John J. Purcell

Topical cyclosporin A in the treatment of anterior segment inflammatory disease.

Topical cyclosporin A was used in the management of 43 patients with a variety of anterior segment inflammatory disorders that had failed corticosteroid treatment. Treatment with topical cyclosporin A ranged from 1 week to 43 months, with a mean treatment period of 13 months. Thirty-five patients (81%) with disorders including highrisk keratoplasty, atopic and vernal keratoconjunctivitis, ligneous conjunctivitis, ulcerative keratitis, and Moorens ulcer had a beneficial result, with resolution, reduction, or prevention of inflammation. Six patients (14%) with scleritis, ocular cicatricial pemphigoid, or endotheliitis showed no clinical improvement. Two patients (5%) had significant ocular discomfort, and the drug had to be discontinued in them. None of the other patients developed local side effects. Twenty-seven of these patients were followed with serial cyclosporin A blood levels and serum creatinine. None of these patients developed measurable drug blood levels or renal toxicity.

Conjunctival Involvement in Primary Systemic Nonfamilial Amyloidosis

There have been few descriptions of external ocular involvement in primary systemic nonfamilial amyloidosis. When amyloid is deposited in the dermis of the eyelid, slight trauma can lead to eyelid ecchymosis. 1 Confluent waxy yellow papules on the eyelids may be diagnostic of primary systemic amyloidosis. Hemorrhage into the conjunctiva is rare, 2 and occurs only in advanced cases with liver failure. 3

Corneal Sensation in Adie's Syndrome

Using the Cochet-Bonnet esthesiometer, we evaluated the corneal sensation of 11 patients with unilateral Adies tonic pupil. We eliminated six other patients with bilateral Adies pupil or disease that lowered corneal sensation. An observed unfamiliar with each patients condition tested 12 clock hour positions in the midperiphery in both eyes of all patients. We studied 30 normal subjects (60 eyes) in a similar fashion. Of those 11 patients with unilateral Adies syndrome, ten had a regional decrease in corneal sensation. The 30 normal subjects examined did not exhibit any significant decrease in corneal sensation in any areas. Our study supports the concept that the lesion of Adies tonic pupil is in the ciliary ganglion or short location where the innervation of the iris sphincter and corneal sensation are found together.

Inheritance of endothelial dystrophy of the cornea.

64 families containing a proband with corneal endothelial dystrophy were examined in order to study the hereditary nature of the disease. Data concerning the frequency of occurrence, severity of the disease, ratio of affected females to males, relationship of the disease with age, and other factors were the subject of a previous report. 7 pedigrees which reflect features of endothelial dystrophy within the 64 families are presented. These features include multiple females in a family being affected, multiple consecutively affected generations, the occurrence of offspring with disease more severe than the parent, and endothelial decompensation (edema) at a relatively young age (less than 40 years of age). The importance of examining family members whenever possible rather than relying on history alone is emphasized. A statistical analysis of the inheritance pattern was performed. Endothelial dystrophy does not seem to follow a strict autosomal dominant pattern even though superficial inspection suggests autosomal dominant inheritance (both males and females affected, successive generations affected, 38% of relatives over the age of 40 years affected). Even though we were unable to determine a specific genetic mode of inheritance in these 64 families with endothelial dystrophy, we do feel that endothelial dystrophy is at least in part an inherited disease. Future investigations might prove sex-linked dominance, genetic heterogeneity, the influence of environmental factors, or a multifactorial etiology.

Clinical Slit Lamp Biomicroscopy and Photo Slit Lamp Biomicrography

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