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Biomedical subjects

Philip G Griffiths

Publications and source records attributed to Philip G Griffiths.

9 recordsLinked to original sources
PubMed2007

Short-term effects of focal argon laser treatment in diabetic maculopathy as demonstrated by optical coherence tomography.

PURPOSE: To assess the short-term effects of argon laser on retinal thickening as demonstrated by optical coherence tomography (OCT). METHODS: A prospectively collected consecutive series of patients undergoing routine focal argon laser treatment for sight-threatening diabetic maculopathy had bilateral OCT performed before laser treatment and 1 hour, 24 hours, and 2 weeks after treatment. The main outcome measure was change in retinal thickness in the region of laser treatment. RESULTS: Forty-six eyes were analyzed. There was a small increase in retinal thickness in the treated area 1 hour after laser treatment, with a mean change from before laser treatment of +2.6 microm (95% confidence interval [CI], +0.2 to + 5.0). However, there was a larger change 24 hours after treatment of +39.0 microm (95% CI, +31.6 to + 46.4) and a significant decrease 2 weeks after treatment of -14.6 microm (95% CI, -21.6 to -7.7) from before laser treatment values. CONCLUSION: Focal argon laser treatment remains the first-line treatment for sight-threatening diabetic maculopathy. This study shows that in the short-term, areas of retinal thickening worsen before settling in response to argon laser treatment as demonstrated by OCT.

Adult↗
PubMed2006

Acute red eye and back pain as a presentation for systemic illness: case report.

BACKGROUND: Acute red eye is a common presentation in both primary and secondary care. Presentation in combination with other systemic symptoms can indicate serious underlying pathology. CASE PRESENTATION: 73-year-old lady presenting with endogenous endophthalmitis and thoracic discitis secondary to sub-acute bacterial endocarditis. CONCLUSION: Acute red eye in combination with systemic symptoms requires immediate investigation. If endogenous endophthalmitis is diagnosed, a source of sepsis should be comprehensively investigated and referral made to individual specialties if necessary.

Acute Disease↗
PubMed2005

A polymorphism at codon 31 of gene p21 is not associated with primary open angle glaucoma in Caucasians.

BACKGROUND: Primary open angle glaucoma (POAG) is considered to be a neurodegenerative optic neuropathy, in which cell death occurs by apoptosis. p21, is an important protective component of the apoptotic pathway, regulating cellular arrest in the presence of DNA damage. An unstable or altered p21 protein could modify the cellular response to genomic injury and abolish the effect of p21. A previous study on a Chinese cohort suggested that the p21 codon 31 polymorphism may alter the state of apoptosis in glaucomatous optic neuropathy, failing to protect the ganglion cells. The aim of this study was to test the hypothesis that a p21 codon 31 polymorphism is associated with POAG on a Caucasian cohort. METHODS: 140 POAG patients and a control group of 73 healthy individuals were included in the study. All the subjects were of Caucasian origin. Genomic DNA was amplified by polymerase chain reaction, followed by enzymatic restriction fragment length polymorphism technique (PCR-RFLP). Patients and controls were genotyped for a single nucleotide polymorphism (C/A transversion) in the third base of codon 31 of p21, which leads to a serine (Ser)/arginine (Arg) substitution. RESULTS: The distribution of the genotypes in the POAG patients showed 128 (91.4%) Ser homozygotes, 10 (7.1%) Ser/Arg heterozygotes and 2 (1.5%) Arg homozygotes. In the control cohort, there were 61 (83.6%) Ser homozygotes and 12 (16.4%) Ser/Arg heterozygotes. No Arg homozygotes were present amongst the control group. Both the allelic and genotypic frequencies of the Ser or Arg residues at codon 31 were not significantly different between POAG patients and controls (Fisher's exact test, P = 0.20 for alleles and P = 0.0561 for genotypes). CONCLUSION: This study suggests that the p21 codon 31 polymorphism does not contribute to the risk of POAG in the Caucasian population.

Aged↗
PubMed2005

Ophthalmoplegia due to mitochondrial DNA disease: the need for genetic diagnosis.

We describe a patient with chronic progressive external ophthalmoplegia (CPEO) who underwent muscle biopsy for suspected mitochondrial disease. In spite of normal histocytochemical cytochrome c oxidase (COX) activity and respiratory chain enzyme measurements in muscle, subsequent molecular genetic analysis revealed the presence of a single, large-scale deletion of mitochondrial DNA (mtDNA). The case serves to illustrate the importance of pursuing the proposed mitochondrial genetic abnormality, even in patients with normal biopsy findings.

Adult↗
PubMed2004

Apolipoprotein E promoter polymorphisms do not have a major influence on the risk of developing primary open angle glaucoma.

PURPOSE: Primary open angle glaucoma (POAG) is a major cause of late onset visual failure of unknown etiology. Recent genetic association studies have implicated the apolipoprotein E (APOE) gene in the pathophysiology of primary open angle glaucoma, but there have been conflicting findings. METHODS: To resolve this issue we studied 140 cases and 73 controls that were carefully phenotyped, and used a logistic regression model to simultaneously analyze the effect of apolipoprotein E genotype and functional polymorphisms in the apolipoprotein E gene promoter while controlling for potentially confounding variables. RESULTS: We found no evidence of an association between the apolipoprotein E promoter region polymorphisms and primary open angle glaucoma. CONCLUSIONS: Apolipoprotein E promoter polymorphisms are unlikely to have a major impact on the pathophysiology of primary open angle glaucoma.

Aged↗
PubMed2004

The role of apolipoprotein E gene polymorphisms in primary open-angle glaucoma.

OBJECTIVE: To test the hypothesis that genetic polymorphisms of the apolipoprotein E (APOE) gene are associated with primary open-angle glaucoma (POAG), based on the association between neurodegenerative diseases and the APOE genotype. METHODS: Genomic DNA was examined from an unrelated cohort of 137 POAG patients and 75 control subjects from the ophthalmology department of the Royal Victoria Infirmary. The APOE allele frequency (epsilon2, epsilon3, and epsilon4 alleles) was studied by polymerase chain reaction amplification of the related locus (19q13.2), enzymatic digestion of the products, gel electrophoresis, and imaging under UV illumination. For statistical analysis, we used a logistic regression model that included intraocular pressure as a continuous variable to study the possible correlation between POAG and APOE allele frequency. RESULTS: Logistic regression analysis showed no statistically significant association between the frequency of the APOE allele and POAG for the population studied, irrespective of the IOP (epsilon2 odds ratio, 0.82; 95% confidence interval, 0.12-5.79 [P =.84]; epsilon3 odds ratio, 0.39; 95% confidence interval, 0.10-1.49 [P =.17]; and epsilon4 odds ratio, 3.84; 95% confidence interval, 0.80-18.49 [P =.09]). CONCLUSION: In our cohort, the APOE genotype does not constitute a risk factor for developing POAG, even in patients with normal-tension glaucoma.Clinical Relevance Apolipoprotein E polymorphisms do not appear to be contributory to POAG.

Aged↗
PubMed2002

The distribution of mitochondrial activity in relation to optic nerve structure.

BACKGROUND: The observation of a buildup of mitochondria at the level of the lamina cribrosa in the optic nerve head has traditionally been attributed to axoplasmic stasis. However, this region is also the transition zone for myelination, resulting in differing energy requirements. OBJECTIVE: To investigate the relationship between myelination and mitochondrial activity in optic nerve tissue. METHODS: Histological, histochemical, and immunocytochemical techniques were used to demonstrate the distribution of myelin, cytochrome-c oxidase activity, and laminar structure in human optic nerve tissue. A study of rabbit optic nerve and retina and unmyelinated human pituitary stalk was also performed. Cytochrome-c oxidase activity in the human optic nerve tissue was measured using microphotometry. RESULTS: There was a striking inverse relationship between myelination and mitochondrial distribution in all tissue studied. Statistical analysis of microphotometric data showed this distribution to be highly significant. CONCLUSION: We caution against the previous inference of a process of axoplasmic stasis and suggest that, instead, the distribution of mitochondria reflects the functional requirement of different regions of the ganglion cell axon. CLINICAL RELEVANCE: Optic neuropathy is associated with several inherited disorders of mitochondria. We suggest that a fine balance exists between energy demand and tissue function in the optic nerve, which may explain why optic nerve pathological features are seen in those with mitochondrial disease.

Adult↗