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W J Shields

Publications and source records attributed to W J Shields.

7 recordsLinked to original sources
PubMed1992

Bilateral progressive essential iris atrophy and keratoconus with coincident features of posterior polymorphous dystrophy: a case report and proposed pathogenesis.

We report the first case known to us of an apparent bilateral association of essential iris atrophy (EIA) and keratoconus (KC), with coincident features of posterior polymorphous dystrophy (PPD). Based on this case and the published natural history and findings of both the irido corneal endothelial (ICE) syndrome and PPD, we propose a new hypothesis for the pathogenesis of the ICE syndrome with associated KC and/or PPD. We suggest that, similar to the genetics of retinoblastoma, the predisposition for either the ICE syndrome or for PPD is inherited as an inactive allele, the so-called "first hit." Inactivation of the second allele, or "second hit," which could occur at any time, might be the product of the background mutation rate or of an environmental trigger. Dedifferentiation or an abnormality in normal development could occur after the first or second hit, resulting in varying clinical patterns. We also concur with other investigators that PPD could be part of the spectrum of the ICE syndrome, owing to similarities in their clinical presentations, histopathology, specular and electron microscopy, and natural history.

Atrophy↗
PubMed1991

Meibomian gland dysfunction in chronic blepharitis.

We examined 57 patients with symptoms of chronic blepharitis using meibomian gland expression, meibography, tear osmolarity, and the Schirmer's test. We also performed meibography on 20 normal patients free of chronic blepharitis. We found that 42 blepharitis patients (74%) had evidence of meibomian gland loss, whereas only four of 20 normal patients (20%) had any gland dropout. We performed cluster analysis on the data from the patients with blepharitis and found that these patients tended to fall into distinct groups with clinically relevant characteristics. We also found that tear osmolarity correlated positively with gland dropout (+0.413) and negatively with excreta volume (-0.499). This study demonstrates that an objective analysis of meibomian gland function may be used to assess chronic blepharitis and define subsets of blepharitis with measurable differences. It also supports the significance of meibomian gland dysfunction on tear osmolarity and the evaporative state of the eye.

Adult↗
PubMed1991

Meibomian gland morphology and tear osmolarity: changes with Accutane therapy.

We evaluated the meibomian gland function of 11 patients before and during treatment with isotretinoin (Accutane) by assessing tear osmolarity, meibomian gland morphology, tear production, rose bengal staining, and meibomian gland excreta. We found, during Accutane use, that meibomian glands appeared significantly less dense and atrophic by meibography. Excreta thickness increased from 1.7 +/- 0.9 to 3.1 +/- 1.2 (p less than 0.005), and expressible excreta volume decreased from 1.52 +/- 0.68 to 1.10 +/- 0.3 (p less than 0.05) (scale 1-4). We also found a significant increase in tear osmolarity from 304.9 +/- 11 to 316.3 +/- 10 mosmol/L (p less than 0.005). There was no significant change in the Schirmer test during treatment. We suggest that the clinical symptoms of blepharitis during Accutane therapy are related to decreased meibomian gland function and consequent increased tear evaporation and tear osmolarity.

Acne Vulgaris↗
PubMedDate not supplied

Corneal infiltrates associated with disposable extended wear soft contact lenses: a report of nine cases.

We report nine cases of corneal infiltrates and/or ulceration in patients using disposable extended wear contact lenses. None of the nine patients had worn the lenses more than the recommended 7 days. Cultures were performed on six of the patients; all cultures were negative. One of the six cultured patients had been treated with topical antibiotics prior to culture. All responded promptly to cessation of lens wear and topical antibiotic therapy. Although all of the infiltrates/ulcers were paracentral, none of the patients sustained any permanent visual loss.

Adult↗
PubMedDate not supplied

Ciguatera in Australia. Occurrence, clinical features, pathophysiology and management.

Ciguatera is a type of food poisoning that results from eating certain tropical fish which have become toxic. It is common in Australia: 175 outbreaks, which involved 527 people, were reported in Queensland between 1965 and 1984. It seems restricted to certain areas around the Australian coastline. Most reports have involved the narrow-barred Spanish mackerel, Scomberomorus commersoni, most of which were caught in southern Queensland waters. Up to 2100 cases may have occurred in north Queensland between 1965 and 1984, which were not recorded by the writers. The symptoms of ciguatera in Australia are similar to those reported elsewhere in the South Pacific. Ciguatoxin acts by increasing the permeability of excitable membranes to sodium ions. This type of membrane is found throughout the body in nerve tissue as well as in heart and skeletal muscle. The treatment of ciguatera remains symptomatic and supportive only. Major advances in treatment for ciguatera and detection of ciguatoxin await the means of producing additional ciguatoxin.

Animals↗