title: Refractive changes in diabetic patients during intensive glycaemic control.
abstract: OBJECTIVE
  To evaluate the clinical course and the characteristics of transient refractive error occurring during intensive glycaemic control of severe hyperglycaemia.
  
  
  METHODS
  28 eyes of patients with persistent diabetes were included in this prospective study. During the observation period, patients underwent general ophthalmological examination and A-mode scan ultrasonography was performed at each examination-at days 1, 3, and 7, and then once every week or every other week until recovery of hyperopia.
  
  
  RESULTS
  A transient hyperopic change occurred in all patients receiving improved control after hyperglycaemia. Hyperopic change developed a mean of 3.4 (SD 2. 0) days after the onset of treatment, and reached a peak at 10.3 (6. 1) days, where the maximum hyperopic change in an eye was 1.47 (0. 87) D (range 0.50-3.75 D). Recovery of the previous refraction occurred between 14 and 84 days after the initial assessment. There was a positive correlation between the magnitude of the maximum hyperopic change and (1) the plasma glucose concentration on admission (p<0.01), (2) the HbA(1c) level on admission (p<0.005), (3) the daily rate of plasma glucose reduction over the first 7 days of treatment (p<0.001), (4) the number of days required for hyperopia to reach its peak (p<0.001), and (5) the number of days required for the development and resolution of hyperopic changes (p<0.0001). There was a negative correlation between the maximum hyperopic change of an eye and baseline value of refraction (p<0.01). During transient hyperopia, no significant changes were observed in the radius of the anterior corneal curvature, axial length, lens thickness, or depth of anterior chamber.
  
  
  CONCLUSIONS
  The degree of transient hyperopia associated with rapid correction of hyperglycaemia is highly dependent on the rate of reduction of the plasma glucose level. A reduction of refractive index in intraocular tissues, especially in lens, appears to be responsible for this hyperopic change.
authors.affiliation: Department of Ophthalmology, Tsukuba University Hospital, Japan. fumiki@iea.att.ne.jp
authors.forename: F
authors.initials: F
authors.lastname: Okamoto
authors.forename: H
authors.initials: H
authors.lastname: Sone
authors.forename: T
authors.initials: T
authors.lastname: Nonoyama
authors.forename: S
authors.initials: S
authors.lastname: Hommura
mesh_terms: D000328:Adult; D000368:Aged; D001786:Blood Glucose / Q000378:metabolism; D003924:Diabetes Mellitus, Type 2 / Q000097:blood / Q000150:complications* / Q000503:physiopathology; D005260:Female; D006801:Humans; D006943:Hyperglycemia / Q000209:etiology / Q000503:physiopathology / Q000628:therapy*; D006956:Hyperopia / Q000097:blood / Q000209:etiology*; D008297:Male; D008875:Middle Aged; D011446:Prospective Studies; D012029:Refraction, Ocular
chemical_list: D001786:Blood Glucose