Skip to content

Advertisement

  • Case report
  • Open Access
  • Open Peer Review

This article has Open Peer Review reports available.

How does Open Peer Review work?

Ground-glass opacity heralding invasive lung adenocarcinoma with prodromal dermatomyositis: a case report

Journal of Cardiothoracic Surgery201813:20

https://doi.org/10.1186/s13019-018-0705-x

Received: 8 November 2017

Accepted: 24 January 2018

Published: 7 February 2018

Abstract

Background

Dermatomyositis, an inflammatory myopathy with cutaneous involvement, is associated with malignancy and often manifests paraneoplastically. While co-occurrence with small cell carcinoma is well attested, primary lung adenocarcinoma, which may present as focal ground-glass opacification on computed tomography of the thorax, is less frequently coincident.

Case presentation

We report the case of a 72-year-old female patient with dermatomyositis — treated with a combination of prednisone, methotrexate, and intravenous immunoglobulin — and an indolent, subsolid, non-hypermetabolic pulmonary lesion, which was determined to be invasive primary lung adenocarcinoma. Supporting a paraneoplastic basis, immunosuppressive therapy was discontinued following tumor excision without relapse of signs or symptoms of dermatomyositis.

Conclusions

While dermatomyositis prodromal to lung adenocarcinoma is not without precedent, association with an indolent, subsolid lesion has, to the best of our knowledge, not been reported. The case described herein illustrates the importance of maintaining a high index of suspicion for malignancy in the setting of dermatomyositis.

Keywords

  • Dermatomyositis
  • Lung adenocarcinoma
  • Subsolid
  • Ground-glass opacity

Background

Idiopathic inflammatory myopathies are a group of diseases of uncertain but presumed autoimmune etiology characterized by weakness and inflammation of the proximal musculature, and include polymyositis (PM), dermatomyositis (DM), sporadic inclusion body myositis, and necrotizing autoimmune myopathy. The best characterized among them, PM and DM, effect insidious dysfunction of the proximal musculature in a symmetric fashion, the progression of which may produce such complications as dysphagia and respiratory failure. Despite their similarities, DM distinguishes itself from PM through a plethora of cutaneous manifestations, including “Gottron’s papules” on the dorsal aspects of the phalangeal joints, the periorbital heliotrope eruption, and rashes distributed characteristically over the back (“shawl sign”), chest (“V sign”), or thighs (“holster sign”) [1]. Since the diagnostic codification of DM and PM by Bohan and Peter [2], many proposals for systematizing the diagnosis of these disorders have been advanced (e.g., [3]). In addition to clinical features, elevations in serum enzyme levels, and histologic and electromyographic evidence, diagnosis is commonly supported by the presence of characteristic autoantibodies, the nature of which may connote a particular disease subtype or impart prognostic significance [4]. Therapy is normally directed toward immunosuppression, by high-dose corticosteroids alone or in conjunction with steroid-sparing agents such as methotrexate and azathioprine, with addition of further agents (e.g., rituximab, intravenous immunoglobulin (IVIG)) as required for refractory illness. Given the association of malignancy with both PM and DM, particularly the latter [5, 6], a thorough diagnostic work-up for its presence is inevitably prompted by a diagnosis of either condition. In many cases, an occult neoplasm is detected at an early stage and with a higher likelihood of successful treatment. While the lung is a frequent site for primary, myositis-associated malignancy, presentation as a subsolid lesion has not been previously reported. We describe herein a case in which DM was the presenting manifestation of invasive adenocarcinoma of the lung, detected by thin-section computed tomography as an indolent nodule with predominantly ground-glass attenuation.

Case presentation

A 72-year-old woman with a history of Graves’ disease treated by radioiodine ablation and no smoking history presented with subacute proximal muscle weakness, accompanied by myalgia and a rash. Dermatologic examination was significant for non-pruritic, macular erythema over the posterior arms; discrete papules on the second and fourth distal interphalangeal joints of the left hand; dusky, reticulated erythema involving the proximal, lateral thighs (evoking the “holster sign” [7]); and linear, erythematous plaques extending inferiorly from the nape. Elevations were noted in the levels of creatine kinase (CK), aldolase, lactate dehydrogenase (LDH), aspartate transaminase (AST), and alanine transaminase (ALT). Suspicion for dermatomyositis prompted initiation of high-dose prednisone (1 mg/kg) on hospital day 2, in spite of which symptoms failed to improve and enzyme levels continued to rise, peaking on hospital day 8 (cf. Fig. 1; peak values were as follows: CK 3108 U/L, aldolase 25.9 U/L, LDH 594 U/L, AST 252 U/L, ALT 344 U/L). Immune serology studies, encompassing general and myositis-specific antibodies, were uniformly negative (ANA, Jo-1, PL-12, PL-7, EJ, OJ, Mi-2, SRP, Ku, U2 snRNP, PM/Scl). Electromyography revealed fibrillations and positive sharp waves, indicative of an irritative myopathic process affecting the proximal muscles. Muscle biopsy demonstrated immune myopathy with perimysial pathology (IMPP). Given the presumptive diagnosis of dermatomyositis, a malignancy work-up was initiated, and computed tomography (CT) of the thorax revealed a 2.1-cm subsolid nodule in the right middle lobe. Relative to a CT scan acquired four years earlier, the nodule was stable in size but had progressed in fractional solidity from 15% (i.e., predominantly ground-glass opacified) to 90% (Fig. 2). PET/CT showed minimal 18F-fluorodeoxyglucose (FDG) avidity (standardized uptake value (SUV) 1.3) in the right middle lobe lesion, consistent with its indolent nature, and no evidence of lymph node or metastatic disease. Given the refractoriness of symptoms to high-dose corticosteroids and biopsy evidence of a DM-spectrum process (IMPP), methotrexate (gradually dose-escalated from 7.5 to 15 mg weekly) and IVIG (2 g/kg monthly) were initiated on hospital day 11. Despite the indolence of the pulmonary lesion, the heightened risk of malignancy in the setting of presumed DM prompted thoracoscopic right middle lobectomy and mediastinal lymph node dissection, which the patient underwent on hospital day 16, after spirometry and diffusion capacity testing demonstrated satisfactory pulmonary function. Histopathologic analysis revealed a 2.1-cm, moderately differentiated, invasive adenocarcinoma, arranged in papillary (60%), acinar (30%), micropapillary (5%), and lepidic (5%) proliferative patterns. There was one intraparenchymal node involved by direct extension; level 4R, 7, and 11 lymph nodes were negative for malignancy. Her stage was pT1cN1M0 or IIB (AJCC 7th edition [8]). Molecular studies of the tumor (specifically, short-read sequencing of a target-enriched library of 130 genes that are frequently mutated in solid tumors) disclosed a constitutively activating mutation of EGFR (c.2156G>C; p.G719A) and a mutation of β-catenin (CTNNB1) within the GSK3 β (GSK3B) phosphorylation region (c.97T>C, p.S33P), with variant allele fractions of 23.5 and 8.6%, respectively. Following surgical excision of the lung tumor, the patient experienced a dramatic improvement in muscle strength and disappearance of the rash. Deltoid and hip-flexor strength increased from 5/10 at the time of surgery to 8/10 within a week. Her enzyme levels continued to decline and were all within the normal range at the time of discharge on hospital day 29. Upon discharge, the corticosteroid dose was tapered from 1 to 0.083 mg/kg/d over a one-month period and the methotrexate discontinued, without relapse of dermatomyositis symptoms; the corticosteroid and IVIG were both discontinued approximately one month thereafter. At the time of writing, the patient continued to show improvements in functional status, and had recently discontinued adjuvant chemotherapy with carboplatin and pemetrexed owing to toxicities.
Figure 1
Fig. 1

Serum creatine kinase levels are displayed with respect to the duration of hospitalization. The upper limit of normal (200 U/L) is indicated by the dashed horizontal line, while the onset of an intervention is indicated by a dashed vertical line. High-dose prednisone (1 mg/kg/d) was started on hospital day 2; methotrexate (MTX, 7.5 mg/week) and intravenous immunoglobulin (IVIG, 2 g/kg/mo) began on hospital day 11; and right middle lobectomy and mediastinal lymph node dissection took place on hospital day 16. Not shown are escalations of the methotrexate dose to 10 mg/week (hospital day 18) and 15 mg/week (hospital day 25), as well as discharge and commencement of the steroid taper, which coincided on hospital day 29

Figure 2
Fig. 2

Slices from chest CT scans acquired four years prior to (left) and at the time of presentation (right), demonstrating an indolent, subsolid lesion in the right middle lobe, the solid fraction of which evolved from 15% (left) to 90% (right)

Discussion

Although the etiology of DM remains to be elucidated, both innate and adaptive arms of the immune system are thought to play important roles, and autoantibodies — classified as either nonspecific, myositis-associated, or myositis-specific — are found in as many as 80% of patients with PM or DM [9]. Numerous myositis-specific autoantigens have been described, including the signal recognition particle (SRP), the helicase Mi-2, and a battery of aminoacyl tRNA synthetases (e.g., histidyl [Jo-1], threonyl [PL-7], alanyl [PL-12], isoleucyl [OJ], glycyl [EJ]), and autoantibodies directed against each are thought to define distinct myositis syndromes: antisynthetase syndrome, for instance, is strongly associated with interstitial lung disease, while Mi-2 autoantibodies are thought to confer reduced risk for a myositis-associated malignancy [10]. Assaying serum for a set of autoantibodies representing the three aforementioned classes was uniformly negative in the patient described in this report. As a putative autoimmune disease, DM has also been found in association with other autoimmune conditions, including Graves’ disease [11, 12], an association observed in the present case.

The incidence of malignancy is elevated in the setting of DM, an association first recognized in 1916 [13, 14] and confirmed by many retrospective analyses, with standardized incidence ratios (SIRs) typically ranging from 3 to 6 [1518]. The temporal association of diagnoses of DM and malignancy [16, 18, 19], and the tendency for resolution of DM symptoms upon treatment of the underlying malignancy [6, 20] are consistent with the notion that malignancy-associated DM is a paraneoplastic phenomenon. While the mechanism underlying the association remains ill-defined, tumoral expression of myositis autoantigens has been proposed as a link whereby an immune-response directed against cancer cells leads to inflammatory destruction of antigenically similar muscle tissue [21]. The association of DM with cancer is broad, comprising many histologic types and tissues of origin, the latter of which tends to reflect the anatomic distribution of cancers observed in a population [22]. Accordingly, the lung is a common site of DM-associated cancer among western populations [15]. A review of 24 cases of coincident PM/DM and primary lung cancer spanning the period 1947–2000 found small cell and squamous cell carcinomas to be the most common histologic types [23]. Since then, myriad reports of DM-associated lung cancer have appeared in the literature [2453]. Combining these reports with those of Fujita et al. [23] gives nearly 50 cases of dermatomyositis-associated, histologically determined lung cancer over the past 70 years, the aggregate analysis of which is presented in Table 1 (many more cases of DM-associated lung cancer have been reported without histologic characterization, e.g., [22]). The most commonly reported histologic type of lung cancer associated with DM is small cell carcinoma (approximately 44%), which is followed by squamous cell carcinoma and adenocarcinoma, each of which account for approximately 17% of reported cases. Given the small, non-systematic sample and the possibility of reporting bias, these frequencies should not be misconstrued as an accurate reflection of the association of lung-cancer histology with dermatomyositis. Among these cases, a history of smoking is common, and in several, including the present one, paraneoplasticity is suggested by the remission of DM shortly after treatment of the associated lung cancer [32, 33, 44, 47].
Table 1

Summary of histologic classification of DM-associated lung malignancies reported in the literature (1947–2017) [2353]

Histology

Cases

Frequency

Small cell carcinoma

21

43.8%

Squamous cell carcinoma

8

16.7%

Adenocarcinoma

8

16.7%

Neuroendocrine

3

6.3%

Undifferentiated

2

4.2%

Other

6

12.5%

Total

48

100.0%

The category “other” comprises mixed histology (e.g., adenosquamous), anaplastic cell carcinoma, alveolar cell carcinoma, giant cell carcinoma, and non-small cell carcinoma not otherwise specified

While previous studies have documented the association between histologic types of lung cancer and DM, little attention has been paid to its association with the molecular basis of malignancy. Genetic analysis of the primary tumor in the present case revealed mutation of the gene encoding EGFR, an event reported to occur in about 10% of cases of non-small cell lung cancer [54]. Point mutations of the codon for G719 account for about 3% of all EGFR mutations in lung cancer; are more common among non-smokers, females, and East Asians [55]; and predict sensitivity to EGFR tyrosine kinase inhibitors [56]. In addition, a mutation was found in the GSK3B phosphorylation region of β-catenin (S33P, which leads to constitutive transactivation of T-cell factor and lymphoid enhancer factor target genes). While β-catenin has been reported to be rarely subject to mutation in lung cancer [57], recent evidence suggests an important role for Wnt/ β-catenin signaling in the progression from lung adenoma to adenocarcinoma [58]. No mutations were found in various other genes implicated in lung adenocarcinoma, including KRAS, ALK, MET, RET, CCND1, TP53, KEAP1, MAP2K1, RIT1, PIK3CA, U2AF1, MDM2, and SETD2 [59]. Whether mutations such as the ones observed bear any relation to paraneoplastic DM remains to be determined.

Finally, the attenuation characteristics of the lesion observed in this case deserve remark inasmuch as an association thereof with paraneoplastic DM is, to our knowledge, without precedent. Ground-glass opacification (GGO) describes an increase in X-ray attenuation which, unlike consolidation, does not obscure underlying vascular and bronchial architecture [60]. Although the finding is generally non-specific, persistence and focality together suggest malignancy, particularly adenocarcinoma or its precursors, the histologic type with which circumscribed subsolid lesions are almost exclusively associated [61, 62]. As a category, subsolid lesions comprise both pure ground-glass-opacified nodules and those with a solid component (part-solid); the GGO component is thought to signify preinvasive growth (atypical adenomatous hyperplasia and adenocarcinoma in situ), and the solid component a nucleus of invasive adenocarcinoma [63]. The consolidation-to-tumor-ratio (CTR), typically defined as the ratio of the maximum linear extents of the solid fraction of the tumor and of the tumor itself, may be used to predict the invasiveness and likelihood of progression of a subsolid lesion [64]. Despite prior claims of association between GGO and EGFR mutation status, a recent meta-analysis found statistically significant association of EGFR mutation status not with pure GGO lesions but with part-solid ones [65]. The majority of subsolid lesions are stable in size; those that grow do so indolently, with reported volume doubling times of 600–900 and 300–500 days for pure GGO and part-solid lesions, respectively [63]. Their typically languorous course explains observations of insignificant FDG uptake [66] — on account of which SUV max thresholds must be adjusted for proper interpretation [62] — and moreover demands prolonged (three to five years) surveillance by CT [67, 68]. Indeed, among a cohort of 218 patients with subsolid nodules that had been stable for 3 years, 14 (6.4%) experienced subsequent growth [69], underscoring the need for vigilance. PET/CT, biopsy, and resection should be pursued for nodules having solid components greater than 8 mm in length, expanding consolidation, or other concerning features [68]. Although sublobar resection has been demonstrated to be equally effective to lobectomy for subsolid nodules [67], the higher recurrence rate for part-solid lesions [70] should be taken into consideration when determining surgical management. In the present case, an indolent GGO lesion evolved within four years to EGFR-mutated, non-hypermetabolic, invasive adenocarcinoma, and is, to our knowledge, the first case of a GGO-predominant pulmonary lesion manifesting as DM.

Conclusions

The case described herein illustrates the importance of maintaining a high index of suspicion for malignancy in the setting of dermatomyositis. The occurrence of a subsolid, indolent, non-hypermetabolic pulmonary lesion, approximately stable in size over a period of four years, in a lifetime nonsmoker may have seemed an unlikely trigger for dermatomyositis, and misapprehension of its significance would have delayed definitive treatment.

Abbreviations

ALT: 

Alanine transaminase

AST: 

Aspartate transaminase

CK: 

Creatine kinase

CT: 

Computed tomography

CTR: 

Consolidation-tumor ratio

DM: 

Dermatomyositis

EGFR: 

Epidermal growth factor receptor

FDG: 

18F-fluorodeoxyglucose

GGO: 

Ground-glass opacity

IMPP: 

Immune myopathy with perimysial pathology

IVIG: 

Intravenous immunoglobulin

LDH: 

Lactate dehydrogenase

PET: 

Positron emission tomography

PM: 

Polymyositis

SIR: 

Standardized incidence ratio

SUV: 

Standardized uptake value

Declarations

Acknowledgements

None declared.

Funding

The study was supported by Stanford Medical Scientist Training Program NIH grant T32-GM007365 (AJB).

Availability of data and materials

Data sharing is not applicable to this article as no datasets were generated or analyzed during the current study.

Authors’ contributions

AJB, DSD, and NLS contributed to design, data collection and analysis, and drafting of the manuscript. All authors contributed to revision of the manuscript. All authors read and approved the final manuscript.

Ethics approval and consent to participate

Not applicable.

Consent for publication

Informed consent for publication was obtained and is available for review by the editor.

Competing interests

None declared.

Publisher’s Note

Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.

Open Access This article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver(http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

Authors’ Affiliations

(1)
Stanford University School of Medicine, Stanford, USA
(2)
Division of Thoracic Surgery, Stanford University School of Medicine, Stanford, USA
(3)
Division of Oncology, Stanford University School of Medicine / Stanford Cancer Institute, Stanford, USA
(4)
Division of Hospital Medicine, Stanford University School of Medicine, Stanford, USA

References

  1. Callen JP. Cutaneous manifestations of dermatomyositis and their management. Curr Rheumatol Rep. 2010; 12(3):192–7.View ArticlePubMedGoogle Scholar
  2. Bohan A, Peter JB. Polymyositis and dermatomyositis (first of two parts). N Engl J Med. 1975; 292(7):344–7.View ArticlePubMedGoogle Scholar
  3. Dalakas MC, Hohlfeld R. Polymyositis and dermatomyositis. Lancet. 2003; 362(9388):971–82.View ArticlePubMedGoogle Scholar
  4. Targoff IN. Humoral immunity in polymyositis/dermatomyositis. J Invest Dermatol. 1993; 100(1):S116–23.View ArticleGoogle Scholar
  5. Sigurgeirsson B, Lindelof B, Edhag O, Allander E. Risk of cancer in patients with dermatomyositis or polymyositis. A population-based study. N Engl J Med. 1992; 326(6):363–7.View ArticlePubMedGoogle Scholar
  6. Andras C, Ponyi A, Constantin T, Csiki Z, Szekanecz E, Szodoray P, et al. Dermatomyositis and polymyositis associated with malignancy: a 21-year retrospective study. J Rheumatol. 2008; 35(3):438–44.PubMedGoogle Scholar
  7. Stephens DH, Schwarzenberger K, Cooper SM. The holster sign: a specific but under recognized skin finding in dermatomyositis. Arthritis Rheum. 2009; 60(Suppl 10):818.Google Scholar
  8. Detterbeck FC, Boffa DJ, Kim AW, Tanoue LT. The eighth edition lung cancer stage classification. Chest. 2017; 151(1):193–203.View ArticlePubMedGoogle Scholar
  9. Nagaraju K, Lundberg IE. Polymyositis and dermatomyositis: pathophysiology. Rheum Dis Clin North Am. 2011; 37(2):159–71.View ArticlePubMedGoogle Scholar
  10. Ghirardello A, Bassi N, Palma L, Borella E, Domeneghetti M, Punzi L, et al. Autoantibodies in polymyositis and dermatomyositis. Curr Rheumatol Rep. 2013; 15(6):335.View ArticlePubMedGoogle Scholar
  11. Selva-O’Callaghan A, Mijares-Boeckh-Behrens T, Solans-Laque R, Molins-Vara T, Olive G, Vilardell-Tarres M. Dermatomyositis and Graves’ disease. Clin Exp Rheumatol. 2001; 19(5):595–6.PubMedGoogle Scholar
  12. Hemminki K, Li X, Sundquist J, Sundquist K. The epidemiology of Graves’ disease: evidence of a genetic and an environmental contribution. J Autoimmun. 2010; 34(3):J307–13.View ArticlePubMedGoogle Scholar
  13. Sterz G. Polymyositis. Berl Klin Wochenshr. 1916; 53:489.Google Scholar
  14. Kankeleit H. Über primaire nichteitrige polymyositis. Dtsch Arch Klin Med. 1916; 120:335–9.Google Scholar
  15. Hill CL, Zhang Y, Sigurgeirsson B, Pukkala E, Mellemkjaer L, Airio A, et al. Frequency of specific cancer types in dermatomyositis and polymyositis: a population-based study. Lancet. 2001; 357(9250):96–100.View ArticlePubMedGoogle Scholar
  16. Chow WH, Gridley G, Mellemkjaer L, McLaughlin JK, Olsen JH, Fraumeni JF. Cancer risk following polymyositis and dermatomyositis: a nationwide cohort study in Denmark. Cancer Causes Control. 1995; 6(1):9–13.View ArticlePubMedGoogle Scholar
  17. Olazagasti JM, Baez PJ, Wetter DA, Ernste FC. Cancer risk in dermatomyositis: a meta-analysis of cohort studies. Am J Clin Dermatol. 2015; 16(2):89–98.View ArticlePubMedGoogle Scholar
  18. Buchbinder R, Forbes A, Hall S, Dennett X, Giles G. Incidence of malignant disease in biopsy-proven inflammatory myopathy. A population-based cohort study. Ann Intern Med. 2001; 134(12):1087–95.View ArticlePubMedGoogle Scholar
  19. Zantos D, Zhang Y, Felson D. The overall and temporal association of cancer with polymyositis and dermatomyositis. J Rheumatol. 1994; 21(10):1855–9.PubMedGoogle Scholar
  20. Ponyi A, Constantin T, Garami M, Andras C, Tallai B, Vancsa A, et al. Cancer-associated myositis: clinical features and prognostic signs. Ann N Y Acad Sci. 2005; 1051:64–71.View ArticlePubMedGoogle Scholar
  21. Casciola-Rosen L, Nagaraju K, Plotz P, Wang K, Levine S, Gabrielson E, et al. Enhanced autoantigen expression in regenerating muscle cells in idiopathic inflammatory myopathy. J Exp Med. 2005; 201(4):591–601.View ArticlePubMedPubMed CentralGoogle Scholar
  22. Zhang W, Jiang SP, Huang L. Dermatomyositis and malignancy: a retrospective study of 115 cases. Eur Rev Med Pharmacol Sci. 2009; 13(2):77–80.PubMedGoogle Scholar
  23. Fujita J, Tokuda M, Bandoh S, Yang Y, Fukunaga Y, Hojo S, et al. Primary lung cancer associated with polymyositis/dermatomyositis, with a review of the literature. Rheumatol Int. 2001; 20(2):81–4.View ArticlePubMedGoogle Scholar
  24. Gentina T, Arbion F, Benard A, Strecker A. Dermatomyositis and small-cell lung cancer: fortuitous association or paraneoplastic syndrome?Rev Pneumol Clin. 2000; 56(3):209–12.PubMedGoogle Scholar
  25. Lee HS, Zang DY, Seo YI, Kim DG, Kim EJ, Ahn JS, et al. A small cell lung cancer concurrently diagnosed with paraneoplastic dermatomyositis. Cancer Res Treat. 2003; 35(2):161–4.View ArticlePubMedGoogle Scholar
  26. Murakami Y, Kanazawa K, Okuno K, Maekawa S, Matsuda Y, Miyamoto Y, et al. High-grade neuroendocrine carcinoma of the lung presenting an unusual spread mimicking pleural mesothelioma associated with dermatomyositis. Am J Med Sci. 2004; 327(4):227–30.View ArticlePubMedGoogle Scholar
  27. Antonioli CM, Airo P. Dermatomyositis associated with lymphoproliferative disorder of NK cells and occult small cell lung carcinoma. Clin Rheumatol. 2004; 23(3):239–41.View ArticlePubMedGoogle Scholar
  28. Mori H, Habe K, Hakamada A, Isoda K, Mizutani H. Relapse of dermatomyositis after 10 years in remission following curative surgical treatment of lung cancer. J Dermatol. 2005; 32(4):290–4.View ArticlePubMedGoogle Scholar
  29. Torchia D, Antiga E, Ricupero L, Caproni M, Fabbri P. Magnetic resonance imaging for paraneoplastic dermatomyositis. Med J Aust. 2007; 187(10):589.PubMedGoogle Scholar
  30. Zangrilli A, Papoutsaki M, Bianchi L, Teoli M, Chimenti S. Bullous dermatomyositis: a marker of poor prognosis and aggressive internal malignancy?Acta Derm Venereol. 2008; 88(4):393–4.PubMedGoogle Scholar
  31. Milanez FM, Pereira CA, Trindade PH, Milinavicius R, Coletta EN. Lung adenocarcinoma, dermatomyositis, and Lambert-Eaton myasthenic syndrome: a rare combination. J Bras Pneumol. 2008; 34(5):333–6.View ArticlePubMedGoogle Scholar
  32. Zang YS, Xiu QY, Fang Z, Li B, Xia TB. Case report: dramatic recovery of lung adenocarcinoma-associated dermatomyositis with targeted lung cancer therapy alone. Oncologist. 2008; 13(1):79–81.View ArticlePubMedGoogle Scholar
  33. Przybylski G, Jarzemska A, Czerniak J, Siemiatkowska K, Gadzinska A, Cieslinski K. A case report of a patient with dermatomyositis as a prodromal sign of lung cancer. Pol Arch Med Wewn. 2008; 118(3):143–7.PubMedGoogle Scholar
  34. Numata T, Kawabata A, Fujita Y, Bono K, Tamura K, Mikami J, et al. A case of small cell lung cancer with dermatomyositis that deteriorated with leukocytopenia due to chemotherapy. Nihon Kokyuki Gakkai Zasshi. 2008; 46(12):1059–64.PubMedGoogle Scholar
  35. Petersen B, Bygum A. Dermatomyositis as a marker of lung cancer. Ugeskr Laeg. 2009; 171(18):1514–5.PubMedGoogle Scholar
  36. Tang MM, Thevarajah S. Paraneoplastic dermatomyositis: a 12-year retrospective review in the Department of Dermatology Hospital Kuala Lumpur. Med J Malaysia. 2010; 65(2):138–42.PubMedGoogle Scholar
  37. Lee WY, Kastelik J, Campbell A, Avery G, McGivern D, Lind M. A case report of dermatomyositis associated with small cell lung cancer. Tumori. 2012; 98(6):158e–61e.PubMedGoogle Scholar
  38. Revannasiddaiah S, Gupta MK, Rastogi M, Kesari AA, Seam RK, Gupta M, Chauhan S, Madabhavi I. Dermatomyositis and chest radiography leading to the diagnosis of lung cancer and subsequent confusions in staging due to the presence of tuberculosis. BMJ Case Rep. 2012; 2012:bcr0120125585.PubMedPubMed CentralGoogle Scholar
  39. Chao G, Fang L, Lu C, Chen Z. Small cell lung cancer presenting as dermatomyositis: mistaken for single connective tissue disease. Rheumatol Int. 2012; 32(6):1737–40.View ArticlePubMedGoogle Scholar
  40. Castro AS, Barroso A, Parente B. Dermatomyositis as the first manifestation of a lung tumor. Rev Port Pneumol. 2013; 19(4):179–83.View ArticlePubMedGoogle Scholar
  41. Nikolaos T, Maria T, Ioannis KD, Georgios L, Nikolaos P, Stamatina D, et al. Dermatomyositis as an early manifestation and a significant clinical precursor of lung cancer: report of a rare case and review of the current literature. Int J Clin Exp Med. 2013; 6(2):105–9.PubMedPubMed CentralGoogle Scholar
  42. Graf SW, Limaye VS, Cleland LG. Gemcitabine-induced radiation recall myositis in a patient with dermatomyositis. Int J Rheum Dis. 2014; 17(6):696–7.View ArticlePubMedGoogle Scholar
  43. Shen C, Che G. Dermatomyositis as an antecedent sign of lung cancer in an eldly patient: a case report. J Thorac Dis. 2014; 6(2):E15–18.PubMedPubMed CentralGoogle Scholar
  44. Bursac DS, Sazdanic-Velikic DS, Tepavac AP, Secen NM. Paraneoplastic dermatomyositis associated with adenocarcinoma of the lung. J Cancer Res Ther. 2014; 10(3):730–2.PubMedGoogle Scholar
  45. Albert TJ, Bastawrous S, Raugi GJ, Hirschmann JV. A 62-year-old man with skin rash and an abnormal chest radiograph. Chest. 2015; 147(3):e90–4.View ArticlePubMedGoogle Scholar
  46. Papakonstantinou E, Kapp A, Raap U. A mild form of dermatomyositis as a prodromal sign of lung adenocarcinoma: a case report. J Med Case Rep. 2016; 10:34.View ArticlePubMedPubMed CentralGoogle Scholar
  47. Zhang X, Wang Y, Ma G, Zhang L, Jing H, DU J. Dermatomyositis as a symptom of primary lung cancer: A case report and review of the literature. Oncol Lett. 2016; 11(5):3413–6.View ArticlePubMedPubMed CentralGoogle Scholar
  48. Dai Y, Li P, Yan S, Xia X, Li Z, Xia M. Lung squamous carcinoma with two paraneoplastic syndromes: dermatomyositis and Lambert-Eaton myasthenic syndrome. Clin Respir J. 2016; 10(4):495–9.View ArticlePubMedGoogle Scholar
  49. Ahumada Pina H, Fuentes Cabrera L, Selame Glena R, Garcia Oneto D, Jimenez Aguilar A, Duran Herrera C, et al. Dermatomyositis as the first manifestation of small cell carcinoma: case report and literature review. Medwave. 2016; 16(10):e6609.View ArticlePubMedGoogle Scholar
  50. Boleto G, Perotin JM, Eschard JP, Salmon JH. Squamous cell carcinoma of the lung associated with anti-Jo1 antisynthetase syndrome: a case report and review of the literature. Rheumatol Int. 2017; 37(7):1203–6.View ArticlePubMedGoogle Scholar
  51. Takashima R, Takamatsu K, Shinkawa Y, Yagita M, Fukui M, Fujita M. Dermatomyositis associated with lung neuroendocrine carcinoma. Intern Med. 2017; 56(6):719–24.View ArticlePubMedPubMed CentralGoogle Scholar
  52. Lee GL, Poulos GA, Zirwas MJ. Dermatomyositis and metastatic lung adenocarcinoma first presenting as calcinosis cutis. J Clin Aesthet Dermatol. 2012; 5(1):47–8.PubMedPubMed CentralGoogle Scholar
  53. Kalinova D, Reshkova V, Rashkov R. Two clinical cases of paraneoplastic dermatomyositis associated with lung cancer with different histopathological characteristics. Neurooncol Open Access. 2016; 1:1.Google Scholar
  54. Vliegen L, Dooms C, De Kelver W, Verbeken E, Vansteenkiste J, Vandenberghe P. Validation of a locked nucleic acid based wild-type blocking PCR for the detection of EGFR exon 18/19 mutations. Diagn Pathol. 2015; 10:57.View ArticlePubMedPubMed CentralGoogle Scholar
  55. Mitsudomi T, Yatabe Y. Epidermal growth factor receptor in relation to tumor development: EGFR gene and cancer. FEBS J. 2010; 277(2):301–8.View ArticlePubMedGoogle Scholar
  56. Lynch TJ, Bell DW, Sordella R, Gurubhagavatula S, Okimoto RA, Brannigan BW, et al. Activating mutations in the epidermal growth factor receptor underlying responsiveness of non-small-cell lung cancer to gefitinib. N Engl J Med. 2004; 350(21):2129–39.View ArticlePubMedGoogle Scholar
  57. Shigemitsu K, Sekido Y, Usami N, Mori S, Sato M, Horio Y, et al. Genetic alteration of the beta-catenin gene (CTNNB1) in human lung cancer and malignant mesothelioma and identification of a new 3p21.3 homozygous deletion. Oncogene. 2001; 20(31):4249–57.View ArticlePubMedGoogle Scholar
  58. Tammela T, Sanchez-Rivera FJ, Cetinbas NM, Wu K, Joshi NS, Helenius K, et al. A Wnt-producing niche drives proliferative potential and progression in lung adenocarcinoma. Nature. 2017; 545(7654):355–9.View ArticlePubMedGoogle Scholar
  59. Network CGAR, et al. Comprehensive molecular profiling of lung adenocarcinoma. Nature. 2014; 511(7511):543–50.View ArticleGoogle Scholar
  60. Hansell DM, Bankier AA, MacMahon H, McLoud TC, Muller NL, Remy J. Fleischner Society: glossary of terms for thoracic imaging. Radiology. 2008; 246(3):697–722.View ArticlePubMedGoogle Scholar
  61. Seki N, Sawada S, Nakata M, Inoue T, Nishimura R, Segawa Y, et al. Lung cancer with localized ground-glass attenuation represents early-stage adenocarcinoma in nonsmokers. J Thorac Oncol. 2008; 3(5):483–90.View ArticlePubMedGoogle Scholar
  62. Ichinose J, Kohno T, Fujimori S, Harano T, Suzuki S, Fujii T. Invasiveness and malignant potential of pulmonary lesions presenting as pure ground-glass opacities. Ann Thorac Cardiovasc Surg. 2014; 20(5):347–52.View ArticlePubMedGoogle Scholar
  63. Kobayashi Y, Mitsudomi T. Management of ground-glass opacities: should all pulmonary lesions with ground-glass opacity be surgically resected?Transl Lung Cancer Res. 2013; 2(5):354–63.PubMedPubMed CentralGoogle Scholar
  64. Asamura H, Hishida T, Suzuki K, Koike T, Nakamura K, Kusumoto M, et al. Radiographically determined noninvasive adenocarcinoma of the lung: survival outcomes of Japan Clinical Oncology Group 0201. J Thorac Cardiovasc Surg. 2013; 146(1):24–30.View ArticlePubMedGoogle Scholar
  65. Cheng Z, Shan F, Yang Y, Shi Y, Zhang Z. CT characteristics of non-small cell lung cancer with epidermal growth factor receptor mutation: a systematic review and meta-analysis. BMC Med Imaging. 2017; 17(1):5.View ArticlePubMedPubMed CentralGoogle Scholar
  66. Sim HJ, Choi SH, Chae EJ, Kim HR, Kim YH, Kim DK, et al. Surgical management of pulmonary adenocarcinoma presenting as a pure ground-glass nodule. Eur J Cardiothorac Surg. 2014; 46(4):632–6.View ArticlePubMedGoogle Scholar
  67. Callister ME, Baldwin DR, Akram AR, Barnard S, Cane P, Draffan J, et al. British Thoracic Society guidelines for the investigation and management of pulmonary nodules. Thorax. 2015; 70(Suppl 2):ii1–54.View ArticlePubMedGoogle Scholar
  68. MacMahon H, Naidich DP, Goo JM, Lee KS, Leung AN, Mayo JR, et al. Guidelines for management of incidental pulmonary nodules detected on CT images: from the Fleischner Society. Radiology. 2017; 284(1):228–43.View ArticlePubMedGoogle Scholar
  69. Cho J, Kim ES, Kim SJ, Lee YJ, Park JS, Cho YJ, et al. Long-term follow-up of small pulmonary ground-glass nodules stable for 3 years: implications of the proper follow-up period and risk factors for subsequent growth. J Thorac Oncol. 2016; 11(9):1453–9.View ArticlePubMedGoogle Scholar
  70. Cho JH, Choi YS, Kim J, Kim HK, Zo JI, Shim YM. Long-term outcomes of wedge resection for pulmonary ground-glass opacity nodules. Ann Thorac Surg. 2015; 99(1):218–22.View ArticlePubMedGoogle Scholar

Copyright

© The Author(s) 2018

Advertisement