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Sense and nonsense of corticosteroid administration in the treatment of ocular toxoplasmosis
  1. E H BOSCH-DRIESSEN,
  2. A ROTHOVA
  1. Donders Institute of Ophthalmology, University Hospital Utrecht, Utrecht, Netherlands
  1. E H Bosch-Driessen, Donders Institute of Ophthalmology, University Hospital Utrecht, E-03-136, Heidelberglaan 100, 3584 CX Utrecht, Netherlands.

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There is no consensus about the use of corticosteroids for the treatment of ocular toxoplasmosis. In clinical practice, corticosteroids are usually given in combination with antiparasitic drugs to reduce the inflammatory reaction during active chorioretinitis and to minimise tissue damage.1 Specifically, in the case of pericentral location, this presumed effect might help to retain central visual acuity and limit scotomas. However, the use of corticosteroids can lead to progression of the underlying infectious disease, as repeatedly demonstrated by the occurrence of fulminant ocular toxoplasmosis following both systemic and periocular administration (Fig 1).2-8 On the other hand, low dose corticosteroid monotherapy has been administered without severe side effects.1 To our knowledge, a well defined study of the effect of corticosteroid monotherapy in ocular toxoplasmosis as well as the additional value of corticosteroids as adjuvant therapy has not been performed. Thus, the use of corticosteroids for the treatment of ocular toxoplasmosis is controversial, and the timing and dosages during the course of the disease are not well defined.

Figure 1

A 23 year old male patient with fulminant toxoplasmic chorioretinitis following periocular corticosteroid injection. Note the multiple lesions, pronounced vasculitis (arteriitis), and extensive exudation in the macular area.

During an acute infection with Toxoplasma gondii, oocysts ingested by the host give rise to the extracellular forms (tachyzoites), which actively penetrate host cells and replicate; subsequently the disease enters the chronic stage when cysts are formed.9 The signal for formation of cysts is not known; the onset and the quality of the host immune response may be an important factor.9 The mechanism of chronic recurrent ocular toxoplasmosis is unknown; it is presumed that the multiplication of parasites, liberated from the cysts, causes damage to adjacent retinal tissue.9 The hypothesis of autoimmunity, directed against retinal S-antigen, has not …

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