Posterior scleritis associated with systemic tuberculosis :A Gupta, V Gupta, Surinder S Pandav, A Gupta, Indian Journal of Ophthalmology

BRIEF REPORT
Year : 2003 | Volume : 51 | Issue : 4 | Page : 347--349

Posterior scleritis associated with systemic tuberculosis

A Gupta, V Gupta, Surinder S Pandav, A Gupta
Postgraduate Institute of Medical Education and Research, Chandigarh, India

Correspondence Address:
A Gupta
Postgraduate Institute of Medical Education and Research, Chandigarh
India

Abstract

Infective isolated posterior scleritis is rare. We report a case of isolated posterior scleritis associated with histopathologically documented systemic tuberculosis, a hitherto unreported association. The patient responded well to a combination of oral corticosteroids with antituberculosis therapy.

How to cite this article:
Gupta A, Gupta V, Pandav SS, Gupta A. Posterior scleritis associated with systemic tuberculosis.Indian J Ophthalmol 2003;51:347-349

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Gupta A, Gupta V, Pandav SS, Gupta A. Posterior scleritis associated with systemic tuberculosis. Indian J Ophthalmol [serial online] 2003 [cited 2023 Mar 25 ];51:347-349
Available from: https://journals.lww.com/ijo/pages/default.aspx/text.asp?2003/51/4/347/14649

Full Text

Scleritis is an uncommon ocular inflammatory disorder most often associated with systemic inflammatory diseases of autoimmune origin. Some cases of anterior scleritis may be caused by microbial infection.[1],[2] Posterior scleritis is predominantly idiopathic or autoimmune or, when infective, is an extension of anterior scleritis. [1],[2],[3] Although anterior scleritis due to Mycobacterium tuberculosis has been reported in literature, isolated posterior scleritis in a patient of systemic tuberculosis has hitherto not been described.[1],[2],[4],[5],[6]We report a patient of isolated posterior scleritis associated with systemic tuberculosis.

Case report

A 45-year-old woman presented with complaints of diminished vision in her left eye of 3 months' duration. She had a history of recurrent anterior uveitis in the left eye. A fine needle aspiration cytology (FNAC) of the cervical lymph nodes performed one year earlier was positive for acid-fast bacilli. She had received anti-tuberculosis chemotherapy, but discontinued after two months due to development of an SLE-like drug reaction. On presentation to us 10 months later, her best corrected visual acuity was 6/6 in the right eye and 6/60 in her left eye. The intraocular pressure was 12 mmHg in the right eye and 16 mmHg in the left eye. Slitlamp biomicroscopy was unremarkable in the right eye while the left eye showed 1+ flare and 1+ cells in the anterior chamber. Fundoscopy of the left eye showed optic disc oedema with choroidal folds in the posterior pole [Figure 1]. Fundus fluorescein angiography showed optic disc hyperfluorescence with alternating dark and light bands in the posterior pole characteristic of choroidal folds [Figure 2]. B-scan ultrasonography revealed sclerochoroidal thickening with high reflectivity along with the presence of fluid in the subTenon space suggestive of posterior scleritis [Figure 3]. Significant investigations included a strongly positive purified protein derivative (PPD) skin test (25 mm induration with central necrosis) and a positive chest X-ray (presence of infiltrates in the right upper zone) suggestive of pulmonary tuberculosis. Other investigations including routine haemogram, erythrocyte sedimentation rate, serum rheumatoid factor, antineutrophilic cytoplasmic antibodies (ANCA), antinuclear factor (ANF), TPHA and ELISA for human immunodeficiency virus (HIV) were unremarkable. She was managed with oral prednisolone 1 mg/kg body weight once daily in combination with supervised anti-tubercular chemotherapy. The anti-tubercular therapy (ATT) was a combination of rifampicin 10 mg/kg, isoniazid 5 mg/kg, pyrazinamide 25 mg/kg and ethambutol 20 mg/kg. The oral prednisolone was tapered over 8 weeks while the antitubercular therapy was given for 9 months. The posterior scleritis resolved over the next 12 weeks and she recovered a visual acuity of 6/9 in the left eye. The optic disc oedema and choroidal folds disappeared [Figure 4]. She has remained asymptomatic over a follow-up period of 18 months.

Discussion

Though uncommon, an infective aetiology of scleritis is known and a number of bacteria, fungi and parasites are implicated in causing scleritis.[1],[2] Typically, infective scleritis manifests as anterior scleritis and occasionally as combined anterior and posterior scleritis or sclerokeratitis. More often than not, it is associated with some predisposing factor such as cataract surgery, scleral buckling surgery, pterygium surgery, suture removal, scleral buckle removal and trauma.[1],[2] Infection-related scleritis can also occur following systemic infection.[3],[4] Scleritis is also reported in patients with systemic tuberculosis. [1],[2],[3],[4],[5],[6]However, we did find any report of isolated posterior scleritis in a patient with systemic tuberculosis in the literature (Medline search).

Our patient had posterior scleritis along with histopathologically proven systemic tuberculosis and responded to a combination of systemic corticosteroids and anti-tubercular chemotherapy. Theoretically, a trial of antituberculosis therapy alone resulting in resolution of the lesion in our patient may have strengthened the causal association with Mycobacterium tuberculosis . But, posterior scleritis is a serious ocular disorder, and a practical treatment rationale demanded corticosteroid therapy in conjunction with ATT. For the same reason, an intraocular sample for histopathological analysis or polymerase chain reaction for Mycobacterium tuberculosis was not performed as the ocular lesion showed an excellent response to our treatment. .

The development of a drug rash or SLE-like rash is well documented following ATT and is most frequently associated with isoniazid. The standard protocol in such patients is to discontinue ATT and reinitiate the drugs one after another. Our patient was treated elsewhere and hence this protocol for reintroduction of ATT drugs was not followed.

We could not establish the presence of any connective tissue disorder in our patient despite thorough investigations. ANF negative SLE is extremely uncommon while ANCA positivity has not shown a very significant association with SLE.[7],[8] Our patient has had no recurrences or relapses in the 18 months of follow-up . This too suggests the likelihood of a non-connective tissue disorder as an aetiology in this patient , though posterior scleritis has been associated with a number of autoimmune disorders including rheumatoid arthritis, periarteritis nodosa, systemic lupus erythematosus and Wegener's granulomatosis. [1],[2],[3]

We feel that intraocular tuberculosis could manifest as isolated posterior scleritis. Oral corticosteroids, given without anti-tubercular drugs in patients of scleral tuberculosis, are likely to worsen the disease in these patients.[5]

References

1	Benson WE. Posterior Scleritis. Surv Ophthalmol 1988;32:297-316.
2	Jackson WB. Infections of the sclera. In: Tabbara KF, Hyndiuk RA, editors: Infections of the Eye . Boston: Little Brown and Company, 1986 . pp 477-87.
3	Riono WP, Hidayat AA, Rao NA. Scleritis: A clinicopathologic study of 55 cases. Ophthalmology 1999;106:1328-33.
4	Hemady R, Sainz M, Raizman MB, Foster SC. Six cases of scleritis associated with systemic infection. Am J Ophthalmol 1992;114:55-62.
5	Nanda M, Pflugfelder SC, Holland S. Mycobacterium tuberculosis scleritis. Am J Ophthalmol 1989;108:736- 37.
6	Bloomfield SE, Mondino B, Gray GF. Scleral tuberculosis. Arch Ophthalmol 1976;94:954-56.
7	Tan EM, Chan EK, Sullivan KF, Sullivan RL. Anitnuclear antibodies (ANAs): Diagnostically specific immune markers and clues towards understanding autoimmunity. Clin Immuno Immunopathol 1988;47:121-41.
8	Molnar K, Kovacs L, Kiss M, Husz S, Dobozy A, Pokorny G. Antineutrophil cytoplasmic antibodies in patients with systemic lupus erythematosus. Clin Exp Dermatol 2002;27:59-61.