Article

Ketoconazole in the treatment of chronic idiopathic central serous chorioretinopathy.

LuEsther T. Mertz Retinal Research Center, Manhattan Eye, Ear & Throat Hospital, New York, New York, USA.
Retina (impact factor: 2.81). 10/2007; 27(7):943-6. DOI:10.1097/IAE.0b013e318050ca69 pp.943-6
Source: PubMed

ABSTRACT To determine the effect of an adrenocorticoid antagonist (ketoconazole) in the treatment of patients with central serous chorioretinopathy (CSC).
Ketoconazole was given at an oral dose of 600 mg per day for 4 weeks. Laboratory monitoring included 24-hour urinary cortisol and liver function tests at baseline, 4 weeks, and 8 weeks. Changes in greatest linear dimension were followed with fluorescein angiography at baseline, 4 weeks, and 8 weeks. Posterior pole anatomy was assessed with optical coherence tomography at baseline, 4 weeks, and 8 weeks. Ophthalmic examination and best-corrected visual acuity were assessed at each interval visit.
Median visual acuity in the study eye remained stable at 20/40 throughout the 8-week follow-up. Median lesion height and greatest linear dimension were stable at 4 weeks and decreased at 8 weeks.
Ketoconazole lowered endogenous cortisol after 4 weeks of 600 mg daily. While median visual acuity, lesion height, and greatest linear dimension remained unchanged during the month of drug treatment, there may have been a delayed therapeutic response seen at 8 weeks.

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    Article: Finasteride for chronic central serous chorioretinopathy.
    Farzin Forooghian, Annal D Meleth, Catherine Cukras, Emily Y Chew, Wai T Wong, Catherine B Meyerle
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    ABSTRACT: To evaluate the safety and efficacy of finasteride, an inhibitor of dihydrotestosterone synthesis, in the treatment of chronic central serous chorioretinopathy. Five patients with chronic central serous chorioretinopathy were prospectively enrolled in this pilot study. Patients were administered finasteride (5 mg) daily for 3 months, after which study medication was withheld and patients were observed for 3 months. Main outcome measures included best-corrected visual acuity, central subfield macular thickness, and subretinal fluid volume as assessed by optical coherence tomography. Serum dihydrotestosterone, serum testosterone, and urinary cortisol were also measured. There was no change in mean best-corrected visual acuity. Mean center-subfield macular thickness and subretinal fluid volume reached a nadir at 3 months and rose to levels that were below baseline by 6 months. The changes in both optical coherence tomography parameters paralleled those in serum dihydrotestosterone level. In four patients, center-subfield macular thickness and/or subretinal fluid volume increased after discontinuation of finasteride. In the remaining patient, both optical coherence tomography parameters normalized with finasteride and remained stable when the study medication was discontinued. Finasteride may represent a novel medical treatment for chronic central serous chorioretinopathy. Larger controlled clinical trials are needed to further assess the efficacy of finasteride for the treatment of central serous chorioretinopathy.
    Retina (Philadelphia, Pa.) 01/2011; 31(4):766-71. · 2.93 Impact Factor
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    Article: Central serous chorioretinopathy: a pathogenetic model.
    Antonio Caccavale, Filippo Romanazzi, Manuela Imparato, Angelo Negri, Anna Morano, Fabio Ferentini
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    ABSTRACT: Despite numerous studies describing predominantly its demography and clinical course, many aspects of central serous chorioretinopathy (CSCR) remain unclear. Perhaps the major impediment to finding an effective therapy is the difficulty of performing studies with large enough cohorts, which has meant that clinicians have focused more on therapy than on a deeper understanding of the pathogenesis of the disease. Hypotheses on the pathogenesis of CSCR have ranged from a basic alteration in the choroid to an involvement of the retinal pigment epithelium (RPE). Starting from evidence that affected subjects often present a personality prone to stress with altered pituitary-hypothalamic axis response (HPA) and that they have higher levels of serum and urinary cortisol and catecholamines than healthy subjects, we hypothesize a cascade of events that may lead to CSCR through hypercoagulability and augmented platelet aggregation. In particular we investigated the role of tissue plasminogen activator, increasing plasminogen activator inhibitor 1 (PAI-1), and plasmin-α2- plasmin inhibitor complexes. We reviewed the different therapeutic approaches, including adrenergic antagonists, carbonic anhydrase inhibitors, mifepristone, ketoconazole, laser photocoagulation, intravitreal injection of bevacizumab, and photodynamic therapy with verteporfin (PDT) and our model of pathogenesis seems to be in agreement with the clinical effects obtained from these treatments. In accord with our thesis, we began to treat a group of patients affected by CSCR with low-dose aspirin (75-100 mg), because of its effectiveness in other vascular diseases and its low ocular and general toxicity with prolonged use. The formulation of a causative model of CSCR enables us to understand how the therapeutic approach cannot be based on a generalized therapy but should be individualized for each patient, and that sometimes a combined strategy of treatment is required. Moreover a complete knowledge of the disease will help to identify patients prone to the most persistent forms of CSCR, and thus help to find a treatment.
    Clinical Ophthalmology 01/2011; 5:239-43.
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Keywords

24-hour urinary cortisol
 
4 weeks
 
8 weeks
 
8-week follow-up
 
adrenocorticoid antagonist
 
best-corrected visual acuity
 
central serous chorioretinopathy
 
delayed therapeutic response
 
greatest linear dimension
 
interval visit
 
ketoconazole
 
lesion height
 
liver function tests
 
Median lesion height
 
Median visual acuity
 
optical coherence tomography
 
oral dose
 
Posterior pole anatomy
 
study eye
 
unchanged
 

Catherine B Meyerle