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Letters to the Editor Letters to the Editor Absence of relation between ments which might alter the bone metabo- E. TOUSSIROT1 G. DUMOULIN2 lism and post-menopausal status. TGFb se- E. RACADOT3 D. WENDLING1 TGF 1 serum levels and rum concentrations were measured as the N.U. NGUYEN2 bone mass in ankylosing TGFb1 isoform by a specific ELISA assay 1Department of Rheumatology and 2Depart- (R&D Systems, Minneapolis, MN, USA) (in- spondylitis patients ment of Physiology, University Hospital J. tra-assay coefficient of variation: 4.9%; in- Minjoz, 3Laboratory of Immunology, Franche ter-assay coefficient of variation: 7.1%). Be- Comté Blood Transfusion Center, Besançon Sirs, fore measuring the active or mature TGFb1 cédex, France. Osteoporosis is a complicating feature of levels, latent TGFb1 present in the patient and Address correspondence to: Prof. Daniel ankylosing spondylitis (AS), as suggested by control serum samples was first activated by Wendling, Department of Rheumatology, the higher incidence of vertebral crush frac- acidification (7). University Hospital J. Minjoz, Boulevard A. tures (1) and decreased bone mineral density No significant difference was observed in Fleming, F-25030 Besançon cédex, France. (BMD) at the spine and femoral neck (2) in serum TGFb1 levels between patients and E-mail: [email protected] this condition. However, the mechanisms of controls (AS versus controls: 40.6 ± 10.5 vs fcomte.fr this osteoporosis still remain to be elucidated. 37.6 ±8.1 pg/ml; t-test: p = 0.25). Similarly, This work was supported by La Société Serum bone markers (serum calcium, phos- circulating TGFb1 did not differ between the Française de Rhumatologie and l’Association phorus, alkaline phosphatases and osteocalcin different patient subgroups (axial [N = 22] or Franc-Comtoise pour la Recherche et [OC]) are normal (3), while urinary excre- peripheral involvement in patients with or l’Enseignement en Rhumatologie. tion of pyridinium crosslinks is increased in without active disease; active disease was de- some AS patients (4). fined by elevated biochemical markers of References We recently studied insulin-like growth fac- disease activity, i.e. ESR ³ 20 mm/h [N = 15] 1. RALSTON SH, URQUHART GDK, BRZESKI M, tor-I (IGF-I) as a bone growth factor, and its or BASDAI ³ 5 [N = 18]). STURROCK RD: Prevalence of vertebral com- main binding protein, insulin-like growth Finally, no relationship between serum TGF- pression fractures due to osteoporosis in anky- losing spondylitis. Br Med J 1990; 300: 563- factor binding protein-3 (IGFBP-3) in AS b1 concentrations and ESR or CRP levels, or 565. patients with lowered BMD (5). In compari- between TGFb1 and the BASDAI score was 2. DEVOGELAER JP, MALDAGUE B, MALGHEM son with healthy subjects, we found normal found (TGFb and ESR: Spearman’s test: r 1 J, NAGANT DE DEUXCHAISNES C: Appendi- IGF-I serum levels and decreased serum con- = 0.06, p = 0.7; TGFb1 and CRP: r = 0.15, p cular and vertebral bone mass in ankylosing centrations of IGFBP-3 in AS, a situation that = 0.4; TGFb1 and BASDAI: r = - 0.06, p = spondylitis. A comparison of plain radiographs could affect osteoblast function and conse- 0.7). with single and dual photon absorptiometry and quently, bone formation. Transforming In this study, we examined circulating TGFb1 with quantitative computed tomography. Ar- growth factor beta (TGFb) is a multifunction- as a bone-promoting cytokine. Our main con- thritis Rheum 1992; 35: 1062-7. 3. WENDLING D, DUMOULIN G: Spondylarthrite al cytokine and a potent stimulator of matrix clusion is that serum TGFb1 is not different formation (6, 7). Additionally, TGFb shares between AS patients and healthy controls and ankylosante et paramètres phosphocalciques. Rev Rhum 1991; 58: 279-81. many biological properties with insulin-like that no change in the levels of this cytokine 4. MARHOFFER W, STRACKE H, MASOUD I et al.: growth factors (6). Four isoforms of TGFb characterize patients with active disease or Evidence of impaired cartilage/bone turnover (TGFb1,2,3, and 5) have to date been identi- peripheral involvement. Unlike IGF-I/IGF- in patients with active ankylosing spondylitis. fied (7). BP-3, our results suggest that TGFb1 is prob- Ann Rheum Dis 1995; 54: 556-9. In this study, we examined the levels of cir- ably not involved in the pathophysiology of 5. TOUSSIROT E, NGUYEN NU, DUMOULIN G, culating TGFb in a series of AS patients; their AS osteoporosis. However, in this study REGNARD J, WENDLING D: Insulin-like growth factor-I and insulin-like growth factor clinical, laboratory and radiological param- TGFb1 was evaluated as a circulating marker eters were previously reported in a study of and it remains to be demonstrated that this binding protein-3 serum levels in ankylosing spondylitis. Br J Rheumatol 1998; 37: 1172-6. IGF-I and IGFBP-3 serum levels (5). The reflects bone concentrations of this growth 6. MARIE P: Growth factors and bone formation same groups of patients and controls were factor. Moreover, we did not evaluate the in osteoporosis: Roles for IGF-I and TGFb. Rev now evaluated for TGFb: 33 AS patients (age other TGFb isoforms (TGFb2,3 and 5). Inter- Rhum [Engl Ed] 1997; 64: 44-53. [mean ± SD]: 38.5 ± 14.8, F/M: 10/23). The estingly, serum TGFb3 was recently reported 7. CENTRELLA M, ROSEN V, HOROWITZ MC, diagnosis in each patient had been made to be increased in women with osteoporosis WOZNEY JM, MCCARTHY TL: Transforming based on the modified New York criteria for (including patients with non-traumatic ver- growth factor-b gene family members, their AS (8). Disease activity was assessed using tebral fractures or decreased lumbar spine receptors, and bone cell function. Endocrine clinical and biological indexes (BASDAI: BMD) (10). Rev 1995; 4: 211-26. 8. VAN DER LINDEN S, VALKENBURG HA, CATS Bath Ankylosing Spondylitis Disease Activ- In addition, TGFb is complexed to a binding A: Evaluation of diagnostic criteria for anky- ity Index (9), erythrocyte sedimentation rate protein which is a vehicle for the release of losing spondylitis. A proposal for modification [ESR] and C-reactive protein [CRP], respec- latent TGFb to matrix (7). Thus, it might also of the New York criteria. Arthritis Rheum 1984; tively). These patients had normal serum be relevant to assess this protein when ex- 27: 361-8. bone markers (serum calcium, OC, total al- amining the role of TGFb in AS. We con- 9. GARRETT S, JENKINSON T, KENNEDY LG, kaline phosphatases, parathyroid hormone clude that the absence of any difference in WHITELOCK H, GAISFORD P, CALIN A: A new approach to defining disease status in anky- and 25OHD3) and decreased lumbar spine serum TGFb1 levels between AS patients and bone mineral density (dual X-ray absorp- controls argues against a major role for this losing spondylitis: the Bath Ankylosing Spond- ylitis Disease Activity Index. J Rheumatol tiometry) compared to the controls (5). The cytokine in the pathogenesis of AS osteoporo- 1994; 21: 2286-91. controls were 23 healthy volonteers (age: sis. However, possible involvement of the 10. GRAINGER DJ, PERCIVAL J, CHIANO M, SPEC- 35.8 ± 9.5 years; 13 men) with no history of other TGFb isoforms in this bone complica- TOR TD: The role of serum TGF-b isoforms as inflammatory disease. Exclusion criteria for tion has not yet been excluded and therefore potential markers of osteoporosis. Osteoporo- patients and controls were conditions or treat- further studies are needed. sis Int 1999; 9: 398-404. 111.
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