Cornea deposits

Chryseosis corneae (deposition of gold crystals in the cornea) occurs rarely in patients treated with a cumulative dose of up to 500 mg of gold, but they occur in nearly all patients who have received 1500 mg or more (28). Deposition of gold as such has no chnical consequences. Gold can occasionally cause a keratitis or keratoconjunctivitis, but these are usually associated with skin involvement and are not a consequence of gold deposits in the cornea. 

The principal problems for sdicone mbber as a viable lens material are the nonpolar nature, which gives Hpid deposits and wettabdity problems and the tendency to adhere to the cornea. Efforts to modify the sdicone lens surface for improved wettabdity have achieved limited success. These efforts include grafting hydrophilic monomers, such as HEMA, GM (150), and NVP (151—153), to the lens surface and plasma treatments of finished lenses. Efforts to improve the movement of sdicone lenses on the cornea with various lens designs have not been successfld, and the cause of lens—cornea adherence, which is not an exclusive problem of sdicone lenses, is an active area of research. 

FIGURE 46-7 Kayser-Fleischer ring in a young boy with Wilson s disease. The brown ring at the edge of the cornea is due to cornea] copper deposition. Courtesy of Dr Jorge Juncos (Emory University). 

Opaque deposits in the cornea and lens may occur with chronic phenothi-azine treatment, especially with CPZ. Although visual acuity is not usually affected, periodic slit-lamp examinations are recommended with use of long-term phenothiazines. Baseline and periodic slit-lamp examinations are also recommended for quetiapine-treated patients because of cataract development and lenticular changes in animal studies. 

Adverse reactions may include transient stinging and burning eye pain/ache browache headache allergic lid reaction conjunctival hyperemia conjunctival or corneal pigmentation ocular irritation (hypersensitivity) localized adrenochrome deposits in conjunctiva and cornea (prolonged use) reversible cystoid macular edema (may result from use in aphakic patients) palpitations tachycardia extrasystoles cardiac arrhythmia hypertension faintness. 

Opacities of the cornea and lens due to deposition of fine particulate matter are a common complication of chlorpromazine therapy but regress after drug withdrawal. The most serious ocular complication is pigmentary retinopathy associated with high-dose thioridazine administration it is an irreversible condition leading to decreased visual acuity and possibly blindness. 

Acute angle closure and difficulty with accommodation can occur from the anticholinergic effects of antipsychotic agents. In addition, pigment deposits may develop in the cornea and lens. Pigmentary retinopathy has been reported with thioridazine. Keratopathy and corneal edema may occur occasionally during pharmacotherapy with chlorpromazine and fluphenazine... 

Deposits in the anterior portions of the eye (cornea and lens) are a common complication of chlorpromazine therapy. They may accentuate the normal processes of aging of the lens. Thioridazine is the only antipsychotic drug that causes retinal deposits, which in advanced cases may resemble retinitis pigmentosa. The deposits are usually associated with "browning" of vision. The maximum daily dose of thioridazine has been limited to 800 mg/d to reduce the possibility of this complication. 

Granular deposits were observed in the conjunctiva and cornea of the eyes of 20 out of the 30 workers in the occupational study of Rosenman et al. (1979), and subjective determination of the degree of silver deposition in the conjunctiva correlated with the duration of employment (see also Moss et al. 1979). Furthermore, the amount of deposition in the eyes was found to correlate significantly with reports of changes in skin color and decreased night vision. The complaint of decreased night vision was also recorded in a study of workers involved in the manufacture of metal silver powders (Rosenman et al. 1987). 

Rungby J. 1986. The silver nitrate prophylaxis of crede causes silver deposition in the cornea of experimental animals. Exp Eye Res 42 93-94. 

Once it is possible to expand a clinically defined and safe cell lineage for transplant, it is also necessary to be able to store the viable cells for subsequent attempts or procedures. This can avoid further surgery on the same patient. This demands the development of crypreservation methods for cells and tissues, involving a tissue bank (blood, skin, bones, cornea, bone marrow, umbilical cord blood, etc.). Cryopreservation must be efficient for long periods of storage, since the frozen cells may be required years after the initial deposit. 

The interesting thing about this report was its striking photographs, in which multiple, small, dark pigment deposits in the conjunctiva were seen in addition, the cornea had multiple, small, discrete, yellowish specks, and both lenses had anterior capsular opacities. 

Webber SK, Domniz Y, Sutton GL, Rogers CM, Lawless MA. Corneal deposition after high-dose chlorpro-mazine hydrochloride therapy. Cornea 2001 20(2) 217-9. 

Deposits in the cornea and lens can complicate long-term chlorpromazine therapy and in vivo confocal imaging of such deposits has now been reported, supposedly for the first time (5). 

Deposits in the lens or cornea probably result from melanin-drug complex deposition and are best detected by slit-lamp examination. These deposits are probably dose-and time-related, since they generally occur only after years of treatment. Fortunately, they are in large part reversible, but if undetected they may progress to interfere with vision. They are most often reported with chlor-promazine or thioridazine and can occur in association with pigmentary changes in the skin. 

Steroid-indnced calcinm deposits in the cornea have been reported. Patients with such persistent epithelial defects snch as postoperative inflammation, penetrating keratoplasty, and a history of herpetic keratitis and dry eye have developed a calcific band keratopathy after topical nse of a steroid phosphate formnlation. 

Examination shows a dusting of gray-white deposits in Bowman s layer or a slight hazing of the cornea early in the course of the disease. It typically starts at 3 and 9 o clock and progresses slowly toward the center, usually taking several months to years to coalesce and form a complete band across the interpalpebral cornea (Figure 26-13). The deposit is separated from the limbus by a clear zone and develops the characteristic Swiss cheese appearance because of the multiple clear areas within the plaque. 

Systemic drugs and their metabolites may reach the cornea and lens via the tear film, limbal vasculature, and also the aqueous hmnor. Deposition may occur, as can direct toxicity to the structures of the cornea and lens. Although corneal opacities secondary to drug therapies are often irreversible with drug cessation or reduction, these opacities may signal more permanent deposits of drug in the lens and, possibly more importantly, the retina. 

The available evidence suggests that gold is deposited in the cornea and lens by circulation in the aqueous fluid in the anterior chamber. 

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