To the Editor:

We thank Drs. Ingegnoli and Cuomo for their comments regarding our study of the potential role of US in the assessment of hand involvement in SSc. In this study, we observed that articular involvement is a common feature in SSc, with approximately half and approximately one-third of SSc patients exhibiting US synovitis and tenosynovitis, respectively. This articular involvement was strikingly underestimated by the single clinical examination.

Regarding tenosynovitis, we observed that in almost half of the cases, the tendons with tenosynovitis were characterized by a hyperechoic tendon sheath thickening that we described as sclerosing tenosynovitis. This pattern was different from the standard tenosynovitis pattern that has been reported in the literature and was specific to SSc patients in comparison to rheumatoid arthritis patients. The pattern predominantly involved the extensor tendons and was associated with the clinical detection of TFRs. Ingegnoli and Cuomo pointed out that this could be related to an increased thickness of the retinacula by US, a thickening of the A1 pulley, or connective tissue infiltrates. Indeed, in another fibrotic disease (i.e., de Quervain's tenosynovitis), the first compartment retinaculum rather than the tendon sheath is thickened, with an inflammatory involvement of the tendons in most of the cases [1]. More recently, Cuomo et al detected increased thickness of the extensor retinaculum at the fourth compartment, which was closely associated with the detection of TFRs, suggesting that this was the lesion underlying the sign [2]. We also evaluated the thickness of the common extensor retinaculum at the fourth compartment between 12 patients with tenosynovitis and 30 healthy controls, but we found no significant difference (mean ± SD 0.98 ± 0.13 mm and 0.97 ± 0.17 mm, respectively; P = 0.77). Therefore, the retinaculum thickness seems to be not universally involved in the sclerosing pattern of tenosynovitis. Tagliafico et al recently reported a thickening of the A1 pulley in SSc patients that was correlated with hand mobility [3]; however, we did not assess this anatomic structure in our study. Another hypothesis is that this sclerosing pattern might be related to fibrosis and particularly to fibrinous deposits on the surface of the tendon sheaths [4]. Because of the clinical meaning of TFRs [5, 6], further studies are warranted to better determine the anatomic structure of this sclerosing tenosynovitis, with particular attention to the A1 pulley and tendon sheaths, and to clarify the best way to assess tenosynovitis in SSc patients and determine its potential input to predict clinical outcomes.

  • Muriel Elhai, MD

  • Henri Guerini, MD

  • Ramin Bazeli, MD

  • Jerôme Avouac, MD, PhD

  • Véronique Freire, MD, FRCPC

  • Jean-Luc Drapé, MD, PhD

  • André Kahan, MD, PhD

  • Yannick Allanore, MD, PhD

  • Paris Descartes University

  • Sorbonne Paris Cité and Cochin Hospital, AP-HP

  • Paris, France