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Journal of Case Reports in Practice (JCRP) 2019; 7(2): 11-13 CASE REPORT 11 Central serous chorioretinopathy in a patient with immune thrombocy- topenic purpura Hamidreza Barkhordari 1 , Mojtaba Poursarajian 2 , 1,2 Geriateric Ophthalmology Research Center, Shahid Sadoughi University of Medical Sciences, Yazd, Iran. ABSTRACT Immune thrombocytopenic purpura (ITP) is a disease characterized by low platelet count (<150,000/mm3). The suitable treatment for newly diagnosed ITP recommend longer courses of corticosteroids (eg, prednisone 1 mg/kg orally for 21 days then tapered off) or IVIg because longer courses of corticosteroids are associated with a longer time to the loss of response. We know that corticosteroids may cause side effects such as cataract, increased intra- ocular pressure and rarely central serous chorioretinopathy. This case report presents a patient with central serous chorioretinopathy after treatment for Immune thrombocytopenic purpura (ITP) that his visual outcome didn’t appropriate responses to our conventional therapy (corticosteroids stop). So we emphasize the thrombocytopenia could be the most responsible for CSCR in immune thrombocytopenic purpura patients. Key words: immune thrombocytopenic purpura (ITP), central serous chorioretinopathy, corticosteroids. INTRODUCTION Corticosteroid medication is recommended for treat- ment of immune thrombocytopenic purpura. It may cause central serous chorioretinopathy (CSCR) that threatens the patients’ visual acuity. For this compli- cation corticosteroid medication should discontinue and another treatment alternated it. We report an im- mune thrombocytopenic purpura (ITP) patient with CSCR simultaneously to use corticosteroid for ITP treatment and sever thrombocytopenia. CASE REPORT A 44-year-old male was diagnosed with immune thrombocytopenic purpura (ITP) because of decrease in platelet count (30,000/mm3) in routine laboratory exam 5 months before referring to us. Corticosteroid (prednisolone 1 mg/kg orally [100 mg]) was admin- istered him for 4 months (platelet count was 40,000/ mm3 after 6 weeks and 27,000/mm3 after 3 months) simultaneous intravenous immunoglobulin (IVIg), platelet concentrate and mabthera (retuximab). At the end, despite long treatment with several drugs, sple- nectomy was done due to resistant thrombocytopenia (platelet count 10,000/mm3). Three months after ini- tiating the corticosteroid treatment, the patient com- plained of blurred vision and decreased visual acu- ity in his right eye. The best-corrected visual acuity (BCVA) was 0.9 in left eye and 0.1 right eye, seeing a dark spot in the center of the visual field; along with metamorphopsia and reduced contrast sensitivity in the right eye. Ocular history was unremarkable. The patient had no significant systemic disease. Slit lamp examinations of anterior segment were normal in both eyes. Intraocular pressure (IOP) measurements were performed via Goldmann applanation tonome- ter and IOP was 12 mmHg in the right eye, 11 mmHg in the left eye. Dilated fundus examination revealed absence of fovea reflex, thickening and elevated macular region in right eye. Fundus examination was normal in left eye. Fundus fluorescein angiography (FA) showed hyperfluorescence as focal fluorescein leaked at the level of the retinal pigmented epithe- lium (RPE), leading to subretinal accumulation of dye at the center of the fovea (smoke stack pattern) in right eye and normal angiographic findings in left eye (Fig. 1). Spectral domain optical coherence tomogra- Correspondence: Mojataba Poursarajian, MD Geriateric Ophthalmology Research Center, Shahid Sadoughi University of Medical Sciences, Yazd, Iran Figure 1, Fundus fluorescein angiogram of both eyes, showed hyperfluorescence as a focal fluorescein leak in RE (Smoke stack pattern) and normal angiogram in LE.

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Page 1: Central serous chorioretinopathy in a patient with immune ...€¦ · C R P ) 21 2: 11-13 CS RPORT 11 Central serous chorioretinopathy in a patient with immune thrombocy - topenic

Journal of Case Reports in Practice (JCRP) 2019; 7(2): 11-13

CASE REPORT

11

Central serous chorioretinopathy in a patient with immune thrombocy-topenic purpuraHamidreza Barkhordari1, Mojtaba Poursarajian2, 1,2Geriateric Ophthalmology Research Center, Shahid Sadoughi University of Medical Sciences, Yazd, Iran.

ABSTRACTImmune thrombocytopenic purpura (ITP) is a disease characterized by low platelet count (<150,000/mm3). The suitable treatment for newly diagnosed ITP recommend longer courses of corticosteroids (eg, prednisone 1 mg/kg orally for 21 days then tapered off) or IVIg because longer courses of corticosteroids are associated with a longer time to the loss of response. We know that corticosteroids may cause side effects such as cataract, increased intra-ocular pressure and rarely central serous chorioretinopathy. This case report presents a patient with central serous chorioretinopathy after treatment for Immune thrombocytopenic purpura (ITP) that his visual outcome didn’t appropriate responses to our conventional therapy (corticosteroids stop). So we emphasize the thrombocytopenia could be the most responsible for CSCR in immune thrombocytopenic purpura patients.

Key words: immune thrombocytopenic purpura (ITP), central serous chorioretinopathy, corticosteroids.

INTRODUCTIONCorticosteroid medication is recommended for treat-ment of immune thrombocytopenic purpura. It may cause central serous chorioretinopathy (CSCR) that threatens the patients’ visual acuity. For this compli-cation corticosteroid medication should discontinue and another treatment alternated it. We report an im-mune thrombocytopenic purpura (ITP) patient with CSCR simultaneously to use corticosteroid for ITP treatment and sever thrombocytopenia.

CASE REPORTA 44-year-old male was diagnosed with immune thrombocytopenic purpura (ITP) because of decrease in platelet count (30,000/mm3) in routine laboratory exam 5 months before referring to us. Corticosteroid (prednisolone 1 mg/kg orally [100 mg]) was admin-istered him for 4 months (platelet count was 40,000/mm3 after 6 weeks and 27,000/mm3 after 3 months) simultaneous intravenous immunoglobulin (IVIg), platelet concentrate and mabthera (retuximab). At the end, despite long treatment with several drugs, sple-nectomy was done due to resistant thrombocytopenia (platelet count 10,000/mm3). Three months after ini-tiating the corticosteroid treatment, the patient com-plained of blurred vision and decreased visual acu-

ity in his right eye. The best-corrected visual acuity (BCVA) was 0.9 in left eye and 0.1 right eye, seeing a dark spot in the center of the visual field; along with metamorphopsia and reduced contrast sensitivity in the right eye. Ocular history was unremarkable. The patient had no significant systemic disease. Slit lamp examinations of anterior segment were normal in both eyes. Intraocular pressure (IOP) measurements were performed via Goldmann applanation tonome-ter and IOP was 12 mmHg in the right eye, 11 mmHg in the left eye. Dilated fundus examination revealed absence of fovea reflex, thickening and elevated macular region in right eye. Fundus examination was normal in left eye. Fundus fluorescein angiography (FA) showed hyperfluorescence as focal fluorescein leaked at the level of the retinal pigmented epithe-lium (RPE), leading to subretinal accumulation of dye at the center of the fovea (smoke stack pattern) in right eye and normal angiographic findings in left eye (Fig. 1). Spectral domain optical coherence tomogra-

Correspondence:Mojataba Poursarajian, MDGeriateric Ophthalmology Research Center, Shahid Sadoughi University of Medical Sciences, Yazd, Iran

Figure 1, Fundus fluorescein angiogram of both eyes, showed hyperfluorescence as a focal fluorescein leak in RE (Smoke stack pattern) and normal angiogram in LE.

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Hamidreza Barkhordari & Mojtaba Poursarajian

12Journal of Case Reports in Practice (JCRP) 2019; 7(2): 11-13

phy showed serous macular detachment as hypore-flective space between the neurosensory retina and RPE with central macular thickness (CMT) of 803 nm (Fig 2). The findings were suggestive of acute central serous chorioretinopathy (CSCR) in right eye. After the patient was diagnosed with steroid-induced CSCR, corticosteroid treatment was stopped. Three months after the cessation of corticosteroid treatment, BCVA do not improved perfectly in right eye. Mac-ular photocoagulation (6 spots with 100-micron size and 70-mw power by Ellex Argon Laser system) over leaking points used to accelerate resolution of the de-tachment. One month later, BCVA was 0.5 and CMT was decreased to 254nm in right eye. (Figs. 3, 4).

DISCUSSIONImmune thrombocytopenic purpura is a disease char-acterized by low platelet count caused by autoanti-body-mediated platelet destruction and the absence of other causes of thrombocytopenia.1 There are new approaches for the treatment of ITP such as corti-costeroids, IVIg, anti-D antibodies, rituximab, and

splenectomy.2 Corticosteroids may cause side effects such as cataract, increased intraocular pressure and rarely central serous chorioretinopathy.3 Early stud-ies showed that CSCR is related to psychological stress, endogenous hypercortisolism and use of cor-ticosteroid medicines.4 Exact mechanism for steroid induced CSCR has not been fully understood yet.4 It has been shown that corticosteroid treatment given through various routes such as oral, inhaled, epidur-al, or intra-articular may cause CSCR.5 However, it may result from inhibition of collagen synthesis, in-creasing permeability of choroidal capillary, and dys-function of ionic pump in the retina pigment epithe-lium.6 Earlier studies showed that many CSCR may resolve spontaneously and just observational therapy was needed for 3–4 months and Some of CSCR cases may resolve with the successful treatment of under-lying pathology or mechanism.7 Shah reported a 24 year-old male with CSCR secondary to prednisolone for treating left sided facial palsy.8 They reported that visual disturbances abated gradually within one week after prednisolone was withdrawn.8 Loo reported 3 patients with CSCR secondary to corticosteroid med-ication for different disease that two of those cases resolved with tapering of corticosteroids and one case was treated by focal laser photocoagulation.9 Shibata used photodynamic therapy for treating two patients with CSCR.10 There are a little reports the CSCR due to thrombocytopenia.11,12,13

In our patient after stopping corticosteroid, BCVA do not improved Pleasant due to Inadequate CSCR resolving, so the corticosteroid usage may not be the alone reason and the thrombocytopenia could be the most responsible for CSCR in our Immune thrombo-cytopenic purpura patient.

CONCLUSIONThis case showed that systemic corticosteroid treat-ment for ITP may cause visual acuity loss due to CSCR but stopping the corticosteroid administration in this patient do not improved visual outcome as ex-pectation. So we emphasize the thrombocytopenia could be the most responsible for CSCR in immune thrombocytopenic purpura patients. Another treat-

Figure 2, Spectral domain optical coherence tomography shows serous macular detachment as hyporeflective space between neurosensory retina and RPE in RE.

Figure 4, Spectral-domain optical coherence tomography scans one months after the macular photocoagulation used. The CSCR was maximally resolved in RE.

Figure 3, Fundus fluorescein angiography (FA) of RE after macular photocoagulation used to accelerate resolution of the detachment.

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Central serous chorioretinopathy in a patient with immune thrombocytopenic purpura

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ment such as IVIG, anti-D, retuximab and Splenec-tomy has shown no significant visual complications.

CONFLICT OF INTERESTNone.

REFERENCES1. Alvina A. Idiopathic thrombocytopenic purpura: laboratory diagnosis and management. Universa Me-dicina 2016;30:126-34.2. Neunert C, Lim W, Crowther M, Cohen A, Solberg L, Crowther MA. The American Society of Hematol-ogy 2011 evidence-based practice guideline for im-mune thrombocytopenia. Blood 2011;117:4190-207.3. Alkin Z, Yilmaz I, Ozkaya A, Yazici AT. Steroid-in-duced central serous chorioretinopathy in a patient with non-arteritic anterior ischemic optic neuropathy. Saudi journal of ophthalmology 2015;29:232-4.4. Tsai D-C, Chen S-J, Huang C-C, et al. Epidemiol-ogy of idiopathic central serous chorioretinopathy in Taiwan, 2001–2006: a population-based study. PLoS One 2013;8:e66858.5. Balakrishnan S, Apsingi S, Manjure SB. Sudden loss of visual acuity following intra-articular steroid injection in to the knee joint: a case report. Cases journal 2008;1:428.6. Cassel GH, Brown GC, Annesley WH. Central se-rous chorioretinopathy: a seasonal variation? British

journal of ophthalmology 1984;68:724-6.7. Vayalambrone D, Ivanova T, Misra A. Atypical cen-tral serous retinopathy in a patient with latent tuber-culosis. BMJ case reports 2012;2012:bcr1120115231.8. Shah SP, Desai CK, Desai MK, Dikshit R. Ste-roid-induced central serous retinopathy. Indian Jour-nal of Pharmacology 2011;43:607.9. Loo J-L, Lee S-Y, Ang C-L. Can long-term corti-costeriods lead to blindness? A case series of central serous chorioretinopathy induced by corticosteroids. Annals of the Academy of Medicine, Singapore 2006;35:496-9.10. Shibata A, Ohkuma Y, Hayashi T, Tsuneoka H. Efficacy of reduced-fluence photodynamic therapy for serous retinal pigment epithelial detachment with choroidal hyperpermeability. Clinical Ophthalmolo-gy (Auckland, NZ) 2013;7:2123.11. Spielberg LH, Leys AM. Retinal and Choroidal Manifestations of Renal Diseases. Retinal and Cho-roidal Manifestations of Selected Systemic Diseases: Springer; 2013:493-519.12. Arévalo JF, Lowder CY, Garcia RA. Retinal and Choroidal Manifestations of Systemic Lupus Er-ythematosus (SLE). Retinal and Choroidal Mani-festations of Selected Systemic Diseases: Springer; 2013:333-52.13. Soriano NCT, Soriano MET. Pregnancy-associat-ed Retinal Diseases. Ophthalmology 2017;3:249-82.

Journal of Case Reports in Practice (JCRP) 2019; 7(2): 11-13