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Articles by C. J. Schofield
Total Records ( 3 ) for C. J. Schofield
  C. J. Schofield , J. D. Ellis , A. Ellingford , A. D. Morris and G. P. Leese
  Aims  To ascertain which perifoveal changes on digital retinal screening in diabetes predict the need for subsequent macular grid or focal laser therapy.

Methods  Between 1 January 2004 and 31 December 2005, all consecutive retinal images where any lesion was within one disc diameter of the fovea were reviewed. Patients were categorized by lesion at screening as having microaneurysm, single blot haemorrhage, multiple blot haemorrhages and exudates or circinate exudates within one disc diameter of the fovea. We compared these retinal images with the findings on slit lamp examination and the related decision for laser photocoagulation.

Results  Four hundred and twenty-four retinal images were identified. Of these, 52 were excluded, principally because of an interval between photography and clinic attendance of greater than 120 days, leaving 372 retinal images in the study group (313 patients). No patients with a single blot haemorrhage required immediate laser therapy at ophthalmology review compared with 13 (23%) of those with multiple blot haemorrhages and 36 (16%) of those with exudates or circinate lesions (P < 0.001). Thirty-nine patients with a single blot haemorrhage who did not require laser therapy underwent ongoing follow-up. None of these underwent laser therapy for maculopathy within the study time frame (9 months from initial screening event).

Conclusions  In this study, no patients with a single blot haemorrhage within one disc diameter of the fovea on digital retinal screening required laser treatment.

  C. J. Schofield , N. Yu , A. S. Jain and G. P. Leese
  Aims  To assess the changing rate of amputation in patients with diabetes over a 7-year period.

Methods  All patients undergoing lower extremity amputation in Tayside, Scotland between 1 January 2000 and 31 December 2006 were identified. Temporal linkage of cases to the diabetes database was used to ascertain which amputations were in patients with diabetes.

Results  The incidence of major amputations fell from 5.1 [95% confidence interval (CI) 3.8-6.4] to 2.9 (95% CI 1.9-3.8) per 1000 patients with diabetes (P < 0.05). There is a clear linear trend in the adjusted incidence of major amputation (P = 0.023 and 0.027 for age- and sex-adjusted, and duration- and sex-adjusted incidences, respectively). The adjusted incidence of total amputations followed decreased linear regression trend over the whole study period when adjusted for age and sex or diabetes duration and sex (P = 0.002).

Conclusions  There has been a significant reduction in the incidence of major lower extremity amputation in patients with diabetes over the 7-year period.

  C. J. Schofield and C. Sutherland
  For many years, the development of insulin resistance has been seen as the core defect responsible for the development of Type 2 diabetes. However, despite extensive research, the initial factors responsible for insulin resistance development have not been elucidated. If insulin resistance can be overcome by enhanced insulin secretion, then hyperglycaemia will never develop. Therefore, a β-cell defect is clearly required for the development of diabetes. There is a wealth of evidence to suggest that disorders in insulin secretion can lead to the development of decreased insulin sensitivity. In this review, we describe the potential initiating defects in Type 2 diabetes, normal pulsatile insulin secretion and the effects that disordered secretion may have on both β-cell function and hepatic insulin sensitivity. We go on to examine evidence from physiological and epidemiological studies describing β-cell dysfunction in the development of insulin resistance. Finally, we describe how disordered insulin secretion may cause intracellular insulin resistance and the implications this concept has for diabetes therapy. In summary, disordered insulin secretion may contribute to development of insulin resistance and hence represent an initiating factor in the progression to Type 2 diabetes.
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