely encountered index families comprised patients with heterogenous features of acromegaly, prolactinoma, and Cushing?s disease. Significantly affected individuals were younger, some were giants, and some harbored more invasive tumors than sporadic patients. The challenge in these rarely encountered and similar families (7) has been that they appear to harbor a mutation in the 11q region, distinct from multiple endocrine neoplasia-1 or any other related tumor suppressor gene. The challenging question in these families has been that the identity of the gene on 11q that predisposes to these traits has remained elusive."

 

There is MUCH MUCH more in this article...well worth reading!!!

 

Hugs,

Robin

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Think I need to print that off & read it.

I've been looking into MEN1. While Bill has abnormal parathyroid results I've read that high cortisol can cause the parathyroid glands to over secrete. I'd much rather think they all only have Cushings.

Judy

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Interesting information on Nelson's, also:

 

"Bertagna and colleagues (19) have now demonstrated that the pathogenesis of Nelson?s syndrome is in fact a reflection of progression of an underlying corticotroph adenoma already present before adrenalectomy. In following 53 patients without corticotroph tumor progression after bilateral adrenalectomy, pituitary hyperplasia or tumor formation developed at a relatively high frequency for the first 6 yr. Thereafter no more patients appear to develop these corticotroph tumors as observed for up to 14 yr. The authors provided evidence that in fact what was termed

Nelson?s syndrome in earlier years was revealed by insensitive pituitary sella x-ray. In contrast, by using available sensitive magnetic resonance imaging, the early underlying tumor can be visualized a priori before adrenalectomy. Thus, the natural history of Nelson?s after adrenalectomy is in reality a reflection of continued tumor growth. The authors, by their analysis, proposed predictors for which patients will in fact develop pituitary hyperplasia and tumors after adrenalectomy and therefore should likely not undergo adrenalectomy. Based on their analysis, these predictors, including early ACTH elevation, an adenoma already visible before adrenalectomy, high ACTH levels after 1,1-

dichlorodiphenildichloroethane suppression or adrenalectomy, and most importantly, the mitotic activity of the original pituitary adenoma if the patient initially underwent surgery for corticotroph adenoma resection before planned adrenalectomy determined the diagnosis."

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