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Criteria for Cure of Acromegaly: A Consensus Statement¹

Department of Internal Medicine/Endocrine Section (A.G.), University of Brescia, Brescia, Italy; Veterans Affairs Medical Center (A.B.), Ann Arbor, Michigan; Endocrine Section, Department of Medicine, Santiago de Compostela University (F.F.C.), Spain; Division of Endocrinology and Metabolism, Ospedale San Luca, University of Milan (F.C.), Milan, Italy; Department of Medicine, University of Illinois at Chicago (L.F.), Chicago, Illinois; Department of Endocrinology, Garvan Institute of Medical Research, St. Vincents Hospital (K.H.), Sydney, Australia; Department of Medicine, Division of Endocrinology and Metabolism, University of Virginia School of Medicine (J.V.), Charlottesville, Virginia; Department of Endocrinology, Radcliffe Infirmary (J.W.), Oxford, United Kingdom; Department of Medicine, Schlosspark Klinik (K.v.W.), Berlin, Germany; and Cedars-Sinai Research Institute, University of California–Los Angeles School of Medicine (S.M.), Los Angeles, California 90048

Address correspondence and requests for reprints to: Shlomo Melmed, Cedars-Sinai Medical Center,8700 Beverly Boulevard, Room 2015, Los Angeles, California 90048. E-mail: melmed{at}csmc.edu

	Abstract

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In February 1999, a workshop was held in Cortina, Italy to develop a consensus defining the criteria for cure of acromegaly. The workshop was sponsored by the University of Brescia and hosted by the Italian Society of Endocrinology. Invited international participants included endocrinologists, neurosurgeons, and radiotherapists skilled in the management of acromegaly. This statement summarizes the consensus achieved in these discussions.

	Therapeutic Goals

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The therapeutic goals in acromegaly are to eliminate morbidity and to reduce mortality to the expected age- and sex-adjusted rates by using safe treatments that remove the tumor mass or control its growth and restore GH secretion and action to normal. The biochemical goals of therapy are to reduce circulating insulin-like growth factor I (IGF-I) levels to normal for age and sex and to reduce serum GH concentrations to less than 1 µg/L after an oral glucose load.

	Baseline Biochemical Parameters

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Baseline biochemical parameters for the diagnosis of acromegaly include a fasting or random GH and IGF measurement. If a random GH level is less than 0.4 µg/L and IGF is in the age- and gender-matched normal range (1, 2), the diagnosis of acromegaly is excluded in a patient who has no other intercurrent illness (Table 1). If either of these levels is not achieved, a glucose tolerance test should be performed with 75 g oral glucose and subsequent measurements of glucose and GH every 30 min over 2 h. During this time, the GH level should fall to 1 µg/L or less for acromegaly to be excluded (3). Although mean integrated 24-h GH levels of less than 2.5 µg/L also exclude acromegaly, these values correlate tightly with results of the glucose suppression test, which is most cost-effective (4). Tests that do not offer additional information for the diagnosis of acromegaly include TRH, GHRH, or GnRH stimulation, measurement of IGF binding protein 3, and studies of spontaneous GH secretion by frequent sampling (5).

	Dynamic Testing

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Failure of GH suppression after glucose loading in the appropriate clinical context suggests the diagnosis of acromegaly, but the results should always be considered in conjunction with an IGF-I measurement because other conditions can cause discordantly elevated GH levels. Using all current commercial assays, the cut-off GH value separating normal subjects from those with acromegaly is less than 1 µg/L. However, with the introduction of newer more sensitive assays it is anticipated that a lower cut-off value can be defined in the future (6).

A paradoxical rise in serum GH provides no additional value beyond that attained by failure to suppress GH. Care needs to be taken in interpretation of the test in the immediate postoperative period due to effects of concomitant glucocorticoid administration and other perioperative medications, including glucose, dopamine, opiates, and anesthetics. Although no data exist regarding the superiority of 75 or 100 g glucose, it is recommended that 75 g be used to achieve a level of standardization. The attained blood glucose levels are of importance with respect to the diagnosis of diabetes mellitus, but do not affect interpretation of the GH result. Although GH responses may differ between male and female subjects and show some influence of age, these factors are not considered important for diagnostic interpretation of the GH response to glucose.

False-positive responses (i.e. failure of normal suppression) may occur in patients with diabetes mellitus, liver disease, renal disease, adolescence, and anorexia nervosa. False negative responses (i.e. normal suppression) may be encountered in acromegaly itself. However, in both situations interpretation should be tempered by the simultaneous availability of IGF-I levels and consideration of the associated clinical findings.

Stimulatory tests

TRH and GnRH stimulation tests of GH secretion have been used as a second tier evaluation of abnormal GH dynamics in the diagnosis of acromegaly and in assessing responses to therapeutic intervention (7). These tests offer no advantage over the OGTT and, as serious side effects may occasionally occur in response to TRH, their use is not recommended for diagnosis. Nearly all patients with acromegaly respond to GH secretagogues, and all have paradoxical inhibitory responses to galanin. However, none of these agents is of proven value in the evaluation of patients with acromegaly at the present time.

Although nearly all patients respond to GHRH stimulation (8), this agent is not of value in the diagnosis of GH-secreting tumors nor in distinguishing them from those with ectopic GHRH secretion. In suspected cases of the rarely encountered latter condition, a serum GHRH level is the preferred test.

	Assays

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The assays used for the diagnosis, management, and follow-up of acromegaly are GH and (total) IGF-I measurements. Both assays should have adequate sensitivity (for GH, at least 0.5 µg/L), established validity, specificity, reliability, and uniform reproducibility (9, 10). IGF-I concentrations must be compared with age-dependent normative data generated across all age groups and both sexes. Systemic diseases, including catabolic states and hepatic or renal failure and malnutrition, may result in lowered IGF-I levels (10). Repeat assay and follow-up may be helpful when IGF-I values are borderline, or clinical and biochemical data are not congruent. Assays for antilymphocyte serum, free IGF-I, IGF binding protein-3, and urinary GH are of no additional independent diagnostic value, but some methods serve currently as research tools (11). Refinements of GH assay performance will likely lead to revised normative criteria of GH suppression after glucose loading, but the clinical relevance of such enhanced sensitivity is not currently apparent. In the rare case of suspected ectopic GHRH syndrome, circulating GHRH concentrations should be measured.

	Using Cure Criteria for Evaluating Treatment

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Definition of cure

Control is achieved when all attributes of disordered GH secretion are restored to normal. Biochemically, this is evident when circulating IGF-I is reduced to an age-adjusted normal range and nadir GH after an oral glucose load is less than 1 µg/L.

Surgery

Ideally, the GH-secreting adenoma should be completely resected, with preservation or subsequent restoration of pituitary function (12). Surgical effectiveness varies greatly depending on expertise in pituitary surgery, both the size and extension of the anatomic mass, and the preoperative level of GH (13, 14, 15, 16). Tumor resection generally results in a rapid and substantial reduction of serum GH levels immediately postoperatively and corresponding lowering of IGF-I levels in the weeks following surgery.

Historically, patients have been classified as "cured" or "noncured." This concept was based on outcomes of surgical interventions with imprecise biochemical evaluation and is misleading for patients and clinicians. If rigorous criteria are used for the interpretation of surgical results (GH nadir after OGTT <1 µg/L), approximately 80% of patients with microadenomas and substantially less than 50% of patients with macroadenomas can be defined as controlled. Patients in whom disease has been controlled, as defined by older criteria, may, in fact, demonstrate increased GH secretion when retested 1 or more years after surgery (17).

Medical treatment

After long-term somatostatin receptor ligand administration, GH levels are suppressed to less than 2.5 µg/L in 65% of patients and IGF-I levels are normalized in 70% of patients (18, 19). New slow-release formulations of long-acting somatostatin receptor ligands result in persistent GH and IGF-I suppression after im depot injection (20, 21). Drug levels peak at 28 days and are sustained for over 4 weeks. Persistently controlled mean GH levels (<2 µg/L) are achieved in over 70% of octreotide-sensitive patients (20). Lanreotide injected every 14 days provides similar GH and IGF-I control (21). High doses of long-acting dopamine receptor agonists rarely normalize IGF-I levels (22, 23), but data on long-term control of GH and IGF-I with these agents is not yet available. Future treatment options may include receptor-subtype selective somatostatin ligands and GH receptor antagonists (24).

Radiotherapy

Beneficial effects of radiotherapy on GH levels are delayed, and about 90% of patients achieve random GH levels of less than 5 µg/L after 18 yr (25). Ineffectiveness of radiotherapy in lowering IGF-I despite attenuation of GH levels has been reported (26). However, shrinkage or at least prevention of continued pituitary tumor mass growth is usually achieved with radiotherapy. Stereotactic radiosurgery is currently under investigation, and early results show that after 1.4 yr, 8 of 16 patients achieve GH levels less than 5 µg/L (27).

	Interpretation of Treatment Outcomes

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Results of the different treatment modalities should be interpreted using the criteria enunciated above and applied for evaluating disease control in assessing disease therapy. Additionally, the efficacy of surgical and radiotherapeutic procedures should be evaluated in the long term by the use of anatomic tools, including magnetic resonance imaging (MRI) and visual field evaluation. Moreover, after these procedures, residual pituitary function should be preserved and hypopituitarism avoided. After surgery and after initiating medical treatment, biochemical assessment should be performed at 6–12 weeks. IGF-I normalization may only occur several months later. After radiotherapy, long-term biochemical assessment is required to assess efficacy and the development of pituitary failure. All patients with acromegaly require periodic lifelong evaluation.

	Clinical outcomes

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The morbidity and mortality associated with active acromegaly comprise a continuum associated with disease activity, requiring effective and sustained long-term treatment. Morbidity and mortality rates are significantly increased due either to a direct deleterious impact of raised GH and IGF-I levels and/or to acromegaly-related co-morbidity, including cardiovascular disease, diabetes, respiratory dysfunction, and sleep apnea. GH levels seem to be the single most important determinant of mortality in acromegaly (28, 29). Importantly, imprecise biochemical assessment (i.e. insufficiently sensitive GH assays and lack of information regarding IGF-I normal ranges) contribute to the uncertainty in the literature regarding dose-response relations between biochemical activity and improvement in morbidity and mortality rates. Nevertheless, the existing epidemiologic information strongly suggests that a decrease in GH level in acromegaly is beneficial and may lead to improved or even normalized mortality rates. Failure to control GH is associated with a 3.5-fold enhanced mortality, as compared to patients in whom GH is controlled whose mortality is not different from controls (14, 15, 30). It is, therefore, recommended that patients with acromegaly, especially those under 40 yr of age, should be treated aggressively to lower the GH/IGF-I indices as close to "normal" as clinically possible. Decrease or even normalization of GH/IGF-I may not always result in consistent reversal of the indices of cardiovascular morbidity, especially hypertension and sleep apnea. Thus, aggressive cotreatment of hypertension, diabetes, heart disease, and hyperlipidemia should be instituted. Sleep apnea should be actively assessed and, if necessary, treated independently. The question of whether increased cerebrovascular morbidity and mortality may be iatrogenic secondary to cranial irradiation, is not resolved.

The association between acromegaly and malignant diseases is not resolved fully. There is increased general mucosal hypertrophy in active acromegaly, which is reflected in the appearance of colonic polyps in a high proportion of acromegalic patients, even at an unusually young age. Colonic polyps are often of a premalignant nature (31). Thus, even though conflicting data exist regarding incidence and mortality from colon cancer in acromegaly, aggressive diagnostic vigilance is justified. All patients should have pan-colonoscopy at diagnosis, and this procedure should be repeated periodically as determined by individual risk factors, including presence of polyps, family history, and presence of skin tags. Screening for breast and prostate cancer should be conducted according to standards used in the general population. Additional basic research assessing GH/IGF-I effects on neoplastic transformation and reevaluation of the clinical use of IGF-I as a marker of disease activity are needed.

The aim of treatment is to control the disease by suppressing GH hyperactivity, reducing the size or impeding the growth of the pituitary mass, and eliminating secondary comorbid complications. Such control of acromegaly may be achieved through either single or combined surgery, radiotherapy, and/or medical treatment. Patients can, thus, be classified depending on the degree of disease control. Good control implies that the patient does not exhibit GH hyperactivity, as measured by available assays, and should enjoy a mortality risk similar to the general population. Inadequate control implies the presence of GH hypersecretion, but minimally enhanced morbidity. Nevertheless, morbidity is inexorable in these patients and ultimately becomes life-threatening. Poor control implies that parameters of GH hyperactivity are present with a high risk of morbidity and mortality. Thus, control of acromegaly depends on evolution of the disease and on therapeutic outcomes (Table 2).

	Footnotes

 
Received April 28, 1999. Revision received September 15, 1999. Rerevision received October 22, 1999. Accepted November 1, 1999.

¹ Participants: M. Arosio, A. Barkan, A. Beckers, A. Bollati, M. Boscaro, P. M. Bouloux, M. Bronstein, A. Burattin, P. Caron, F. F. Casa-nueva, F. Cavagnini, P. Chanson, R. N. Clayton, D. Cocchi, A. M. Colao, E. Degli Uberti, M. Doga, E. Erfurth, S. Ezzat, L. Frohman, R. Gaillard, M. Gasperi, M. Giovanelli, A. Giustina, G. Giustina, A. Grossman, R. Gunnarsson, K. Ho, I. Jackson, P. Jaquet, J. Jorgensen, D. Kleinberg, E. Laws, G. Lombardi, M. Losa, D. Ludecke, P. Maffei, G. Maira, J. Marek, G. Marini, E. Martino, C. Mascadri, S. Melmed, F. Minuto, H. Orskov, A. Pedtroncelli, A. Pinchera, H. Quabbe, M. Sheppard, N. Sicolo, G. Tamburrano, G. Tolis, A. Van Der Lely, J. D. Veldhuis, K. Von Werder, J. A. H. Wass, and S. Webb.

Supported by an unrestricted educational grant by Ipsen Pharmaceuticals to the University of Brescia (Brescia, Italy).

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				A. Colao, R. Pivonello, M. Galderisi, P. Cappabianca, R. S. Auriemma, M. Galdiero, L. M. Cavallo, F. Esposito, and G. Lombardi Impact of Treating Acromegaly First with Surgery or Somatostatin Analogs on Cardiomyopathy J. Clin. Endocrinol. Metab., July 1, 2008; 93(7): 2639 - 2646. [Abstract] [Full Text] [PDF]

				A. Fusco, M. C. Zatelli, A. Bianchi, V. Cimino, L. Tilaro, F. Veltri, F. Angelini, L. Lauriola, V. Vellone, F. Doglietto, et al. Prognostic Significance of the Ki-67 Labeling Index in Growth Hormone-Secreting Pituitary Adenomas J. Clin. Endocrinol. Metab., July 1, 2008; 93(7): 2746 - 2750. [Abstract] [Full Text] [PDF]

				L. Nachtigall, A. Delgado, B. Swearingen, H. Lee, R. Zerikly, and A. Klibanski Changing Patterns in Diagnosis and Therapy of Acromegaly over Two Decades J. Clin. Endocrinol. Metab., June 1, 2008; 93(6): 2035 - 2041. [Abstract] [Full Text] [PDF]

				U Plockinger and T Reuter Pegvisomant increases intra-abdominal fat in patients with acromegaly: a pilot study. Eur. J. Endocrinol., April 1, 2008; 158(4): 467 - 471. [Abstract] [Full Text] [PDF]

				A. Colao and G. Lombardi Should We Still Use Glucose-Suppressed Growth Hormone Levels for the Evaluation of Acromegaly? J. Clin. Endocrinol. Metab., April 1, 2008; 93(4): 1181 - 1182. [Full Text] [PDF]

				M. P Matta, E. Couture, L. Cazals, D. Vezzosi, A. Bennet, and P. Caron Impaired quality of life of patients with acromegaly: control of GH/IGF-I excess improves psychological subscale appearance Eur. J. Endocrinol., March 1, 2008; 158(3): 305 - 310. [Abstract] [Full Text] [PDF]

				A. Tagliafico, E. Resmini, R. Nizzo, F. Bianchi, F. Minuto, D. Ferone, and C. Martinoli Ultrasound Measurement of Median and Ulnar Nerve Cross-Sectional Area in Acromegaly J. Clin. Endocrinol. Metab., March 1, 2008; 93(3): 905 - 909. [Abstract] [Full Text] [PDF]

				R. Baldelli, L. De Marinis, A. Bianchi, R. Pivonello, V. Gasco, R. Auriemma, G. Pasimeni, V. Cimino, M. Appetecchia, M. Maccario, et al. Microalbuminuria in Insulin Sensitivity in Patients with Growth Hormone-Secreting Pituitary Tumor J. Clin. Endocrinol. Metab., March 1, 2008; 93(3): 710 - 714. [Abstract] [Full Text] [PDF]

				C. L Ronchi, E. Rizzo, A. G Lania, R. Pivonello, S. Grottoli, A. Colao, E. Ghigo, A. Spada, M. Arosio, and P. Beck-Peccoz Preliminary data on biochemical remission of acromegaly after somatostatin analogs withdrawal Eur. J. Endocrinol., January 1, 2008; 158(1): 19 - 25. [Abstract] [Full Text] [PDF]

				A. Colao, R. Pivonello, R. S Auriemma, M. Galdiero, S. Savastano, and G. Lombardi Beneficial effect of dose escalation of Octreotide-LAR as first-line therapy in patients with acromegaly Eur. J. Endocrinol., November 1, 2007; 157(5): 579 - 587. [Abstract] [Full Text] [PDF]

				M. Bex, R. Abs, G. T'Sjoen, J. Mockel, B. Velkeniers, K. Muermans, and D. Maiter AcroBel the Belgian registry on acromegaly: a survey of the 'real-life' outcome in 418 acromegalic subjects Eur. J. Endocrinol., October 1, 2007; 157(4): 399 - 409. [Abstract] [Full Text] [PDF]

				G. T'Sjoen, M. Bex, D. Maiter, B. Velkeniers, and R. Abs Health-related quality of life in acromegalic subjects: data from AcroBel, the Belgian Registry on acromegaly Eur. J. Endocrinol., October 1, 2007; 157(4): 411 - 417. [Abstract] [Full Text] [PDF]

				E. O. Vik-Mo, M. Oksnes, P.-H. Pedersen, T. Wentzel-Larsen, E. Rodahl, F. Thorsen, T. Schreiner, S. Aanderud, and M. Lund-Johansen Gamma knife stereotactic radiosurgery for acromegaly Eur. J. Endocrinol., September 1, 2007; 157(3): 255 - 263. [Abstract] [Full Text] [PDF]

				C. Schmid, P.-A. Krayenbuehl, R.-L. Bernays, C. Zwimpfer, F. E. Maly, and P. Wiesli Growth Hormone (GH) Receptor Isoform in Acromegaly: Lower Concentrations of GH but Not Insulin-Like Growth Factor-1 in Patients with a Genomic Deletion of Exon 3 in the GH Receptor Gene Clin. Chem., August 1, 2007; 53(8): 1484 - 1488. [Abstract] [Full Text] [PDF]

				P. Maison, A.-I. Tropeano, I. Macquin-Mavier, A. Giustina, and P. Chanson Impact of Somatostatin Analogs on the Heart in Acromegaly: A Metaanalysis J. Clin. Endocrinol. Metab., May 1, 2007; 92(5): 1743 - 1747. [Abstract] [Full Text] [PDF]

				M. Georgitsi, A. Raitila, A. Karhu, K. Tuppurainen, M. J. Makinen, O. Vierimaa, R. Paschke, W. Saeger, R. B. van der Luijt, T. Sane, et al. Molecular diagnosis of pituitary adenoma predisposition caused by aryl hydrocarbon receptor-interacting protein gene mutations PNAS, March 6, 2007; 104(10): 4101 - 4105. [Abstract] [Full Text] [PDF]

				A N Paisley, K Hayden, A Ellis, J Anderson, G Wieringa, and P J Trainer Pegvisomant interference in GH assays results in underestimation of GH levels Eur. J. Endocrinol., March 1, 2007; 156(3): 315 - 319. [Abstract] [Full Text] [PDF]

				L. Sze, C. Schmid, K. E Bloch, R. Bernays, and M. Brandle Effect of transsphenoidal surgery on sleep apnoea in acromegaly Eur. J. Endocrinol., March 1, 2007; 156(3): 321 - 329. [Abstract] [Full Text] [PDF]

				G. F Taboada, R. M Luque, W. Bastos, R. F C Guimaraes, J. B Marcondes, L. M C Chimelli, R. Fontes, P. J P Mata, P. N. Filho, D. P Carvalho, et al. Quantitative analysis of somatostatin receptor subtype (SSTR1-5) gene expression levels in somatotropinomas and non-functioning pituitary adenomas Eur. J. Endocrinol., January 1, 2007; 156(1): 65 - 74. [Abstract] [Full Text] [PDF]

				S. Melmed Acromegaly N. Engl. J. Med., December 14, 2006; 355(24): 2558 - 2573. [Full Text] [PDF]

				S.-C. Hua, Y.-H. Yan, and T.-C. Chang Associations of remission status and lanreotide treatment with quality of life in patients with treated acromegaly Eur. J. Endocrinol., December 1, 2006; 155(6): 831 - 837. [Abstract] [Full Text] [PDF]

				R. Kauppinen-Makelin, T. Sane, H. Sintonen, H. Markkanen, M. J. Valimaki, E. Loyttyniemi, L. Niskanen, A. Reunanen, U.-H. Stenman, and and the Finnish Acromegaly Study Group Quality of Life in Treated Patients with Acromegaly J. Clin. Endocrinol. Metab., October 1, 2006; 91(10): 3891 - 3896. [Abstract] [Full Text] [PDF]

				P. J Trainer, J. Barth, C. Sturgeon, G. Wieringaon, and on behalf of the collaborative Consensus statement on the standardisation of GH assays. Eur. J. Endocrinol., July 1, 2006; 155(1): 1 - 2. [Full Text] [PDF]

				A. Colao, R. Pivonello, R. S. Auriemma, F. Briganti, M. Galdiero, F. Tortora, F. Caranci, S. Cirillo, and G. Lombardi Predictors of Tumor Shrinkage after Primary Therapy with Somatostatin Analogs in Acromegaly: A Prospective Study in 99 Patients J. Clin. Endocrinol. Metab., June 1, 2006; 91(6): 2112 - 2118. [Abstract] [Full Text] [PDF]

				S Pekic, M Doknic, D Miljic, M Joksimovic, J Glodic, M Djurovic, C Dieguez, F Casanueva, and V Popovic Ghrelin test for the assessment of GH status in successfully treated patients with acromegaly. Eur. J. Endocrinol., May 1, 2006; 154(5): 659 - 666. [Abstract] [Full Text] [PDF]

				P. J. Jenkins, P. Bates, M. N. Carson, P. M. Stewart, J. A. H. Wass, and on behalf of the UK National Acromegaly Register S Conventional Pituitary Irradiation Is Effective in Lowering Serum Growth Hormone and Insulin-Like Growth Factor-I in Patients with Acromegaly J. Clin. Endocrinol. Metab., April 1, 2006; 91(4): 1239 - 1245. [Abstract] [Full Text] [PDF]

				R. Cozzi, M. Montini, R. Attanasio, M. Albizzi, G. Lasio, S. Lodrini, P. Doneda, L. Cortesi, and G. Pagani Primary Treatment of Acromegaly with Octreotide LAR: A Long-Term (Up to Nine Years) Prospective Study of Its Efficacy in the Control of Disease Activity and Tumor Shrinkage J. Clin. Endocrinol. Metab., April 1, 2006; 91(4): 1397 - 1403. [Abstract] [Full Text] [PDF]

				F. Bogazzi, C. Cosci, C. Sardella, A. Costa, L. Manetti, M. Gasperi, G. Rossi, L. Bartalena, and E. Martino Identification of Acromegalic Patients at Risk of Developing Colonic Adenomas J. Clin. Endocrinol. Metab., April 1, 2006; 91(4): 1351 - 1356. [Abstract] [Full Text] [PDF]

				H. D. White, A. M. Ahmad, B. H. Durham, S. Chandran, A. Patwala, W. D. Fraser, and J. P. Vora Effect of Active Acromegaly and Its Treatment on Parathyroid Circadian Rhythmicity and Parathyroid Target-Organ Sensitivity J. Clin. Endocrinol. Metab., March 1, 2006; 91(3): 913 - 919. [Abstract] [Full Text] [PDF]

				H. Markkanen, T. Pekkarinen, M. J. Valimaki, H. Alfthan, R. Kauppinen-Makelin, T. Sane, and U.-H. Stenman Effect of Sex and Assay Method on Serum Concentrations of Growth Hormone in Patients with Acromegaly and in Healthy Controls Clin. Chem., March 1, 2006; 52(3): 468 - 473. [Abstract] [Full Text] [PDF]

				A. Colao, R. Attanasio, R. Pivonello, P. Cappabianca, L. M. Cavallo, G. Lasio, A. Lodrini, G. Lombardi, and R. Cozzi Partial Surgical Removal of Growth Hormone-Secreting Pituitary Tumors Enhances the Response to Somatostatin Analogs in Acromegaly J. Clin. Endocrinol. Metab., January 1, 2006; 91(1): 85 - 92. [Abstract] [Full Text] [PDF]

				C. L. Ronchi, V. Varca, P. Beck-Peccoz, E. Orsi, F. Donadio, A. Baccarelli, C. Giavoli, E. Ferrante, A. Lania, A. Spada, et al. Comparison between Six-Year Therapy with Long-Acting Somatostatin Analogs and Successful Surgery in Acromegaly: Effects on Cardiovascular Risk Factors J. Clin. Endocrinol. Metab., January 1, 2006; 91(1): 121 - 128. [Abstract] [Full Text] [PDF]

				J Ayuk and M C Sheppard Growth hormone and its disorders Postgrad. Med. J., January 1, 2006; 82(963): 24 - 30. [Abstract] [Full Text] [PDF]

				G. Minniti, V. Esposito, M. Piccirilli, A. Fratticci, A. Santoro, and M.-L. Jaffrain-Rea Diagnosis and management of pituitary tumours in the elderly: a review based on personal experience and evidence of literature Eur. J. Endocrinol., December 1, 2005; 153(6): 723 - 735. [Abstract] [Full Text] [PDF]

				S Melmed, F Casanueva, F Cavagnini, P Chanson, L A Frohman, R Gaillard, E Ghigo, K Ho, P Jaquet, D Kleinberg, et al. Consensus statement: medical management of acromegaly Eur. J. Endocrinol., December 1, 2005; 153(6): 737 - 740. [Abstract] [Full Text] [PDF]

				R. A. Feelders, M. Bidlingmaier, C. J. Strasburger, J. A. M. J. L. Janssen, P. Uitterlinden, L. J. Hofland, S. W. J. Lamberts, A. J. van der Lely, and W. W. de Herder Postoperative Evaluation of Patients with Acromegaly: Clinical Significance and Timing of Oral Glucose Tolerance Testing and Measurement of (Free) Insulin-Like Growth Factor I, Acid-Labile Subunit, and Growth Hormone-Binding Protein Levels J. Clin. Endocrinol. Metab., December 1, 2005; 90(12): 6480 - 6489. [Abstract] [Full Text] [PDF]

				A. L. Barkan, P. Burman, D. R. Clemmons, W. M. Drake, R. F. Gagel, P. E. Harris, P. J. Trainer, A. J. van der Lely, and M. L. Vance Glucose Homeostasis and Safety in Patients with Acromegaly Converted from Long-Acting Octreotide to Pegvisomant J. Clin. Endocrinol. Metab., October 1, 2005; 90(10): 5684 - 5691. [Abstract] [Full Text] [PDF]

				C. A. Hurty and B. Flatland Feline Acromegaly: A Review of the Syndrome J. Am. Anim. Hosp. Assoc., September 1, 2005; 41(5): 292 - 297. [Abstract] [Full Text] [PDF]

				G M Besser, P Burman, and A F Daly Predictors and rates of treatment-resistant tumor growth in acromegaly Eur. J. Endocrinol., August 1, 2005; 153(2): 187 - 193. [Abstract] [Full Text] [PDF]

				R. Fahlbusch, B. v Keller, O. Ganslandt, J. Kreutzer, and C. Nimsky Transsphenoidal surgery in acromegaly investigated by intraoperative high-field magnetic resonance imaging Eur. J. Endocrinol., August 1, 2005; 153(2): 239 - 248. [Abstract] [Full Text] [PDF]

				A. P Silva, K. Bethmann, F. Raulf, and H. A Schmid Regulation of ghrelin secretion by somatostatin analogs in rats Eur. J. Endocrinol., June 1, 2005; 152(6): 887 - 894. [Abstract] [Full Text] [PDF]

				S. V. Rowles, L. Prieto, X. Badia, S. M. Shalet, S. M. Webb, and P. J. Trainer Quality of Life (QOL) in Patients with Acromegaly Is Severely Impaired: Use of a Novel Measure of QOL: Acromegaly Quality of Life Questionnaire J. Clin. Endocrinol. Metab., June 1, 2005; 90(6): 3337 - 3341. [Abstract] [Full Text] [PDF]

				N. R. Biermasz, A. M. Pereira, J. W. A. Smit, J. A. Romijn, and F. Roelfsema Morbidity after Long-Term Remission for Acromegaly: Persisting Joint-Related Complaints Cause Reduced Quality of Life J. Clin. Endocrinol. Metab., May 1, 2005; 90(5): 2731 - 2739. [Abstract] [Full Text] [PDF]

				J. J. Puder, S. Nilavar, K. D. Post, and P. U. Freda Relationship between Disease-Related Morbidity and Biochemical Markers of Activity in Patients with Acromegaly J. Clin. Endocrinol. Metab., April 1, 2005; 90(4): 1972 - 1978. [Abstract] [Full Text] [PDF]

				A. A. Sakharova, E. V. Dimaraki, W. F. Chandler, and A. L. Barkan Clinically Silent Somatotropinomas May Be Biochemically Active J. Clin. Endocrinol. Metab., April 1, 2005; 90(4): 2117 - 2121. [Abstract] [Full Text] [PDF]

				P. Nomikos, M. Buchfelder, and R. Fahlbusch The outcome of surgery in 668 patients with acromegaly using current criteria of biochemical 'cure' Eur. J. Endocrinol., March 1, 2005; 152(3): 379 - 387. [Abstract] [Full Text] [PDF]

				C. L. Ronchi, V. Varca, C. Giavoli, P. Epaminonda, P. Beck-Peccoz, A. Spada, and M. Arosio Long-Term Evaluation of Postoperative Acromegalic Patients in Remission with Previous and Newly Proposed Criteria J. Clin. Endocrinol. Metab., March 1, 2005; 90(3): 1377 - 1382. [Abstract] [Full Text] [PDF]

				M. Terzolo, G. Reimondo, M. Gasperi, R. Cozzi, R. Pivonello, G. Vitale, A. Scillitani, R. Attanasio, E. Cecconi, F. Daffara, et al. Colonoscopic Screening and Follow-Up in Patients with Acromegaly: A Multicenter Study in Italy J. Clin. Endocrinol. Metab., January 1, 2005; 90(1): 84 - 90. [Abstract] [Full Text] [PDF]

				H. Bihan, C. Espinosa, H. Valdes-Socin, S. Salenave, J. Young, S. Levasseur, P. Assayag, A. Beckers, and P. Chanson Long-Term Outcome of Patients with Acromegaly and Congestive Heart Failure J. Clin. Endocrinol. Metab., November 1, 2004; 89(11): 5308 - 5313. [Abstract] [Full Text] [PDF]

				E. J. M. Zirkzee, E. P. M. Corssmit, N. R. Biermasz, P. A. Brouwer, F. T. Wiggers-De Bruine, L. J. M. Kroft, M. A. Van Buchem, F. Roelfsema, A. M. Pereira, J. W. A. Smit, et al. Pituitary Magnetic Resonance Imaging Is Not Required in the Postoperative Follow-Up of Acromegalic Patients with Long-Term Biochemical Cure after Transsphenoidal Surgery J. Clin. Endocrinol. Metab., September 1, 2004; 89(9): 4320 - 4324. [Abstract] [Full Text] [PDF]

				J. Ayuk, R. N. Clayton, G. Holder, M. C. Sheppard, P. M. Stewart, and A. S. Bates Growth Hormone and Pituitary Radiotherapy, But Not Serum Insulin-Like Growth Factor-I Concentrations, Predict Excess Mortality in Patients with Acromegaly J. Clin. Endocrinol. Metab., April 1, 2004; 89(4): 1613 - 1617. [Abstract] [Full Text] [PDF]

				C. Schmid, P. Wiesli, R. Bernays, K. Bloch, J. Zapf, C. Zwimpfer, C. Ghirlanda, and M. Brandle Decrease in sE-Selectin after Pituitary Surgery in Patients with Acromegaly Clin. Chem., March 1, 2004; 50(3): 650 - 652. [Full Text] [PDF]

				D. Rizzoni, E. Porteri, A. Giustina, C. De Ciuceis, I. Sleiman, G. E. M. Boari, M. Castellano, M. L. Muiesan, S. Bonadonna, A. Burattin, et al. Acromegalic Patients Show the Presence of Hypertrophic Remodeling of Subcutaneous Small Resistance Arteries Hypertension, March 1, 2004; 43(3): 561 - 565. [Abstract] [Full Text] [PDF]

				A. Colao, D. Ferone, P. Marzullo, and G. Lombardi Systemic Complications of Acromegaly: Epidemiology, Pathogenesis, and Management Endocr. Rev., February 1, 2004; 25(1): 102 - 152. [Abstract] [Full Text] [PDF]

				O. Serri, C. Beauregard, and J. Hardy Long-Term Biochemical Status and Disease-Related Morbidity in 53 Postoperative Patients with Acromegaly J. Clin. Endocrinol. Metab., February 1, 2004; 89(2): 658 - 661. [Abstract] [Full Text] [PDF]

				A. Mukherjee, J. P. Monson, P. J. Jonsson, P. J. Trainer, and S. M. Shalet Seeking the Optimal Target Range for Insulin-Like Growth Factor I during the Treatment of Adult Growth Hormone Disorders J. Clin. Endocrinol. Metab., December 1, 2003; 88(12): 5865 - 5870. [Abstract] [Full Text] [PDF]

				R. Attanasio, R. Baldelli, R. Pivonello, S. Grottoli, L. Bocca, V. Gasco, M. Giusti, G. Tamburrano, A. Colao, and R. Cozzi Lanreotide 60 mg, a New Long-Acting Formulation: Effectiveness in the Chronic Treatment of Acromegaly J. Clin. Endocrinol. Metab., November 1, 2003; 88(11): 5258 - 5265. [Abstract] [Full Text] [PDF]

				L. Spinelli, M. Petretta, G. Verderame, G. Carbone, A. A. Venetucci, A. Petretta, W. Acampa, D. Bonaduce, A. Colao, and A. Cuocolo Left Ventricular Diastolic Function and Cardiac Performance during Exercise in Patients with Acromegaly J. Clin. Endocrinol. Metab., September 1, 2003; 88(9): 4105 - 4109. [Abstract] [Full Text] [PDF]

				P. De, D. A. Rees, N. Davies, R. John, J. Neal, R. G. Mills, J. Vafidis, J. S. Davies, and M. F. Scanlon Transsphenoidal Surgery for Acromegaly in Wales: Results Based on Stringent Criteria of Remission J. Clin. Endocrinol. Metab., August 1, 2003; 88(8): 3567 - 3572. [Abstract] [Full Text] [PDF]

				R. Cozzi, R. Attanasio, M. Montini, G. Pagani, G. Lasio, S. Lodrini, M. Barausse, M. Albizzi, D. Dallabonzana, and A. M. Pedroncelli Four-Year Treatment with Octreotide-Long-Acting Repeatable in 110 Acromegalic Patients: Predictive Value of Short-Term Results? J. Clin. Endocrinol. Metab., July 1, 2003; 88(7): 3090 - 3098. [Abstract] [Full Text] [PDF]

				R. Attanasio, P. Epaminonda, E. Motti, E. Giugni, L. Ventrella, R. Cozzi, M. Farabola, P. Loli, P. Beck-Peccoz, and M. Arosio Gamma-Knife Radiosurgery in Acromegaly: A 4-Year Follow-Up Study J. Clin. Endocrinol. Metab., July 1, 2003; 88(7): 3105 - 3112. [Abstract] [Full Text] [PDF]

				A. Colao, L. Spinelli, P. Marzullo, R. Pivonello, M. Petretta, C. Di Somma, G. Vitale, D. Bonaduce, and G. Lombardi High Prevalence of Cardiac Valve Disease in Acromegaly: An Observational, Analytical, Case-Control Study J. Clin. Endocrinol. Metab., July 1, 2003; 88(7): 3196 - 3201. [Abstract] [Full Text] [PDF]

				R. N. Clayton Cardiovascular Function in Acromegaly Endocr. Rev., June 1, 2003; 24(3): 272 - 277. [Abstract] [Full Text] [PDF]

				A. Giustina and S. Melmed Acromegaly Consensus: The Next Steps J. Clin. Endocrinol. Metab., April 1, 2003; 88(4): 1913 - 1914. [Full Text] [PDF]

				Z Merza Modern treatment of acromegaly Postgrad. Med. J., April 1, 2003; 79(930): 189 - 194. [Abstract] [Full Text] [PDF]

				J. J. Kopchick, C. Parkinson, E. C. Stevens, and P. J. Trainer Growth Hormone Receptor Antagonists: Discovery, Development, and Use in Patients with Acromegaly Endocr. Rev., October 1, 2002; 23(5): 623 - 646. [Abstract] [Full Text] [PDF]

				G. Weckbecker, U. Briner, I. Lewis, and C. Bruns SOM230: A New Somatostatin Peptidomimetic with Potent Inhibitory Effects on the Growth Hormone/Insulin-Like Growth Factor-I Axis in Rats, Primates, and Dogs Endocrinology, October 1, 2002; 143(10): 4123 - 4130. [Abstract] [Full Text] [PDF]

				J. Ayuk, S. E. Stewart, P. M. Stewart, and M. C. Sheppard Long-Term Safety and Efficacy of Depot Long-Acting Somatostatin Analogs for the Treatment of Acromegaly J. Clin. Endocrinol. Metab., September 1, 2002; 87(9): 4142 - 4146. [Abstract] [Full Text] [PDF]

				A. Colao, M. De Rosa, R. Pivonello, A. Balestrieri, P. Cappabianca, A. Di Sarno, V. Rochira, C. Carani, and G. Lombardi Short-Term Suppression of GH and IGF-I Levels Improves Gonadal Function and Sperm Parameters in Men with Acromegaly J. Clin. Endocrinol. Metab., September 1, 2002; 87(9): 4193 - 4197. [Abstract] [Full Text] [PDF]

				N. R. Adams, J. R. Briegel, and K. A. Ward The impact of a transgene for ovine growth hormone on the performance of two breeds of sheep J Anim Sci, September 1, 2002; 80(9): 2325 - 2333. [Abstract] [Full Text] [PDF]

				P. J. Trainer Acromegaly--Consensus, What Consensus? J. Clin. Endocrinol. Metab., August 1, 2002; 87(8): 3534 - 3536. [Full Text] [PDF]

				E. V. Dimaraki, C. A. Jaffe, R. DeMott-Friberg, W. F. Chandler, and A. L. Barkan Acromegaly with Apparently Normal GH Secretion: Implications for Diagnosis and Follow-Up J. Clin. Endocrinol. Metab., August 1, 2002; 87(8): 3537 - 3542. [Abstract] [Full Text] [PDF]

				P. U. Freda Somatostatin Analogs in Acromegaly J. Clin. Endocrinol. Metab., July 1, 2002; 87(7): 3013 - 3018. [Full Text] [PDF]

				A. Colao, L. Spinelli, A. Cuocolo, S. Spiezia, R. Pivonello, C. di Somma, D. Bonaduce, M. Salvatore, and G. Lombardi Cardiovascular Consequences of Early-Onset Growth Hormone Excess J. Clin. Endocrinol. Metab., July 1, 2002; 87(7): 3097 - 3104. [Abstract] [Full Text] [PDF]

				A. C. F. Costa, A. Rossi, C. E. Martinelli Jr., H. R. Machado, and A. C. Moreira Assessment of Disease Activity in Treated Acromegalic Patients Using a Sensitive GH Assay: Should We Achieve Strict Normal GH Levels for a Biochemical Cure? J. Clin. Endocrinol. Metab., July 1, 2002; 87(7): 3142 - 3147. [Abstract] [Full Text] [PDF]

				C. Parkinson, W. M. Drake, M. E. Roberts, K. Meeran, G. M. Besser, and P. J. Trainer A Comparison of the Effects of Pegvisomant and Octreotide on Glucose, Insulin, Gastrin, Cholecystokinin, and Pancreatic Polypeptide Responses to Oral Glucose and a Standard Mixed Meal J. Clin. Endocrinol. Metab., April 1, 2002; 87(4): 1797 - 1804. [Abstract] [Full Text] [PDF]

				Ph. Caron, A. Beckers, D. R. Cullen, M. I. Goth, B. Gutt, P. Laurberg, A. M. Pico, M. Valimaki, and W. Zgliczynski Efficacy of the New Long-Acting Formulation of Lanreotide (Lanreotide Autogel) in the Management of Acromegaly J. Clin. Endocrinol. Metab., January 1, 2002; 87(1): 99 - 104. [Abstract] [Full Text] [PDF]

				C. Parkinson, W. D. J. Ryder, and P. J. Trainer The Relationship between Serum GH and Serum IGF-I in Acromegaly Is Gender-Specific J. Clin. Endocrinol. Metab., November 1, 2001; 86(11): 5240 - 5244. [Abstract] [Full Text] [PDF]

				M. Andersen, C. H. Jensen, R. K. Stoving, J. B. Larsen, H. D. Schroder, B. Teisner, and C. Hagen Fetal Antigen 1 in Healthy Adults and Patients with Pituitary Disease: Relation to Physiological, Pathological, and Pharmacological GH Levels J. Clin. Endocrinol. Metab., November 1, 2001; 86(11): 5465 - 5470. [Abstract] [Full Text] [PDF]

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