Indian Journal of Nuclear Medicine
Home | About IJNM | Search | Current Issue | Past Issues | Instructions | Ahead of Print | Online submissionLogin 
Indian Journal of Nuclear Medicine
  Editorial Board | Subscribe | Advertise | Contact
Users Online: 265 Print this page  Email this page Small font size Default font size Increase font size


 
 Table of Contents     
CASE REPORT
Year : 2016  |  Volume : 31  |  Issue : 4  |  Page : 283-285  

Fluorine-18 fluorodeoxyglucose positron emission tomography/computed tomography in idiopathic pulmonary fibrosis: A new ray of hope!


1 Department of Pulmonary Medicine, Topiwala National Medical College and B. Y. L. Nair Hospital, Mumbai, Maharashtra, India
2 Radiation Medicine Centre (BARC), Tata Memorial Hospital Annexe, Parel, Mumbai, Maharashtra, India

Date of Web Publication19-Sep-2016

Correspondence Address:
Jyotsna M Joshi
Department of Pulmonary Medicine, Topiwala National Medical College and B. Y. L. Nair Hospital, Mumbai - 400 008, Maharashtra
India
Login to access the Email id

Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0972-3919.187456

Rights and Permissions
   Abstract 


Idiopathic pulmonary fibrosis (IPF) is a progressive interstitial lung disease with median survival of 2–3 years. It is described as fibroproliferative rather than pro-inflammatory disorder with limited treatment options. IPF diagnostics and therapeutics are a hot topic of current research. We describe a case elaborating the utility of the whole body positron emission tomography with 2-deoxy-2-(fluorine-18) fluoro-D-glucose (F-18 FDG) integrated with computed tomography technique in IPF. The area of most intense pulmonary F--18 FDG uptake corresponded to regions of honeycombing suggesting metabolically active disease amenable to pharmacologic intervention. Additional F--18 FDG uptake was seen in mediastinal nodes implying an extrapulmonary component of disease.

Keywords: Fluorine-18 fluoro-D-glucose, honeycombing, idiopathic pulmonary fibrosis, positron emission tomography/computed tomography


How to cite this article:
Desai U, Karkhanis VS, Basu S, Joshi JM. Fluorine-18 fluorodeoxyglucose positron emission tomography/computed tomography in idiopathic pulmonary fibrosis: A new ray of hope!. Indian J Nucl Med 2016;31:283-5

How to cite this URL:
Desai U, Karkhanis VS, Basu S, Joshi JM. Fluorine-18 fluorodeoxyglucose positron emission tomography/computed tomography in idiopathic pulmonary fibrosis: A new ray of hope!. Indian J Nucl Med [serial online] 2016 [cited 2019 May 19];31:283-5. Available from: http://www.ijnm.in/text.asp?2016/31/4/283/187456




   Introduction Top


Idiopathic pulmonary fibrosis (IPF) is a progressive interstitial lung disease (ILD) occurring primarily in older adults, limited to the lungs, and associated with the radiologic and/or histopathologic pattern of usual interstitial pneumonia (UIP).[1] Clinical and radiological correlation is sufficient to establish the diagnosis of IPF. Limited treatment modalities and poor survival have made researchers integrate newer diagnostics and therapeutics in search of effective therapy. Role of positron emission tomography (PET) with 2-deoxy-2-(fluorine-18) fluoro-D-glucose (F-18 FDG) integrated with computed tomography (CT) has been studied recently in patients with IPF. We describe a case elaborating the findings of this noninvasive radiology technique in IPF.


   Case Report Top


A 70-year-old man ex-smoker was referred to our outpatient department with symptoms of progressive exertional dyspnea and dry cough since 1 year. On general examination, he had the presence of exercise desaturation from of 95% to 75% and Grade III clubbing. On chest auscultation, bibasilar fine crackles were noted.

Chest X-ray showed a bilateral reticulonodular pattern with right upper lobe fibrosis [Figure 1]. Hematological and biochemical blood investigations were within normal limits. High-resolution computed tomography (HRCT) of thorax showed bilateral reticular opacities with honeycombing in peripheral subpleural areas and interlobular, intralobular septal thickening with traction bronchiectasis, and few ground-glass opacities (GGOs) most marked in lower lobes. Spirometry showed severe restrictive abnormality with forced vital capacity of 0.85 L (26% of predicted). Diffusion capacity of lungs for carbon monoxide could not be performed. F-18 FDG PET/CT showed moderate grade F-18 FDG avid (maximum standardized uptake value (SUVmax) - 4.35) uptake in bilateral reticular opacities [Figure 2]a with relatively high grade F-18 FDG (SUVmax - 6–6.6) uptake in honeycombed areas [Figure 2]b. Low-grade FDG uptake was noted in the ground glass areas with multiple F-18 FDG avid (SUVmax - 8.72) mediastinal lymph nodes [Figure 2]c. His two-dimensional echocardiography showed a pulmonary artery systolic pressure as estimated by tricuspid regurgitation jet method of 35 mmHg. Dual-energy X-ray absorptiometry scan showed osteopenia.
Figure 1: Chest X-ray (posteroanterior view) showing a bilateral reticulonodular pattern with right upper lobe fibrosis

Click here to view
Figure 2: (a) High-resolution computed tomography and corresponding fluorine-18 fluoro-D-glucose positron emission tomography/computed tomography image showing moderate grade fluorine-18 fluoro-D-glucose avid (maximum standardized uptake value - 4.35) uptake in bilateral reticular opacities. (b) High-resolution computed tomography and corresponding fluorine-18 fluoro-D-glucose positron emission tomography/computed tomography image showing high-grade fluorine-18 fluoro-D-glucose (maximum standardized uptake value - 6–6.6) uptake in honeycombed areas. (c) High-resolution computed tomography and corresponding fluorine-18 fluoro-D-glucose positron emission tomography/computed tomography image showing multiple fluorine-18 fluoro-D-glucose avid (maximum standardized uptake value - 8.72) mediastinal lymph nodes

Click here to view


With clinicoradiological correlation, the patient was diagnosed as a case of IPF with mild pulmonary hypertension and osteopenia. He was initiated on therapy with pirfenidone and offered pulmonary rehabilitation.


   Discussion Top


A specific UIP pattern has been described with respect to HRCT of the chest in IPF. Clinical history and characteristic HRCT pattern are the key to diagnosis with a multidisciplinary approach for the treatment of these patients.[1] HRCT has a positive predictive value of 96% and has made the role of surgical lung biopsy obsolete in IPF.[2] However, HRCT is a purely structural imaging on which only indirect inferences regarding metabolism can be made based on degrees of fibrosis and GGO. Hence, newer diagnostics and therapeutics have been explored in IPF. Advances in molecular biology and technology have opened a Pandora's box. One of the newer modalities, F-18 FDG PET/CT is recently studied in IPF. The principle of F-18 FDG uptake in the disease process by tissues is a marker of glucose utilization, correlating with certain types of tissue metabolism (malignancy, infection, and inflammation). Glucose transporter-1 (Glut-1), the predominant Glut in the lung, is responsible for F-18 FDG uptake. Studies have shown F-18 FDG PET to be more sensitive than HRCT in detecting early disease in IPF, and also allow early detection of therapeutic response.[3] The first few studies of F-18 FDG PET/CT evaluation in IPF were by Meissner et al.[4] and Kim et al.[5] They concluded that SUV ratio reflected disease activity of IPF, and it had a positive correlation with fibrosis score or total score on HRCT.[6] Groves et al.[6] documented novel findings of intense pulmonary F-18 FDG uptake corresponding to regions of honeycombing on HRCT of IPF patients and increased F-18 FDG in mediastinal nodes implying an extrapulmonary component of disease. Both of these were seen in our case. The prevailing ILD hypothesis states that chronic inflammatory process injures the lung and modulates the lung fibrogenesis, leading to the end-stage fibrotic scar.[7] Honeycombing is pathognomonic of this irreversible established fibrotic disease; hence, F-18 FDG-PET evidence of increased Glut-1–mediated glucose metabolism at these sites is an interesting contradictory finding. Whether honeycombing represents burnt-out disease or a metabolically active fibrotic process has been debated on by the authors.[6] They postulated that the raised F-18 FDG uptake in patients with changes of honeycombing was a reflection of increased fibroblast metabolism that expresses Glut-1.

Another theory states F-18 FDG-PET uptake in fibrotic lung diseases is due to inflammatory cells and erythrocytes within regions of neovascularization and not by an increased metabolic rate of epithelial cells.[8] Turner-Warwick first implicated aberrant vascular remodeling in the pathogenesis of IPF, demonstrating anastomoses between the systemic and pulmonary microvasculature, and extensive neovascularization within areas of fibrosis.[9] Keane et al.[10] proposed that in IPF, an imbalance in the expression of angiogenic chemokines (CXCL5 and CXCL8) versus angiostatic factors (CXCL10) existed, favoring net angiogenesis. Fibroblasts appeared to be the predominant source of CXCL8 in the interstitium of IPF supporting their role in the angiogenic activity in this disease. Although the explanation for the raised F-18 FDG uptake at sites of honeycombing remains unclear, the findings suggested that effective pharmacologic intervention is possible in these. In a recent study,[11] it was shown that SUVmax was higher in IPF patients with disease progression than in those with stable disease suggesting that F-18 FDG PET/CT may play a role in predicting the progression of IPF.

To conclude, implications of F-18 FDG uptake on F-18 FDG PET/CT in IPF are still under research, and no robust evidence is yet available on its exact use. However, F-18 FDG PET/CT has shown interesting results in early diagnosis, predicting therapy response, and progression of disease. Further studies are required to explore and establish its utility.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.

 
   References Top

1.
Raghu G, Collard HR, Egan JJ, Martinez FJ, Behr J, Brown KK, et al. An official ATS/ERS/JRS/ALAT statement: Idiopathic pulmonary fibrosis: Evidence-based guidelines for diagnosis and management. Am J Respir Crit Care Med 2011;183:788-824.  Back to cited text no. 1
[PUBMED]    
2.
Gotway MB, Freemer MM, King TE Jr. Challenges in pulmonary fibrosis 1: Use of high resolution CT scanning of the lung for the evaluation of patients with idiopathic interstitial pneumonias. Thorax 2007;62:546-53.  Back to cited text no. 2
    
3.
Win T, Thomas BA, Lambrou T, Hutton BF, Screaton NJ, Porter JC, et al. Areas of normal pulmonary parenchyma on HRCT exhibit increased FDG PET signal in IPF patients. Eur J Nucl Med Mol Imaging 2014;41:337-42.  Back to cited text no. 3
[PUBMED]    
4.
Meissner HH, Soo Hoo GW, Khonsary SA, Mandelkern M, Brown CV, Santiago SM. Idiopathic pulmonary fibrosis: Evaluation with positron emission tomography. Respiration 2006;73:197-202.  Back to cited text no. 4
[PUBMED]    
5.
Kim BS, Kang WJ, Oh SW, Lee JW, Lim I, Lee DS, et al. Assessment of disease activity of idiopathic pulmonary fibrosis (IPF) using FDG PET and high-resolution computed tomography (HRCT). J Nucl Med 2007;48:124.  Back to cited text no. 5
    
6.
Groves AM, Win T, Screaton NJ, Berovic M, Endozo R, Booth H, et al. Idiopathic pulmonary fibrosis and diffuse parenchymal lung disease: Implications from initial experience with 18F-FDG PET/CT. J Nucl Med 2009;50:538-45.  Back to cited text no. 6
[PUBMED]    
7.
Selman M, King TE, Pardo A; American Thoracic Society; European Respiratory Society; American College of Chest Physicians. Idiopathic pulmonary fibrosis: Prevailing and evolving hypotheses about its pathogenesis and implications for therapy. Ann Intern Med 2001;134:136-51.  Back to cited text no. 7
[PUBMED]    
8.
El-Chemaly S, Malide D, Yao J, Nathan SD, Rosas IO, Gahl WA, et al. Glucose transporter-1 distribution in fibrotic lung disease: Association with [18 F]-2-fluoro-2-deoxyglucose-PET scan uptake, inflammation, and neovascularization. Chest 2013;143:1685-91.  Back to cited text no. 8
[PUBMED]    
9.
Turner-Warwick M. Precapillary systemic-pulmonary anastomoses. Thorax 1963;18:225-37.  Back to cited text no. 9
[PUBMED]    
10.
Keane MP, Arenberg DA, Lynch JP 3rd, Whyte RI, Iannettoni MD, Burdick MD, et al. The CXC chemokines, IL-8 and IP-10, regulate angiogenic activity in idiopathic pulmonary fibrosis. J Immunol 1997;159:1437-43.  Back to cited text no. 10
[PUBMED]    
11.
Park J, Shim HK, Lee SS. Clinical utility of F-18 FDG PET/CT in progression of idiopathic pulmonary fibrosis. J Nucl Med 2015;56:1729.  Back to cited text no. 11
    


    Figures

  [Figure 1], [Figure 2]



 

Top
  
 
  Search
 
  
    Similar in PUBMED
   Search Pubmed for
   Search in Google Scholar for
 Related articles
    Access Statistics
    Email Alert *
    Add to My List *
* Registration required (free)  

 
  In this article
    Abstract
   Introduction
   Case Report
   Discussion
    References
    Article Figures

 Article Access Statistics
    Viewed1024    
    Printed8    
    Emailed0    
    PDF Downloaded81    
    Comments [Add]    

Recommend this journal