HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH RSS TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Figures Only Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Lebtahi, R. Articles by Crestani, B. Search for Related Content PubMed PubMed Citation Articles by Lebtahi, R. Articles by Crestani, B.

Increased Uptake of ¹¹¹In-Octreotide in Idiopathic Pulmonary Fibrosis

¹ Department of Nuclear Medicine, Hôpital Bichat, Assistance Publique-Hôpitaux de Paris, Paris, France; ² Department of Pneumology, Hôpital Bichat, Assistance Publique-Hôpitaux de Paris, Paris, France; ³ Department of Radiology, Hôpital Bichat, Assistance Publique-Hôpitaux de Paris, Paris, France; ⁴ INSERM Unit 700, Faculté Xavier Bichat, Université Paris 7 Denis Diderot, Paris, France; ⁵ EA 3512, Faculté Xavier Bichat, Université Paris 7 Denis Diderot, Paris, France; ⁶ Department of Radiology, Hôpital Avicenne, Assistance Publique Hôpitaux de Paris, Université Paris 13, Paris, France; and ⁷ Division of Cell Biology and Experimental Cancer Research, Institute of Pathology, University of Berne, Berne, Switzerland

Correspondence: For correspondence or reprints contact: Rachida Lebtahi, MD, PhD, Service de Médecine Nucléaire, Hôpital Bichat, 46 rue Henri Huchard, 75018 Paris, France. E-mail: rachida.lebtahi{at}bch.aphp.fr

Idiopathic pulmonary fibrosis (IPF) is characterized by an uncontrolled accumulation and activation of lung fibroblasts. A modulation of fibroblast activation has been observed in various systems with octreotide, a synthetic somatostatin analog with strong affinity for the somatostatin receptor subtype 2 (sst₂). One aim of our study was to evaluate the expression of somatostatin receptors in the lungs of patients with IPF. A second aim was to evaluate the relationship between ¹¹¹In-octreotide uptake and the effect of pulmonary fibrosis as assessed by lung function tests and parameters and by radiologic findings. Methods: We investigated 11 patients with IPF, 6 patients with pulmonary fibrosis associated with systemic sclerosis (SSc), and 19 patients with disease not of the lung (control patients). The expression of somatostatin receptors was evaluated in vivo using ¹¹¹In-octreotide scintigraphy. We evaluated the relationship between ¹¹¹In-octreotide uptake and the activity of pulmonary fibrosis as assessed by lung function tests, bronchoalveolar lavage (BAL) cellularity, and high-resolution CT (HRCT) of the chest. Planar images and thoracic SPECT (24 h) were performed after injection of 222 MBq of ¹¹¹In-octreotide. Lung uptake was quantified using the lung-to-background ratio (L/B). In addition, the expression of sst₂ was evaluated in vitro, in frozen lung-tissue samples using autoradiography, and in human cultures of lung fibroblasts using a ligand-binding assay. Results: Compared with lung uptake in control patients (median L/B, 1.25; range, 1.14–1.49), lung uptake was increased in all 11 IPF patients (median L/B, 2.63; range, 1.59–3.13; P < 0.001) and in 4 of 6 SSc patients (median L/B, 1.68; range, 1.42–2.16). The L/B was lower in SSc patients than in IPF patients (P = 0.011). Increased uptake correlated with the alteration of lung function (carbon monoxide diffusing capacity [ = –0.655; P = 0.038], diffusing capacity for carbon monoxide and alveolar volume ratio [ = –0.627; P = 0.047], vital capacity [ = –0.609; P = 0.054], and total lung capacity [ = –0.598; P = 0.058]) and with the intensity of alveolitis (total BAL cellularity [ = 0.756; P = 0.045], neutrophil counts [ = 0.738; P = 0.05]), and HRCT fibrosis score ( = 0.673; P = 0.007). Autoradiography suggested that vascular structures were a prominent binding site. Lung fibroblasts expressed somatostatin receptors in vitro as measured by binding assay. Conclusion: Our preliminary results identified an increased expression of sst₂ in (mainly idiopathic) pulmonary fibrosis. Lung uptake correlates with the alteration of lung function and with the intensity of alveolitis.

Key Words: somatostatin receptors • pulmonary fibrosis • fibroblasts

This article has been cited by other articles:

				V. R. Muzykantov Chair's Summary Proceedings of the ATS, August 15, 2009; 6(5): 398 - 402. [Full Text] [PDF]

				P. Rogliani, M. Mura, M. Assunta Porretta, and C. Saltini Review: New perspectives in the treatment of idiopathic pulmonary fibrosis Therapeutic Advances in Respiratory Disease, April 1, 2008; 2(2): 75 - 93. [Abstract] [PDF]

				R Borie, A Fabre, F Prost, J Marchal-Somme, R Lebtahi, S Marchand-Adam, M Aubier, P Soler, and B Crestani Activation of somatostatin receptors attenuates pulmonary fibrosis Thorax, March 1, 2008; 63(3): 251 - 258. [Abstract] [Full Text] [PDF]