Administration Of Topical Corticosteroids Research Articles

Cytokine immunoreactivity in seasonal rhinitis: regulation by a topical corticosteroid.

Seasonal allergic rhinitis is characterized by the development of nasal mucosal inflammation in response to natural allergen exposure, and is prevented by the administration of topical corticosteroids. Interleukin-4 (IL-4), IL-5, and IL-6 may have important roles in this process, and in vitro the gene transcription for each of these cytokines is inhibited by corticosteroids. In this study we have therefore investigated the effect of seasonal allergen exposure on the expression of immunoreactivity for IL-4, IL-5, and IL-6 in nasal mucosal biopsies, and the effect of regular prophylactic treatment with the topical corticosteroid, fluticasone propionate. Following a nasal mucosal biopsy out of season, patients were randomized double-blind to receive 6 wk of treatment during the pollen season with either topical fluticasone nasal spray (200 micrograms daily) or matching placebo. Each subject underwent a repeat nasal biopsy at the end of the 6-wk treatment period. Seasonal increases in epithelial eosinophils (p = 0.046), submucosal eosinophils (p = 0.001), and epithelial mast cells (p = 0.055) occurred in the placebo--but not the fluticasone-treated patients. Submucosal mast cell numbers did not change in either group. Immunoreactivity for IL-4 and IL-6 was localized predominantly to mast cells while IL-5 was found in both mast cells and eosinophils. Numbers of IL-4+ cells in the nasal submucosa were significantly suppressed by treatment with fluticasone (p = 0.0003 for monoclonal antibody [mAb] 3H4, p = 0.041 for mAb 4D9). In contrast, fluticasone treatment failed to influence the number of IL-5 and IL-6 immunoreactive cells.(ABSTRACT TRUNCATED AT 250 WORDS)

Clinical and Prognostic Features of Rectal Sparing in Ulcerative Colitis

Thirty patients with ulcerative colitis who had been followed clinically for more than 5 years were studied. Patients with total or left-sided colitis were investigated to evaluate the significance of rectal sparing in the prognosis of the disease. Patients were divided into two groups, one with complete or relative sparing of the rectum and the other with homogeneous lesions ranging from the rectum to the proximal colon based on endoscopic findings. The administration of topical corticosteroids seemed to have little effect on rectal sparing. However, the relapse index was significantly higher in patients with rectal sparing. The intractability index, representing the ratio of the duration of the active stage to the investigation period, was also higher, though not significantly so, in this group. The results suggest that rectal sparing may give information about intractability or a tendency to relapse.

Immunosuppressive Agents in Penetrating Keratoplasty

One of the problems with corneal grafting is the occurrence of rejection. Immune reaction is considered to be an important cause of graft failure. Early recognition of such graft reaction can frequently be treated successfully with intensive topical administration of corticosteroids. Generally, I prefer to add systemic corticosteroids and immunosuppressive agents such as azathioprine. In the present study two cases are described to illustrate the use of azathioprine and demonstrate that even severe and recurrent graft reactions can be successfully treated with immunosuppressive agents.

Early Corneal Findings in Cogan's Syndrome

We evaluated the ocular manifestations of Cogan's syndrome in 13 consecutive patients. The most frequent and earliest ocular finding was bilateral peripheral subepithelial keratitis consisting of faint, nummular lesions. The subepithelial keratitis was responsive to topical administration of corticosteroids. Peripheral subepithelial keratitis was seen in four patients and strongly suspected on review of history in three additional patients. Deep stromal keratitis was seen in two patients, while only one patient developed classic findings of Cogan's syndrome, ie. interstitial keratitis with vascularization. Additionally, five patients presented with noncomeal ocular inflammatory disease and deafness (atypical Cogan's syndrome). Early subepithelial keratitis in Cogan's syndrome may be mistakenly diagnosed as trival ocular inflammatory disease, and suppressed by topical corticosteroids, resulting in delayed diagnosis of Cogan's syndrome in the absence of classic corneal findings. Early diagnosis of Cogan's syndrome is important inasmuch as prompt treatment of cochlear symptoms with systemic corticosteroids may prevent or ameliorate deafness.

The prognosis of corticosteroid-responsive individuals.

Response of intraocular pressure to topical corticosteroid administration is determined genetically, and the genes that determine corticosteroid responsiveness of IOP and primary open angle glaucoma are considered closely related. To elucidate the relationship between corticosteroid responsiveness and primary open angle glaucoma, 35 patients with high corticosteroid responsiveness were followed up without therapy for at least ten years. During the follow-up period, a sustained rises in IOP greater than 21 mm Hg developed in five of 22 originally normotensive subjects. In two cases, glaucomatous field changes were demonstrated along with pressure elevation. Of 13 originally ocular hypertensives, further rise of IOP associated with glaucomatous field changes developed in seven. Results strongly indicate that pressure elevation is more likely to develop in corticosteroid-responsive individuals and the glaucomatous field defects are more likely to develop in responsive are compared with nonresponsive subjects.

Corneal Ulcers Associated with Goldenhar Syndrome

Two patients with Goldenhar syndrome developed corneal ulcers. Previous acid burn of the cornea and prolonged topical corticosteroid administration occurred in Patient 1. Predisposing ocular anomalies in patients with Goldenhar syndrome include corneal hypesthesia; keratoconjunctivitis sicca, and exposure secondary to eyelid colobomas, lacrimal gland and duct anomalies, dermoids and lipodermoids, and neurologic deficits. Serious ocular morbidity may be prevented by searching for and adequately treating these predisposing factors. It is possible that embryonic events contribute to ocular complications in Goldenhar syndrome, in part, by causing hypoplasia or abnormal function of the trigeminal and facial nerves.

Visual field changes in ocular hypertension. A computer-based analysis.

A minicomputer system has been developed to digitize and store visual field data. In 110 cortiocosteroid-nonresponding subjects aged 10 to 75, the area of the i4e and i2e isopters and of the blind spot changed linearly as a function of age. Within this population the same visual field parameters were randomly distributed with respect to intraocular pressure. In 32 cortiocosteroid responders (increase in intraocular pressure to over 31 mm Hg after topical administration of corticosteroids) with normal visual fields, the central visual field area (i2e isopter) was reduced as a nonlinear function of IOP. Increases in IOP in excess of 8 mm Hg were required to produce significant mean reductions in central visual field area.

Treatment of traumatic hyphaema.

A series of 131 successive hospitalized cases of traumatic hyphaema after blunt injury of the eye were treated with complete bed-rest for 6 days and double eye-patching but without any topical medication. Seven patients (5.3%) had a secondary bleeding. The visual acuities of 115 patients were tested, and 105 regained their normal vision, i.e. 1.0 or over. These results are no better than those reported in series treated with moderate bed-rest for 3-4 days combined with topical administration of corticosteroids and mydriatics. The results indicate that our present treatment may be unnecessarily severe.