Elsevier

Medical Hypotheses

Volume 73, Issue 3, September 2009, Pages 435-437
Medical Hypotheses

A new strategy of treatment with low-dosage acetyl salicylic acid in patients affected by central serous chorioretinopathy

https://doi.org/10.1016/j.mehy.2009.03.036Get rights and content

Summary

Central serous chorioretinopathy (CSCR) is an ocular disease characterized by serous detachment of the neurosensory retina at the posterior pole, with or without an associated retinal pigment epithelium (RPE) detachment. It is associated with different systemic diseases although the pathogenesis is unknown. Different therapies have been applied to treat CSCR with poor results. We reviewed the literature and found that in all the diseases associated with CSCR plasminogen activator inhibitor 1 (PAI-1) was increased. Acetyl salicylic acid (Aspirin) is effective in lowering PAI-1 levels and platelets aggregation; as such we decided to treat patients affected by CSCR with low dose Aspirin.

From January 2005 to December 2008 we enrolled 107 patients, 85 male and 22 female, affected with active CSCR or the multifocal variant.

Aspirin was administrated at an oral dose of 100 mg. per day for a month and then 100 mg. every other day for five months.

After the first week of therapy and for the following three months the visual acuity improved and remained stable to the end of the follow-up (median follow-up 20 months).

A recurrence of the disease interested the 6% of the patients.

In this study low-dose Aspirin was able to treat central serous chorioretinopathy with a quick recovery of the visual acuity and a reduced number of recurrences during the follow-up.

Besides the effectiveness of the treatment with Aspirin supports our observation regarding the role of impaired fibrinolysis and increased platelets aggregation in the choriocapillaris as genesis of CSCR.

Introduction

Central serous chorioretinopathy (CSCR) is characterized by serous detachment of the neurosensory retina at the posterior pole, with or without an associated retinal pigment epithelium (RPE) detachment.

The idiopathic form of CSCR affects young and middle-aged people, more males than females [1], [2], that have as common denominator a type A or a stressful personality.

CSCR has been described in association with bone marrow and solid organ transplantation [3], [4], giant cell arteritis [5], lupus erythematosus, Crohn’s disease, ulcerative colitis, paraproteinemias and primitive or secondary Cushing’s syndrome [6], [7].

In the many of these cases, the onset of the CSCR seem to be a consequence of treatment with corticosteroids or directly to hypercortisolism in Cushing’s syndrome.

CSCR is also associated with pregnancy, in particular in the setting of preeclampia, hemodialysis or untreated hypertension [8].

Finally, an interesting correlation between Helicobacter pilory (HP) infection and CSCR is emerging [9], [10], [11], [12].

Idiopathic CSCR is often a self-limited disease with a good functional prognosis. However thirty to fifty percent of patients [1], [2], [13], [14]. CSCR has a relapsing course with recurrent neurosensory detachments, progressive decompensation of the RPE and consequent impairment of the visual acuity.

The pathogenesis of CSCR is debated nevertheless an increasing number of studies seem to point out that a focal, transient or persistent, occlusion of the choriocapillaries is responsible for the RPE decompensation and the following retinal neurosensory detachment [15], [16], [17], [18], [19].

This hypotheses is well demonstrated by fluorangiography (FAG), indocyanine green angiograhy (ICGA) and optical coherence tomography (OCT) findings [20], [21], [22], [23].

Hypercoagulation induced by steroids seems to explain the link between steroids therapy and the onset of CSCR.

In some diseases associated with CSCR, in particular when a relative hypercortisolism can be identified, the focal occlusion of the choroidal capillaries can be explained by an immune-mediated mechanism, such as damage of the vascular endothelial cells from impaired fibrinolysis and platelets mediated clotting [24].

It was found out that patients affected by CSCR have an adaptive response to stress with an increased cathecolamine secretion and a hypothalamus–pituitary–adrenal (HPA) axis stimulation inducing a relative hypercortisolism [24], [25].

In idiopathic CSRC endogenous glucocorticoids seem to be more involved than catecholamines in the development of the disease.

Section snippets

The hypothesis

The literature suggests that in all these diseases plasminogen activator inhibitor 1 (PAI-1) was increased [26], [27], [28], [29], [30], [31], [32], [33].

In addition Iijima et al. demonstrated that elevated levels of PAI 1 were found in patients with CSCR [34].

In light of this association of elevated levels of PAI 1 and CSRC, we decided to treat patients affected by CSCR with low-dosage acetyl salicylic acid (Aspirin)100mg as this antiplatelet medication is effective in decreasing the PAI-1

Evaluation of the hypothesis

From January 2005, we started to treat patients with CSCR with low-dose acetyl salicylic acid (100 mg).

We performed a prospective case series study from January 2005 to December 2008 enrolling consecutively 107 patients, 85 male and 22 female, 110 eyes, affected with active classic CSCR or the multifocal variant. 41 patients experienced a relapsing disease in the past two years.

At the admission a complete ophthalmic examination was undertaken in all patients with fluorescein angiography (FA) and

Consequences of the hypothesis and discussion

In past years different therapies were applied to treat CSCR with poor results.

Acetazolamide treatment was effective only to short the time for clinical resolution, but has no effect on either final visual acuity or recurrence rate of the disease [37].

On the other hand, corticosteroids sometimes used till few years ago, has been reported to precipitate the disease [38], [39] and their use should be considered controindicated because they may aggravate the permeability alteration that already

Acknowledgments

The authors thank Dr. Ralph Levinson, Department of Ophthalmology at UCLA, and Dr. Luciano Prosperi for their suggestions and comments. This study could not take the light without them.

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