Trichomegaly of the Eyelashes After Lung Cancer … · clinical response of lung cancer to EGFR...
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Wareef Kabbani Department of Pathology, University of Texas Southwestern Medical Center, Dallas, TX ACKNOWLEDGMENT Supported by Physician-Scientist KO8 Award (1K08NS051843) (J.B.); Clinical Scientist Development Award, Doris Duke Charitable Foundation (J.B.); and V Scholar Award, V Foundation for Cancer Research (J.B.). We thank Beni Stewart and Dorothy Smith for figure editing. AUTHORS’ DISCLOSURES OF POTENTIAL CONFLICTS OF INTEREST The author(s) indicated no potential conflicts of interest. REFERENCES 1. Lam JS, Shvarts O, Leppert JT, et al: Postoperative surveillance protocol for patients with localized and locally advanced renal cell carcinoma based on a validated prognostic nomogram and risk group stratification system. J Urol 174:466-472, 2005 2. Brugarolas J: Renal-cell carcinoma: Molecular pathways and therapies. N Engl J Med 356:185-187, 2007 3. Motzer RJ, Hutson TE, Tomczak P, et al: Sunitinib versus interferon alfa in metastatic renal-cell carcinoma. N Engl J Med 356:115-124, 2007 4. Hudes G, Carducci M, Tomczak P, et al: Temsirolimus, interferon alfa, or both for advanced renal-cell carcinoma. N Engl J Med 356:2271-2281, 2007 5. Chu TF, Rupnick MA, Kerkela R, et al: Cardiotoxicity associated with tyrosine kinase inhibitor sunitinib. Lancet 370:2011-2019, 2007 6. Wullschleger S, Loewith R, Hall MN: TOR signaling in growth and metabolism. Cell 124:471-484, 2006 7. Brugarolas J, Vazquez F, Reddy A, et al: TSC2 regulates VEGF through mTOR-dependent and -independent pathways. Cancer Cell 4:147-158, 2003 8. Serruys PW, Kutryk MJ, Ong AT: Coronary-artery stents. N Engl J Med 354:483-495, 2006 9. Dutcher JP, Szczylik C, Tannir N, et al: Correlation of survival with tumor histology, age, and prognostic risk group for previously untreated patients with advanced renal cell carcinoma (adv RCC) receiving temsirolimus (TEMSR) or interferon-alpha (IFN). J Clin Oncol 26:18s, 2007 (abstr 5033) 10. Atkins MB, Hidalgo M, Stadler WM, et al: Randomized phase II study of multiple dose levels of CCI-779, a novel mammalian target of rapamycin kinase inhibitor, in patients with advanced refractory renal cell carcinoma. J Clin Oncol 22:909-918, 2004 11. Raymond E, Alexandre J, Faivre S, et al: Safety and pharmacokinetics of escalated doses of weekly intravenous infusion of CCI-779, a novel mTOR inhibitor, in patients with cancer. J Clin Oncol 22:2336-2347, 2004 12. Boni JP, Leister C, Bender G, et al: Population pharmacokinetics of CCI-779: Correlations to safety and pharmacogenomic responses in patients with advanced renal cancer. Clin Pharmacol Ther 77:76-89, 2005 DOI: 10.1200/JCO.2008.16.4590 ■ ■ ■ Trichomegaly of the Eyelashes After Lung Cancer Treatment with the Epidermal Growth Factor Receptor Inhibitor Erlotinib A 57-year-old white woman who had never smoked pre- sented with a history of isolated coughing for several months. Com- puted tomography scans of the chest demonstrated a 2.5 4.5-cm right-middle-lobe tumor, widespread bilateral pulmonary nodules consistent with metastases, and enlarged lymph nodes in the subcari- nal, paratracheal, and prevascular regions (Fig 1, yellow arrows). Fine- needle aspiration biopsy of the lesion revealed bronchogenic adenocarcinoma. Magnetic resonance imaging of the brain revealed four subcentimeter metastatic lesions with minimal edema. Polymer- ase chain reaction-based sequencing of DNA of the epidermal growth factor receptor (EGFR) gene revealed an 18-base pair deletion in exon 19 of the EGFR gene, which has been previously reported in patients with lung tumors that responded to erlotinib. 1-3 The patient received whole-brain radiation therapy with a total of 30 Gy in ten fractions. She then received systemic front-line therapy with single agent erlo- tinib (standard oral dose, 150 mg). Her disease demonstrated a major response to erlotinib; the diffuse pulmonary nodules disappeared 6 weeks after she started therapy, while the primary right-middle–lobe tumor shrank down to 1.0 4.0 cm 2 2 months later and remained stable for over 1 year (Fig 1). Thirteen months after the initiation of systemic therapy, clear progression of disease was noted, with devel- opment of new pulmonary nodules and an increase in the size of the right-middle–lobe tumor. Since the addition of bevacizumab did not provide better tumor control, further treatment was switched to the chemotherapy doublet of carboplatin and paclitaxel, which reinduced a durable partial response. During her therapy with erlotinib, the patient experienced a mild rash on her face, chest, and back, which was treated with emolients and topical clindamycin. She had mild paro- nychia, which improved after topical therapy. The patient experienced alopecia after brain radiotherapy, and it persisted with very slow hair regrowth while she was receiving erlotinib. She had growth of dark, thick, coarse hairs on the dorsal aspect of her fingers as well. Three weeks after starting erlotinib, the patient noticed an accelerated growth of her eyelashes, which interfered with her wearing glasses because the lashes pushed against the lenses. She had to trim her eyelashes with scissors on a weekly basis. Close examination revealed marked bilateral coarse, thick, elongated irregular growth of the eye- lashes, with marked darkening and curling of the terminal ends (Fig 2). These changes resolved after erlotinib was discontinued when disease progressed. Hypertrichosis of the eyelashes, or eyelash trichomegaly, was originally described in the setting of rare congenital conditions such as Oliver-McFarlane syndrome, 4 oculocutaneous albinism type I, 5 or familial hypertrichosis. 6 Although it may be encountered in the con- text of generalized acquired hypertrichosis, 7 hypertrichosis of the eye- lashes is more often an isolated finding. It is defined as an increase in the length, thickness, stiffness, curling, and pigmentation of existing eyelashes. 8 Acquired trichomegaly of the eyelashes has been repeatedly described in case series of patients infected with HIV type 1 9 or in association with uveitis. 10 Trichomegaly has been reported in some patients secondary to therapy with a drug such as the antiretroviral agent zidovudine (a reverse transcriptase inhibitor), 11 and is usually associated with poor tolerance to the drug. Topical ocular hypotensive (antiglaucoma) agents such as latanoprost 12 and bimatoprost 13 have on rare occasions caused trichomegaly of the eyelashes. Other ocular topical treatments such as cyclosporine 14 and systemic therapy with the anticonvulsant topiramate 8 also have been reported to cause trichomegaly. The condition was noted in some recipients of solid organ transplants who were given cyclosporine 15 or tacrolimus. 16 Acquired trichomegaly was reported in isolated cases of patients with dermatomyositis 17 and systemic lupus erythematosus 18 (Table 1). In cancer patients, trichomegaly must be distinguished from a rare para- neoplastic syndrome, the acquired hypertrichosis lanuginosa, charac- terized in adults by the abnormal growth of lanugo-type hair, confined to the face and neck and concomitant with the spread of an internal malignancy. 19,20 Trichomegaly can occur in patients with cancer in the setting of a paraneoplastic syndrome, 21 or secondary to anticancer Braiteh et al 3460 © 2008 by American Society of Clinical Oncology JOURNAL OF CLINICAL ONCOLOGY Information downloaded from jco.ascopubs.org and provided by at US Oncology on December 28, 2012 from 67.66.44.224 Copyright © 2008 American Society of Clinical Oncology. All rights reserved.
Transcript of Trichomegaly of the Eyelashes After Lung Cancer … · clinical response of lung cancer to EGFR...
Wareef KabbaniDepartment of Pathology, University of Texas Southwestern Medical Center,Dallas, TX
ACKNOWLEDGMENTSupported by Physician-Scientist KO8 Award (1K08NS051843) (J.B.);Clinical Scientist Development Award, Doris Duke CharitableFoundation (J.B.); and V Scholar Award, V Foundation for CancerResearch (J.B.). We thank Beni Stewart and Dorothy Smith forfigure editing.
AUTHORS’ DISCLOSURES OF POTENTIAL CONFLICTS OF INTERESTThe author(s) indicated no potential conflicts of interest.
REFERENCES1. Lam JS, Shvarts O, Leppert JT, et al: Postoperative surveillance protocol
for patients with localized and locally advanced renal cell carcinoma based on avalidated prognostic nomogram and risk group stratification system. J Urol174:466-472, 2005
2. Brugarolas J: Renal-cell carcinoma: Molecular pathways and therapies.N Engl J Med 356:185-187, 2007
3. Motzer RJ, Hutson TE, Tomczak P, et al: Sunitinib versus interferon alfa inmetastatic renal-cell carcinoma. N Engl J Med 356:115-124, 2007
4. Hudes G, Carducci M, Tomczak P, et al: Temsirolimus, interferon alfa, orboth for advanced renal-cell carcinoma. N Engl J Med 356:2271-2281, 2007
5. Chu TF, Rupnick MA, Kerkela R, et al: Cardiotoxicity associated withtyrosine kinase inhibitor sunitinib. Lancet 370:2011-2019, 2007
6. Wullschleger S, Loewith R, Hall MN: TOR signaling in growth andmetabolism. Cell 124:471-484, 2006
7. Brugarolas J, Vazquez F, Reddy A, et al: TSC2 regulates VEGF throughmTOR-dependent and -independent pathways. Cancer Cell 4:147-158, 2003
8. Serruys PW, Kutryk MJ, Ong AT: Coronary-artery stents. N Engl J Med354:483-495, 2006
9. Dutcher JP, Szczylik C, Tannir N, et al: Correlation of survival with tumorhistology, age, and prognostic risk group for previously untreated patients withadvanced renal cell carcinoma (adv RCC) receiving temsirolimus (TEMSR) orinterferon-alpha (IFN). J Clin Oncol 26:18s, 2007 (abstr 5033)
10. Atkins MB, Hidalgo M, Stadler WM, et al: Randomized phase II study ofmultiple dose levels of CCI-779, a novel mammalian target of rapamycin kinaseinhibitor, in patients with advanced refractory renal cell carcinoma. J Clin Oncol22:909-918, 2004
11. Raymond E, Alexandre J, Faivre S, et al: Safety and pharmacokinetics ofescalated doses of weekly intravenous infusion of CCI-779, a novel mTORinhibitor, in patients with cancer. J Clin Oncol 22:2336-2347, 2004
12. Boni JP, Leister C, Bender G, et al: Population pharmacokinetics ofCCI-779: Correlations to safety and pharmacogenomic responses in patients withadvanced renal cancer. Clin Pharmacol Ther 77:76-89, 2005
DOI: 10.1200/JCO.2008.16.4590
■ ■ ■
Trichomegaly of the Eyelashes After LungCancer Treatment with the Epidermal
Growth Factor Receptor Inhibitor Erlotinib
A 57-year-old white woman who had never smoked pre-sented with a history of isolated coughing for several months. Com-puted tomography scans of the chest demonstrated a 2.5 � 4.5-cmright-middle-lobe tumor, widespread bilateral pulmonary nodulesconsistent with metastases, and enlarged lymph nodes in the subcari-nal, paratracheal, and prevascular regions (Fig 1, yellow arrows). Fine-needle aspiration biopsy of the lesion revealed bronchogenicadenocarcinoma. Magnetic resonance imaging of the brain revealedfour subcentimeter metastatic lesions with minimal edema. Polymer-ase chain reaction-based sequencing of DNA of the epidermal growthfactor receptor (EGFR) gene revealed an 18-base pair deletion in exon19 of the EGFR gene, which has been previously reported in patientswith lung tumors that responded to erlotinib.1-3 The patient receivedwhole-brain radiation therapy with a total of 30 Gy in ten fractions.She then received systemic front-line therapy with single agent erlo-tinib (standard oral dose, 150 mg). Her disease demonstrated a majorresponse to erlotinib; the diffuse pulmonary nodules disappeared 6weeks after she started therapy, while the primary right-middle–lobetumor shrank down to 1.0 � 4.0 cm2 2 months later and remainedstable for over 1 year (Fig 1). Thirteen months after the initiation ofsystemic therapy, clear progression of disease was noted, with devel-opment of new pulmonary nodules and an increase in the size of theright-middle–lobe tumor. Since the addition of bevacizumab did notprovide better tumor control, further treatment was switched to thechemotherapy doublet of carboplatin and paclitaxel, which reinduceda durable partial response. During her therapy with erlotinib, thepatient experienced a mild rash on her face, chest, and back, which wastreated with emolients and topical clindamycin. She had mild paro-nychia, which improved after topical therapy. The patient experiencedalopecia after brain radiotherapy, and it persisted with very slow hairregrowth while she was receiving erlotinib. She had growth of dark,
thick, coarse hairs on the dorsal aspect of her fingers as well. Threeweeks after starting erlotinib, the patient noticed an acceleratedgrowth of her eyelashes, which interfered with her wearing glassesbecause the lashes pushed against the lenses. She had to trim hereyelashes with scissors on a weekly basis. Close examination revealedmarked bilateral coarse, thick, elongated irregular growth of the eye-lashes, with marked darkening and curling of the terminal ends (Fig2). These changes resolved after erlotinib was discontinued whendisease progressed.
Hypertrichosis of the eyelashes, or eyelash trichomegaly, wasoriginally described in the setting of rare congenital conditions such asOliver-McFarlane syndrome,4 oculocutaneous albinism type I,5 orfamilial hypertrichosis.6 Although it may be encountered in the con-text of generalized acquired hypertrichosis,7 hypertrichosis of the eye-lashes is more often an isolated finding. It is defined as an increase inthe length, thickness, stiffness, curling, and pigmentation of existingeyelashes.8 Acquired trichomegaly of the eyelashes has been repeatedlydescribed in case series of patients infected with HIV type 19 or inassociation with uveitis.10 Trichomegaly has been reported in somepatients secondary to therapy with a drug such as the antiretroviralagent zidovudine (a reverse transcriptase inhibitor),11and is usuallyassociated with poor tolerance to the drug. Topical ocular hypotensive(antiglaucoma) agents such as latanoprost12 and bimatoprost13 haveon rare occasions caused trichomegaly of the eyelashes. Other oculartopical treatments such as cyclosporine14 and systemic therapy withthe anticonvulsant topiramate8 also have been reported to causetrichomegaly. The condition was noted in some recipients of solidorgan transplants who were given cyclosporine15 or tacrolimus.16
Acquired trichomegaly was reported in isolated cases of patients withdermatomyositis17 and systemic lupus erythematosus18 (Table 1). Incancer patients, trichomegaly must be distinguished from a rare para-neoplastic syndrome, the acquired hypertrichosis lanuginosa, charac-terized in adults by the abnormal growth of lanugo-type hair, confinedto the face and neck and concomitant with the spread of an internalmalignancy.19,20 Trichomegaly can occur in patients with cancer in thesetting of a paraneoplastic syndrome,21 or secondary to anticancer
Braiteh et al
3460 © 2008 by American Society of Clinical Oncology JOURNAL OF CLINICAL ONCOLOGY
Information downloaded from jco.ascopubs.org and provided by at US Oncology on December 28, 2012 from 67.66.44.224Copyright © 2008 American Society of Clinical Oncology. All rights reserved.
therapy with interferon-�.22 With the introduction of EGFR inhibi-tors in clinical practice, clinicians have observed numerous cutaneousadverse effects, such as acneiform rash, pruritus, and, less frequently,xerosis, paronychia, skin fissures, and telangiectasia.23 After treatmentwith the recombinant anti-EGFR antibody cetuximab, generalizeddiffuse trichomegaly can occur.24 Eyelash trichomegaly has been en-countered after treatment with cetuximab as well25 and after the EGFRtyrosine kinase inhibitors erlotinib26,27 and gefitinib.28,29 In thesecases, trichomegaly occurred after about 2 months of therapy and was
reversible after cessation of the medication. Because of the risk oftrichiasis and secondary corneal ulceration,27 it has been recom-mended that patients with trichomegaly who complain of symptomsof eye irritation be seen by an ophthalmologist, because other ocularconditions such as conjunctivitis and keratoconjunctivitis sicca cancomplicate anti-EGFR therapy. Trimming and epilation have beenfound to be satisfactory, safe therapeutic options. As illustrated in ourcase report, sensitivity to EGFR tyrosine kinase inhibitors in non–small-cell lung adenocarcinomas has been associated with somaticmutations in the EGFR gene1-3 with subsequent constitutive ligand-independent activation of the receptor kinase and prolonged kinaseactivity after ligand stimulation.2,30. EGFR tyrosine kinase domainmutations are mainly either in-frame deletions in exon 19, a single-point missense mutation in exon 21, or in-frame duplications, inser-tions, or both in exon 20.31 Retrospective data showed averageresponse rates to EGFR tyrosine kinase inhibitors of approximately75% for tumors with EGFR mutations, and, in contrast, less than 10%for tumors with the wild-type EGFR gene.32 The patient presentedhere had a deletion mutation in exon 19, and exhibited an excellentlong-lasting response to erlotinib. The exact incidence of eyelashtrichomegaly is unknown, and the condition remains sporadicallyreported. Although it appears to be a class effect associated with EGFRinhibitors, the occurrence of eyelash trichomegaly in relation to EGFRmutations is unknown. Whether eyelash trichomegaly correlates with
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Baseline After six weeks of erlotinib
Fig 1.
Fig 2.
Diagnosis in Oncology
www.jco.org © 2008 by American Society of Clinical Oncology 3461Information downloaded from jco.ascopubs.org and provided by at US Oncology on December 28, 2012 from 67.66.44.224
Copyright © 2008 American Society of Clinical Oncology. All rights reserved.
clinical response of lung cancer to EGFR inhibitors or whether itoccurs as an unrelated adverse event remains to be evaluated on alarger scale. We are planning to investigate further the effect of erlo-tinib on the eyelashes of patients with lung cancer who receive erlo-tinib for adjuvant therapy or for secondary prevention.
Fadi Braiteh and Razelle KurzrockDepartment of Investigational Cancer Therapeutics, Phase I Program, TheUniversity of Texas M.D. Anderson Cancer Center; and The University ofTexas Graduate School of Biomedical Sciences Houston, Houston, TX
Faye M. JohnsonDepartment of Thoracic/Head and Neck Medical Oncology, The University ofTexas M.D. Anderson Cancer Center; and The University of Texas GraduateSchool of Biomedical Sciences Houston, Houston, TX
AUTHORS’ DISCLOSURES OF POTENTIAL CONFLICTS OF INTERESTThe author(s) indicated no potential conflicts of interest.
REFERENCES1. Cohen EE, Rosen F, Stadler WM, et al: Phase II trial of ZD1839 in recurrent
or metastatic squamous cell carcinoma of the head and neck. J Clin Oncol21:1980-1987, 2003
2. Lynch TJ, Bell DW, Sordella R, et al: Activating mutations in the epidermalgrowth factor receptor underlying responsiveness of non–small-cell lung cancerto gefitinib. N Engl J Med 350:2129-2139, 2004
3. Van Doorn R, Kirtschig G, Scheffer E, et al: Follicular and epidermalalterations in patients treated with ZD1839 (Iressa), an inhibitor of the epidermalgrowth factor receptor. Br J Dermatol 147:598-601, 2002
4. Oliver GL, McFarlane DC: Congenital trichomegaly with associated pig-mentary degeneration of the retina, dwarfism, and mental retardation. ArchOphthalmol 74:169-171, 1965
5. Ziakas NG, Jogiya A, Michaelides M: A case of familial trichomegaly inassociation with oculocutaneous albinism type 1. Eye 18:863-864, 2004
6. Harrison DA, Mullaney PB: Familial trichomegaly. Arch Ophthalmol 115:1602-1603, 1997
7. Aghaei S, Dastgheib L: Acquired eyelash trichomegaly and generalizedhypertrichosis associated with breast anomaly. Dermatol Online J 12:19, 2006
8. Santmyire-Rosenberger BR, Albert M: Acquired trichomegaly with topira-mate. J Am Acad Dermatol 53:362-363, 2005
9. Kaplan MH, Sadick NS, Talmor M: Acquired trichomegaly of the eyelashes:A cutaneous marker of acquired immunodeficiency syndrome. J Am AcadDermatol 25:801-804, 1991
10. Bayer A, Bagkesen H, Sobaci G: Acquired trichomegaly in uveitis. Can JOphthalmol 42:101-106, 2007
11. Klutman NE, Hinthorn DR: Excessive growth of eyelashes in a patient withAIDS being treated with zidovudine. N Engl J Med 324:1896, 1991
12. Elgin U, Batman A, Berker N, et al: The comparison of eyelashlengthening effect of latanoprost therapy in adults and children. Eur JOphthalmol 16:247-250, 2006
13. Centofanti M, Oddone F, Chimenti S, et al: Prevention of dermatologicside effects of bimatoprost 0.03% topical therapy. Am J Ophthalmol 142:1059-1060, 2006
14. Pucci N, Massai C, Bernardini R, et al: Eyelash length in children with vernalkeratoconjunctivitis: Effect of treatment with cyclosporine eye drops. Int J Im-munopathol Pharmacol 20:595-599, 2007
15. Weaver DT, Bartley GB: Cyclosporine-induced trichomegaly. Am J Oph-thalmol 109:239, 1990
16. Ward KM, Barnett C, Fox LP, et al: Eyelash trichomegaly associated withsystemic tacrolimus. Arch Dermatol 142:248, 2006
17. Sharma RC, Mahajan VK, Sharma NL, et al: Trichomegaly of the eyelashesin dermatomyositis. Dermatology 205:305, 2002
18. Santiago M, Travassos AC, Rocha MC, et al: Hypertrichosis in systemiclupus erythematosus (SLE). Clin Rheumatol 19:245-246, 2000
19. Slee PH, van der Waal RI, Schagen van Leeuwen JH, et al: Paraneoplastichypertrichosis lanuginosa acquisita: Uncommon or overlooked? Br J Dermatol157:1087-1092, 2007
20. Vulink AJ, ten Bokkel HD: Acquired hypertrichosis lanuginosa: A rarecutaneous paraneoplastic syndrome. J Clin Oncol 25:1625-1626, 2007
21. Velez A, Kindelan JM, Garcia-Herola A, et al: Acquired trichomegaly andhypertrichosis in metastatic adenocarcinoma. Clin Exp Dermatol 20:237-239, 1995
22. Hernandez-Nunez A, Fernandez-Herrera J, Buceta LR, et al: Trichomegalyfollowing treatment with interferon alpha-2b. Lancet 359:1107, 2002
23. Santoro F, Cozzani E, Parodi A: Cutaneous adverse effects during therapywith an epidermal growth factor receptor (EGFR) inhibitor. J Dermatolog Treat17:160-161, 2006
24. Kerob D, Dupuy A, Reygagne P, et al: Facial hypertrichosis induced bycetuximab, an anti-EGFR monoclonal antibody. Arch Dermatol 142:1656-1657, 2006
25. Bouche O, Brixi-Benmansour H, Bertin A, et al: Trichomegaly of theeyelashes following treatment with cetuximab. Ann Oncol 16:1711-1712, 2005
26. Carser JE, Summers YJ: Trichomegaly of the eyelashes after treatmentwith erlotinib in non–small-cell lung cancer. J Thorac Oncol 1:1040-1041, 2006
27. Lane K, Goldstein SM: Erlotinib-associated trichomegaly. Ophthal PlastReconstr Surg 23:65-66, 2007
28. Pascual JC, Banuls J, Belinchon I, et al: Trichomegaly following treatmentwith gefitinib (ZD1839). Br J Dermatol 151:1111-1112, 2004
29. Shah NT, Kris MG, Pao W, et al: Practical management of patients withnon–small-cell lung cancer treated with gefitinib. J Clin Oncol 23:165-174, 2005
30. Hirsch FR, Varella-Garcia M, McCoy J, et al: Increased epidermal growthfactor receptor gene copy number detected by fluorescence in situ hybridizationassociates with increased sensitivity to gefitinib in patients with bronchioloalveo-lar carcinoma subtypes: A Southwest Oncology Group Study. J Clin Oncol23:6838-6845, 2005
31. Shigematsu H, Lin L, Takahashi T, et al: Clinical and biological featuresassociated with epidermal growth factor receptor gene mutations in lungcancers. J Natl Cancer Inst 97:339-346, 2005
32. Riely GJ, Politi KA, Miller VA, et al: Update on epidermal growth factor receptormutations in non-small cell lung cancer. Clin Cancer Res 12:7232-7241, 2006
DOI: 10.1200/JCO.2008.16.9391
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Table 1. Reported Causes of Eyelash Trichomegaly
Congenital eyelash trichomegalyOliver-McFarlane syndrome4
Oculocutaneous albinism type I5
Acquired eyelash trichomegalySystemic disease
Dermatomyositis17
Systemic lupus erythematosus18
Systemic infectionHuman immunodeficiency virus infection or acquired immunodeficiency
syndrome9
Uveitis10
Paraneoplastic syndromeRenal cell cancer21
Side effect of topical ophthalmic drug therapyOcular hypotensive agents (antiglaucoma)
Latanoprost,12 bimatoprost13
ImmunosuppressorsCyclosporine14
Adverse effect of systemic drug therapyInterferon
Interferon-alpha22
AnticonvulsantsTopimarate8
ImmunosuppressorsCyclosporine,15 tacrolimus16
Anti-EGFR recombinant antibodyCetuximab24,25
EGFR tyrosine kinase inhibitorsErlotininib,26,27 gefitinib28,29
Abbreviation: EFGR, epidermal growth factor receptor.
Braiteh et al
3462 © 2008 by American Society of Clinical Oncology JOURNAL OF CLINICAL ONCOLOGY
Information downloaded from jco.ascopubs.org and provided by at US Oncology on December 28, 2012 from 67.66.44.224Copyright © 2008 American Society of Clinical Oncology. All rights reserved.
