Ocular findings in systemic lupus erythematosus

Systemic lupus erythematosus [SLE] is a chronic multisystem autoimmune disease. Ocular complications occur in up to one-third of patients with SLE. The ocular findings may represent the initial manifestation of the disease and may lead to severe ocular morbidity and loss of vision. Early diagnosis and prompt management of patients with SLE are mandatory and require collaboration between the ophthalmologist and the rheumatologist

Regression of peripapillary choroidal neovascular membrane in a patient with sarcoidosis after oral steroid therapy

Choroidal neovascular membrane [CNV] may occur in patients with posterior uveitis. Treatment of patients with corticosteroids induces regression of the inflammation in the posterior pole with downregulation of many cytokines including vascular endothelial growth factors. We report herewith, a case of biopsy proven sarcoidosis that developed posterior uveitis and peripapillary CNV membrane and subretinal hemorrhage with fluid. The patient was treated with systemic steroids. She demonstrated progressive regression of the CNV membrane and complete resolution of the subretinal hemorrhage and fluids. In conclusion, control of the posterior segment inflammation is crucial in the resolution of the CNV membrane in uveitis and the intravitreal anti-vascular endothelial growth factor may not be always indicated

Ocular manifestations of graft-versus-host disease

Allogeneic hematopoietic stem cell transplantation [HSCT] has evolved over the past two decades to become the standard of care for hematologic and lymphoid malignancies. Major ocular complications after allogeneic HSCT have been increasing in number and severity. Graft-versus-host disease [GVHD] remains a major cause of ocular morbidity after allogeneic HSCT. The main objective of this review is to elucidate the ocular complications in patients developing GVHD following HSCT. Ocular complications secondary to GVHD are common and include dry eye syndrome, acquisition of ocular allergy from donors with allergic disorders. Eyelid changes may occur in GVHD leading to scleroderma-like changes. Patients may develop poliosis, madarosis, vitiligo, lagophthalmos, and entropion. The cornea may show filamentary keratitis, superficial punctate keratitis, corneal ulcers, and peripheral corneal melting which may lead to perforation in severe cases. Scleritis may also occur which can be anterior or posterior. Keratoconjunctivis sicca appears to be the most common presentation of GVHD. The lacrimal glands may be involved with mononuclear cell infiltration of both the major and accessory lacrimal glands and decrease in tear production. Severe dry eye syndrome in patients with GVHD may develop conjunctival scarring, keratinization, and cicatrization of the conjunctiva. Therapy of GVHD includes systemic immunosuppression and local therapy. Surgical treatment in refractory cases includes surgical intervention to improve the manifestation of GVHD of the eye. This may include tarsorrhapy, prose lenses, punctal occlusions and corneal transplantation

Late onset corneal ectasia after LASIK surgery

To report late onset corneal ectasia following myopic LASIK. Methods: A retrospective cohort case series. Nineteen patients with late onset corneal ectasia following LASIK procedure were examined at The Eye Center, Riyadh, Saudi Arabia. Patients underwent LASIK for myopia with spherical equivalent ranging from -1.4 to -13.75 diopters. Age and gender, history of systemic or local diseases, and time of onset of corneal ectasia were recorded. Eye examination and corneal topographical analyses were done before and after LASIK surgery. Results: Nineteen patients [29 eyes] with late onset corneal ectasia were identified from 1998 to 2008 in 13 male and six female patients. The mean follow-up period was 108 +/- 23 months [range 72-144 months]. No patient had pre-operative identifiable risk factors for corneal ectasia and the mean time of onset was 57 +/- 24 months [range 24-120 months after LASIK]. The pre-operative values included mean central pachymetry 553 +/- 25 urn, mean keratometry reading of 42.9 +/- 1.5 diopters, average oblique cylinder of 1.4 +/- 1.2 diopters, posterior surface elevation of 26 +/- 2.1 diopters, corneal flap thickness of 160 urn, mean spherical equivalent of -5.6 +/- 3.6 diopters, and calculated residual corneal stromal bed thickness was 288 +/- 35 um. Three [5 eyes] patients developed ectasia after pregnancy. Three [4 eyes] patients developed corneal ectasia following severe adenoviral keratoconjunctivitis and had positive PCR for adenovirus type 8. Conclusions: Corneal ectasia may develop many years after LASIK surgery and symptoms could go undetected for some time. Pregnancy and adenoviral keratoconjunctivitis occurred post-opera-tively in six patients

Pattern of childhood blindness at a referral center in Saudi Arabia

An understanding of the causes of blindness and the magnitude of the problem is crucial in designing effective intervention and prevention programs. We undertook this retrospective review to determine the causes of childhood blindness at an eye referral center. We reviewed charts of children who presented between August 1997 and August 2003. All children had a complete ophthalmologic examination. Blindness was defined as a visual acuity <20/400, visual impairment as visual acuity between 20/400 and 20/60, and visual loss as a visual acuity <20/60. A total of 5217 children included 220 [59%] males and 152 [41%] females [age range 2 to 18 years, mean age, 10 years]. One hundred twelve [2%] were blind and 260 [5%] had visual impairment. The most common causes of bilateral blindness included optic nerve diseases, retinal disorders, and cataract. The most common causes of unilateral blindness included trauma, retinal diseases, refractive errors, and optic nerve diseases. The most common causes of bilateral visual impairment included refractive errors, corneal diseases, retinal disorders, cataract, and congenital nystagmus. Genetically determined disorders were observed in 37 [70%] of 53 patients with bilateral blindness, and in 52 [56%] of 93 patients with bilateral visual impairment. The incidence of consanguinity among parents of children with acquired causes was 2 [3%] of 59 patients compared to 34 [38%] of 89 among genetically determined causes [P<0.001]. Genetically determined disorders continue to play an important role in the causation of childhood blindness among patients attending our referral center in Saudi Arabia. Genetic counseling, early eye screening of children and public education may help in the prevention of visual disorders in children

Azithromycin prophylaxis and treatment of murine toxoplasmosis

To evaluate the azithromycin effects alone and in combination with other agents in the prophylaxis and treatment of murine toxoplasmosis. A total of 280 BALB/c mice were included, and 2 x 103 Toxoplasma organisms of the RH strain Toxoplasma gondii strain ATCC50174 were given intraperitoneally to each mouse. In experiment one, 40 animals were given azithromycin 200 milligram/kilogram/daily for 3 days starting the day of inoculation, 40 mice were control. In experiment 2, the treatment was started 48 hours after inoculation and given daily for 3 days: one group received azithromycin 200 milligram/kilogram/day, the second group received pyrimethamine 25 milligram/kilogram/day, and the sulfadiazine 100 milligram/kilogram/day. The third group was control. In experiment 3, 7 groups of animals received one of the following [1] none, [2] azithromycin 200 milligram/kilogram/day, [3] pyrimethamine 25 milligram/kilogram/day and sulfadiazine 100 milligram/kilogram/day, [4] azithromycin and sulfadiazine, [5] azithromycin and pyrimethamine, [6] azithromycin with sulfadiazine and pyrimethamine, [7] sulfadiazine alone. Treatment was initiated 72 hours after inoculation for 3 days. The study was conducted at the Animal Care Facility of King Saud University, Riyadh, Kingdom of Saudi Arabia. Animals that received azithromycin simultaneously with inoculation survived, and all control animals died. All animals died in groups receiving single drug therapy. Animals treated with azithromycin and sulfadiazine showed a survival rate of 40%, sulfadiazine and pyrimethamine 40%, or azithromycin with sulfadiazine and pyrimethamine 95% [p<0.0001]. Azithromycin alone was found to be effective in the prophylaxis of murine toxoplasmosis. Combination therapy was effective in the treatment of murine toxoplasmosis

Changing pattern of childhood blindness in Saudi Arabia

We studied 187 patients attending special educational institutions in Saudi Arabia who were blind before the age of 14. All patients underwent complete ophthalmological evaluation. The visual acuity in 31% of the patients was no light perception and in 58% light perception to counting fingers at 3 feet [1 m]. 70% were blind before age 2. Prior to 1962 acquired diseases led to blindness in 75% of the patients. From 1962 onwards genetically determined diseases accounted for 84% of childhood blindness. 56% of this group were the product of consanguineous marriages. On the other hand in the group who acquired blindness only 14% were from cosanguineous marriages [p<0.0001]. We here describe guidelines for the prevention of childhood blindness in Saudi Arabia

Toxoplasmosis in a group of glucose-6-phosphate dehydrogenase deficient patients

This was a retrospective study that aimed at evaluating the relative risk of Toxoplasma infection in patients with glucose-6-phosphate dehydrogenase deficiency as compared to a control group with no glucose-6-phosphate dehydrogenase deficiency. Ninety-one blood donor volunteers had serology testing from Toxoplasma gondii and were screened for glucose-6-phosphate dehydrogenase deficiency by a qualitative method using fluorescent spot test. They were all males and their ages ranged from 17 to 52 years. Fifty-three persons [58%] were glucose-6-phosphate dehydrogenase deficient and 38 [42%] were glucose-6-phosphate dehydrogenase normal. In the glucose-6-phosphate dehydrogenase deficient group, 31 [58.5%] had positive titers for Toxoplasma; while in the glucose-6-phosphate dehydrogenase normal group 9 persons [24%] had positive titers for Toxoplasma. The relative risk of infection was 2.5 times more in the glucose-6-phosphate dehydrogenase deficient group, a statistically significant difference with a p value of 0.002. Glucose-6-phosphate dehydrogenase deficiency seems to increase the risk for Toxoplasma infection by 2.5 fold probably due to decreased killing effect, of phagocytic cells

Decrease in tear bioavailability of ciprofloxacin in eyes with carbon containing eyeliners

We studied the tear bioavailability of topical ciprofloxacin 0.3% eyedrops in eyes having an eyeliner and compared the level to the fellow eye without the eyeliner. We enrolled a total of 10 patients; 6 females and 4 males, with an age range of 32 to 40 years. One drop of ciprofloxacin 0.3% was instilled in each eye; one eye had carbon-based eyeliner placed at the lid margin and the fellow eye had no eyeliner. Tear samples were collected at 1 and 5 hours following the application of topical ciprofloxacin. At one hour, the mean ciprofloxacin tear concentration in eyes with eyeliner was 1.67 mg/1 compared to 2.35 mg/1 in eyes without eyeliner [p <0.05]. At 5 hours, the mean concentration of ciprofloxacin was 0.17 mg/1 in eyes with eyeliner and 0.24 mg/1 in eyes without the eyeliner [p <0.1]. Application of carbon-based eyeliner may cause a decrease in the bioavailability of ciprofloxacin in the tear film compared to eyes without the eyeliner. It is proposed that carbon may cause adsorption of the ciprofloxacin and decrease the bioavailability of ciprofloxacin in the tear film. Patients on topical ciprofloxacin may have to be asked to avoid the use of carbon-based eyeliners