Horm Metab Res 2010; 42(8): 613-618
DOI: 10.1055/s-0030-1255032
Humans, Clinical

© Georg Thieme Verlag KG Stuttgart · New York

Body Composition After Endogenous (Cushing's Syndrome) and Exogenous (Rheumatoid Arthritis) Exposure to Glucocorticoids

E. Resmini1 , C. Farkas1 , B. Murillo1 , M. J. Barahona1 , 2 , A. Santos1 , M. A. Martínez-Momblán1 , O. Roig1 , J. Ybarra1 , C. Geli3 , S. M. Webb1
  • 1Instituto de Investigación Biomédica (IIB)-Sant Pau, Endocrinology/Medicine Department and Centro de Investigación Biomédica en Red de Enfermedades Raras (CIBER-ER, Unidad 747) ISCIII; Universitat Autonoma de Barcelona, Spain
  • 2Endocrinology Department, Hospital Universitari Mútua de Terrassa, Barcelona, Spain
  • 3Rheumatology Department, Hospital Sant Pau, Barcelona, Spain
Further Information

Publication History

received 03.03.2010

accepted 03.05.2010

Publication Date:
31 May 2010 (online)

Abstract

Exposure to chronic glucocorticoid (GC) excess determines changes in body composition. The aim of the study was to compare body composition in women exposed to endogenous hypercortisolism (Cushing's syndrome, CS), exogenous glucocorticoid treatment (rheumatoid arthritis, RA) and controls. Fifty-one CS women, 26 RA women treated with low-dose prednisone (5 mg/day or 10 mg/2 days), and 78 female controls were included. Fourteen CS patients were hypercortisolemic, 37 in remission (10 required hydrocortisone substitution after surgery). Body composition parameters were measured by dual-energy X-ray absorptiometry scanning (DEXA). RA patients had a greater waist-hip ratio (WHR) (p<0.01), less lean body mass (LBM) (p<0.01), and lumbar bone mineral density (BMD) (p<0.01) than controls. CS patients, globally and those with cured disease, had more total fat (both percentage and kg) and trunk fat percentage, and less whole body-BMD than RA patients (p<0.05, p<0.01, p<0.05, respectively). Active CS patients had less whole body-BMD and more LBM than RA patients (p<0.05, p=0.01, respectively). Cured CS patients not taking hydrocortisone had more total fat [both percentage (p<0.05) and kg (p<0.05)], trunk fat percentage (p<0.05), lumbar BMD (p<0.01) than RA patients. Cured CS patients requiring hydrocortisone only differed from RA patients by smaller WHR (p<0.01). All the differences in BMD disappeared when the data were reanalyzed including only the estrogen-deficient groups. Hypercortisoliof CS determines an irreversible increase in body fat, greater than in RA. Endogenous and exogenous exposure to GC negatively affects body composition by increasing the WHR. There appears to be no additional effect on BMD in estrogen-deficient women.

References

  • 1 Burt MG, Gibney J, Ho KK. Characterization of the metabolic phenotypes of Cushing's syndrome and growth hormone deficiency: a study of body composition and energy metabolism.  Clin Endocrinol. 2006;  64 436-443
  • 2 Shaker JL, Lukert BP. Osteoporosis associated with excess glucocorticoids.  Endocrinol Metab Clin N Am. 2005;  34 341-356
  • 3 Fernandez-Rodriguez E, Stewart PM, Cooper MS. The pituitary-adrenal axis and body composition.  Pituitary. 2009;  12 105-115
  • 4 Niu CS, Yeh CH, Yeh MF, Cheng JT. Increase of adipogenesis by ginsenoside (Rh2) in 3T3-L1 cell via an activation of glucocorticoid receptor.  Horm Metab Res. 2009;  41 271-276
  • 5 Rockall AG, Sohaib SA, Evans D, Kaltsas G, Isidori AM, Monson JP, Besser GM, Grossman AB, Reznek RH. Computed tomography assessment of fat distribution in male and female patients with Cushing's syndrome.  Eur J Endocrinol. 2003;  149 561-567
  • 6 Ueland T, Kristo C, Godang K, Aukrust P, Bollerslev J. Interleukin-1 receptor antagonist is associated with fat distribution in endogenous Cushing's syndrome: a longitudinal study.  J Clin Endocrinol Metab. 2003;  88 1492-1496
  • 7 Pirlich M, Biering H, Gerl H, Ventz M, Schmidt B, Ertl S, Lochs H. Loss of body cell mass in Cushing's syndrome: effect of treatment.  J Clin Endocrinol Metab. 2002;  87 1078-1084
  • 8 Colao A, Pivonello R, Spiezia S, Faggiano A, Ferone D, Filippella M, Marzullo P, Cerbone G, Siciliani M, Lombardi G. Persistence of increased cardiovascular risk in patients with Cushing's disease after 5 years of successful cure.  J Clin Endocrinol Metab. 1999;  84 2664-2672
  • 9 Lewis JG, Borowski KK, Shand BI, George PM, Scott RS. Plasma sex hormone-binding globulin, corticosteroid-binding globulin, cortisol, and free cortisol levels in outpatients attending a lipid disorders clinic: a cross-sectional study of 1 137 subjects.  Horm Metab Res. 2010;  42 274-279
  • 10 Majithia V, Geraci SA. Rheumatoid arthritis: diagnosis and management.  Am J Med. 2007;  120 936-939
  • 11 Boland EW, Headley NE. Results of long-continued cortisone administration in rheumatoid arthritis.  Calif Med. 1975;  74 416-423
  • 12 Arnett FC, Edworthy SM, Bloch DA, McShane DJ, Fries JF, Cooper NS, Healey LA, Kaplan SR, Liang MH, Luthra HS, Medsger Jr TA, Mitchel DM, Neustadt DH, Pinals RS, Schaller JG, Sharp JT. The American Rheumatism association 1987. Revised criteria for the classification of Rheumatoid Arthritis.  Arthritis Rheum. 1988;  31 315-323
  • 13 Wilson TA, Blizzard RM. Adrenal insufficiency in childhood. In: Lavin N, (ed.) Manual of Endocrinology and Metabolism. Boston: Little, Brown & Co; 1986: 189
  • 14 Arnaldi G, Mancini T, Polenta B, Boscaro M. Cardiovascular risk in Cushing's syndrome.  Pituitary. 2004;  7 253-256
  • 15 Albiger N, Testa RM, Almoto B, Ferrari M, Bilora F, Petrobelli F, Pagnan A, Mantero F, Scaroni C. Patients with Cushing's syndrome have increased intimal media thickness at different vascular levels: comparison with a population matched for similar cardiovascular risk factors.  Horm Metab Res. 2006;  38 405-410
  • 16 Huxley R, Mendis S, Zheleznyakov E, Reddy S, Chan J. Body mass index, waist circumference and waist-hip ratio as predictors of cardiovascular risk-a review of the literature.  Eur J Clin Nutr. 2010;  64 16-22
  • 17 Barahona MJ, Sucunza N, Resmini E, Fernández-Real JM, Ricart W, Moreno-Navarrete JM, Puig T, Farrerons J, Webb SM. Persistent body fat mass and inflammatory marker increases after long-term cure of Cushing's syndrome.  J Clin Endocrinol Metab. 2009;  94 3365-3371
  • 18 Leong GM, Abad V, Charmandari E, Reynolds JC, Hill S, Chrousos GP, Nieman LK. The effects of child-and adolescent-onset endogenous Cushing syndrome on bone mass, body composition and growth: a 7-year prospective study into young adulthood.  J Bone Miner Res. 2007;  22 110-118
  • 19 Pivonello R, Faggiano A, Lombardi G, Colao A. The metabolic syndrome and cardiovascular risk in Cushing's syndrome.  Endocrinol Metab Clin N Am. 2005;  34 327-339
  • 20 Stewart PM. Tissue-specific Cushing's syndrome, 11β-hydroxysteroid dehydrogenases and the redefinition of corticosteroid hormone action.  Eur J Endocrin. 2003;  149 163-168
  • 21 Tomlinson JW, Walker EA, Bujalska IJ. 11β-Hydroxysteroid Dehydrogenase type 1: a tissue-specific regulator of glucocorticoid response.  End Rev. 2004;  25 831-866
  • 22 Bujalska IJ, Kumar S, Stewart PM. Does central obesity reflect “Cushing's disease of the omentum”?.  The Lancet. 1997;  349 1210-1213
  • 23 Chrousos GP. The role of stress and the hypothalamic-pituitary-adrenal axis in the pathogenesis of the metabolic syndrome: neuro-endocrin and target tissue-related causes.  Int J Obes. 2000;  24 50-55
  • 24 Kola B, Christ-Crain M, Lolli F, Arnaldi G, Giacchetti G, Boscaro M, Grossman AB, Korbonits M. Changes in AMP-activated protein kinase as a mechanism of visceral obesity in Cushing's syndrome.  J Clin Endocrinol Metab. 2008;  93 4969-4973
  • 25 Pecori Giraldi F, Andrioli M, De Marinis L, Bianchi A, Giampietro A, De Martin M, Sacco E, Scacchi M, Pontecorvi A, Cavagnini F. Significant GH deficiency after long-term cure by surgery in adult patients with Cushing's disease.  Eur J Endocrinol. 2007;  156 233-239
  • 26 Burt MG, Gibney J, Ho KK. Characterization of the metabolic phenotypes of Cushing's syndrome and growth hormone deficiency: a study of body composition and energy metabolism.  Clin Endocrinol (Oxf). 2006;  64 436-443
  • 27 Webb SM, Mo D, Lamberts SW, Melmed S, Cavagnini F, Pecori Giraldi F, Strasburger CJ, Zimmermann AG, Woodmansee WW. Metabolic, cardiovascular, and cerebrovascular outcomes in growth hormone-deficient subjects with previous Cushing's disease or non-functioning pituitary adenoma.  J Clin Endocrinol Metab. 2010;  95 630-638
  • 28 McLeod KM, Johnson CS. Identifying women with low bone mass: a systematic review of screening tools.  Geriatr Nurs. 2009;  30 164-173
  • 29 Sherk VD, Palmer IJ, Bemben MG, Bemben DA. Relationships between body composition, muscular strength, and bone mineral density in estrogen-deficient postmenopausal women.  J Clin Densitom. 2009;  12 292-298
  • 30 Barahona MJ, Sucunza N, Resmini E, Fernández-Real J, Ricart W, Moreno J, Puig T, Wägner A, Rodriguez-Espinosa J, Farrerons J, Webb S. Deleterious effects of glucocorticoid replacement on bone in women after long-term remission of Cushing's syndrome.  J Bone Miner Res. 2009;  24 1841-1846
  • 31 Kanazawa I, Yamaguchi T, Yano S, Hayashi K, Yamauchi M, Sugimoto T. Inhibition of the mevalonate pathway rescues the dexamethasone-induced suppression of the mineralization in osteoblasts via enhancing bone morphogenetic protein-2 signal.  Horm Metab Res. 2009;  41 612-616
  • 32 Westhovens R, Nijs J, Taelman V, Dequeker J. Body composition in rheumatoid arthritis.  Br J Rheumatol. 1997;  36 444-448

Correspondence

E. ResminiMD 

Department of Endocrinology

Hospital de Sant Pau

C. S. Antoni Maria Claret n.167

08025 Barcelona

Spain

Phone: +34/9355/37 917

Fax: +34/9355/65 602

Email: eresmini@santpau.cat

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