Diabetic retinopathy in people aged 70 years or older. The Oulu Eye Study

AIMS—To evaluate the presence and severity of diabetic retinopathy and the value of retinopathy screening in people aged 70 years or older.
METHODS—In a population based study on 500 of 560 eligible (89%) people aged 70 years or older, signs of diabetic retinopathy were evaluated through dilated pupils by an ophthalmologist using photographic and/or ophthalmoscopic methods.
RESULTS—23% of the study population (113/500) had diabetes mellitus. Signs of diabetic retinopathy were found in 24 people (21% of the diabetic population). Retinopathy changes were graded as mild to moderate non-proliferative retinopathy (NPDR) in 40 eyes (18 people), severe NPDR (preproliferative) in five eyes (four people), and proliferative in three eyes (two people). Preproliferative or proliferative changes were present in four people (3.5% of the diabetic population) and diabetic maculopathy was diagnosed in nine (8% of the diabetic population). Laser treatment was considered to be indicated in seven people for maculopathy, and in two for proliferative changes. In four people the visual acuity was reduced to a low vision level as a result of diabetic retinopathy.
CONCLUSION—In spite of the high prevalence of diabetes mellitus in the elderly population, the prevalence of vision threatening diabetic retinopathy, particularly proliferative retinopathy, is low. Ophthalmoscopically, reliable information on fundus changes could be obtained in 94%, but photographs were gradable in only 76% of the diabetic population. Therefore, the value of photographic screening for diabetic retinopathy in this age group is poor in comparison with younger age groups.

     

Diabetic retinopathy in Down's syndrome

AIM—To determine the prevalence of diabetic retinopathy in patients with Down's syndrome and diabetes mellitus.
METHOD—Nine patients with Down's syndrome and diabetes mellitus were assessed. Factors recorded included type and duration of diabetes, level of diabetic control, blood pressure, urinalysis, and results of ophthalmological examination.
RESULTS—The duration of diabetes ranged from 8 to 41 years (mean 17.6 years). All had satisfactory glycaemic control and blood pressure measurements on the low side of normal (mean 106.6/70 mm Hg). One patient had early background diabetic retinopathy. The remainder had no evidence of diabetic retinopathy.
CONCLUSION—The low prevalence of diabetic retinopathy in these Down's syndrome patients, despite the long duration, is an interesting finding. It suggests some inherent protective factor against the development of diabetic retinopathy in this patient subgroup.

Keywords: Down's syndrome; retinopathy; diabetes; hypertension     

Evidence that upregulation of serum IGF-1 concentration can trigger acceleration of diabetic retinopathy

BACKGROUND—Acute reduction of chronic hyperglycaemia can accelerate early diabetic retinopathy. In adolescent patients with Mauriac's syndrome, this phenomenon is related to an upregulation of subnormal serum IGF-1 levels.
AIM—To obtain longitudinal data on serum IGF-1 and retinopathy status in poorly controlled adult insulin dependent (type 1) diabetic patients without Mauriac's syndrome, in whom hyperglycaemia is reduced by intensive insulin therapy.
METHODS—Four patients with chronic severe insulin deficiency and early microangiopathy were studied prospectively. Changes in plasma glucose, HbA_1c, serum IGF-1 levels, proteinuria, retinopathy, and clinical status were followed up closely.
RESULTS—Reducing hyperglycaemia from >16 mmol/l (equivalent to HbA_1c >11%) to <10 mmol/l (HbA_1c <8%) within 5 months increased serum IGF-1 levels by 70-220%. While proteinuria and symptomatic neuropathy regressed, retinopathy progressed from the mild to the severe non-proliferative stage with maculopathy (n=4), and to the proliferative stage (n=1). Laser coagulation was commenced upon the appearance of sight threatening macular oedema (n=4).
CONCLUSION—Upregulation of serum IGF-1 preceding retinal deterioration in these patients suggests a cause-effect relation, consistent with earlier experimental and clinical data.

Keywords: diabetes mellitus; macular oedema; metabolic control; intensive therapy; glycated haemoglobin A_1c; growth factors     

Retinal vessel dilatation and elongation precedes diabetic macular oedema

AIMS/BACKGROUND—Retinal vessel dilatation is a well known phenomenon in diabetes. In this study, the theory of whether excessive changes in diameter and length of retinal vessels occur in the development of diabetic macular oedema was tested, supporting a hypothesis that the development of diabetic macular oedema may be linked to hydrostatic pressure changes described in Starling's law.
METHODS—From fundus photographs of diabetic patients attending a regular eye screening programme, the diameter and segment length of retinal vessels were measured in three retinopathy groups (12 patients each) with diabetic macular oedema (DMO), background retinopathy and no retinopathy, over a period of approximately 4 years, ending at the time of diagnosis of diabetic macular oedema in the DMO group.
RESULTS—A statistically significant dilatation and elongation of retinal arterioles, venules, and their macular branches was found before the diagnosis of macular oedema in the DMO group. No significant changes were found in the other two groups.
CONCLUSION—It is suggested that Starling's law applies to the formation of oedema in the retina as in other tissues.

     

VEGF localisation in diabetic retinopathy

AIM—To determine the staining pattern of vascular endothelial growth factor (VEGF) at different stages of diabetic retinopathy (including post-laser photocoagulation) and to compare staining in excised fibrovascular and fibrocellular (non-diabetic) preretinal membranes.
METHODS—Immunohistochemical localisation of VEGF, using antibodies raised against VEGF₁₆₅ and VEGF_121,165,189, was carried out on specimens of normal human retina (n=15), diabetic retinas ((a) with no overt retinopathy (n=19), (b) with intraretinal vascular abnormalities but no proliferative retinopathy (n=6), (c) with active proliferative retinopathy (n=6), (d) with no residual proliferative retinopathy after photocoagulation therapy (n=15)), excised diabetic fibrovascular membranes (n=19), and non-diabetic fibrocellular membranes (n=7). The degree and pattern of immunostaining was recorded.
RESULTS—In general, VEGF was absent from the majority of normal retinas. VEGF staining was apparent in most diabetic tissues but the staining pattern was dependent on both the specificity of the antibody used and the category of tissue. Staining with the VEGF₁₆₅ antibody was generally confined to endothelial cells and perivascular regions while the VEGF_121,165,189 antibody was also associated with extravascular components of the inner retina. Intensity of immunostaining of diabetic eyes was dependent on the severity of retinopathy being least in diabetics with no overt retinopathy and greatest in retinas with proliferative retinopathy. Interestingly, the intensity of immunostaining in diabetic retinas which had undergone laser surgery for proliferative retinopathy was reduced to basal levels. Moderate to intense immunostaining was observed in all fibrovascular and fibrocellular membranes examined.
CONCLUSIONS—This study supports a circumstantial role for VEGF in the pathogenesis of both the preclinical and proliferative stages of diabetic retinopathy.

Keywords: vascular endothelial growth factor; VEGF; diabetes; diabetic retinopathy     

Altered retrobulbar vascular reactivity in early diabetic retinopathy

AIM/BACKGROUND—In diabetic eye disease the factors leading to compromised circulation and the resulting loss of visual function are poorly understood. Although retinal circulation has been widely investigated, it accounts for only a fraction of total eye blood flow. Blood flow was investigated in the larger vessels feeding the eye in patients with early diabetic retinopathy.
METHODS—Eleven patients with early diabetes with minimal or no retinopathy and 11 healthy controls were evaluated for retrobulbar blood flow velocity using colour Doppler imaging for the ophthalmic and central retinal arteries. Patients and subjects were tested while breathing room air and again under conditions of isocapnic hyperoxia.
RESULTS—Hyperoxia induced a significant change in the central retinal artery end diastolic velocity (EDV) (p = 0.008) and resistance index (RI) (p = 0.032) in normal subjects, but not in diabetic patients. Consequently, during hyperoxia, the diabetic patients were significantly higher for EDV (p = 0.006) and significantly lower for RI (p = 0.002) compared with normal controls. Hyperoxia caused no significant change in either group in the ophthalmic artery; nevertheless, under isocapnic hyperoxia conditions the diabetic patients had lower peak systolic velocity (p = 0.05) and lower RI (p = 0.05) than normal subjects.
CONCLUSIONS—Imposition of isocapnic hyperoxia produces significant differences in the ophthalmic and central retinal artery blood flow velocities in diabetic patients with early disease when compared with normal subjects. These results demonstrate that diabetic patients with minimal or no retinopathy suffer from irregular ocular vascular function in the major vessels feeding the eye.

     

Serum total renin, an independent marker of the activity and severity of retinopathy in patients with IDDM

BACKGROUND/AIMS—Recent studies have demonstrated marked renin and prorenin concentration gradients between ocular tissues and blood, and local expression of the renin-angiotensin system (RAS) in the eye. The authors determined whether serum total renin, which mostly consists of prorenin, is a marker of the activity and severity of diabetic retinopathy independent of other microvascular complications.
METHODS—Total renin concentrations (TRC) were measured with a time resolved immunofluorometric assay in 38 patients with IDDM (age 34 (SD 7) years, duration of disease 22 (7) years, serum creatinine 95 (15) µmol/l, urinary albumin excretion rate (UAER) 207 (829) µg/min, HbA_1c 8.5% (1.2%)), and in 13 matched normal subjects. All subjects were carefully characterised with respect to the presence and severity of retinopathy (RP score), nephropathy, and neuropathy using seven different tests of autonomic neuropathy.
RESULTS—Serum TRC was on average twofold higher in IDDM (396 (SE 211) ng/l) than in normal subjects (201 (88) ng/l, p<0.001). It was nearly twofold higher in patients with preproliferative or active proliferative retinopathy requiring careful follow up or therapy (TRC 596 (268) ng/l, n=11) compared with those with quiescent proliferative retinopathy after laser treatment (TRC 338 (183) ng/l, p<0.01, n=5); moderately severe non-proliferative retinopathy (337 (106) ng/l, p<0.01, n=13), no retinopathy, or only minimal non-proliferative retinopathy (270 (43) ng/l, p<0.001, n=9). In multiple linear regression analysis, RP score (p<0.01), but not the UAER or any index of autonomic neuropathy, was an independent determinant of serum TRC, and explained 32% of its variation (R=0.57, p<0.005).
CONCLUSIONS—Serum TRC in patients with diabetic retinopathy is increased independent of renal function and autonomic neuropathy, especially in those with severe active changes requiring careful follow up or treatment. These findings support the idea that diabetic retinopathy is the most important determinant of serum TRC in patients with IDDM, and that TRC is produced when retinopathy is active.

Keywords: diabetes; prorenin/total renin; retinopathy; nephropathy; neuropathy     

Prevalence of diabetic retinopathy in patients with diabetes mellitus diagnosed after the age of 70 years

AIMS/BACKGROUND—A hospital based prevalence study was undertaken to estimate the prevalence of diabetic retinopathy (DR) in patients diagnosed as having diabetes mellitus after the age of 70 years. The prevalence of visually threatening retinopathy at the time of diagnosis of diabetes was also determined. The association between prevalence of DR and duration of diabetes mellitus, mode of treatment, HbA_1c levels, presence of hypertension, and sex of patient was examined and a comparison was drawn between this study and earlier prevalence studies of DR in older type II diabetics.
METHODS—Using data on the Irish Diabetic Retinopathy Register located in the Mater Misericordiae Hospital, Dublin, all patients who were diagnosed as having type II diabetes mellitus after the age of 70 years were invited to attend for ophthalmic review. Medical records were examined to determine the duration of diabetes mellitus, mode of treatment, recent HbA_1c levels, and the presence of systemic hypertension.
RESULTS—Of the 150 patients examined, 21 (14%) had some form of DR and 10 of these patients (6.6%) had visually threatening retinopathy or previously treated visually threatening retinopathy. Five patients (3.3%) presented with visually threatening retinopathy at the time of diagnosis of diabetes. Those patients with DR had a significantly higher median duration of diabetes (5.0 years) compared with those patients without DR (3.5 years). A significantly higher proportion of patients with DR required treatment with insulin and a correspondingly lower proportion of patients without DR were controlled on diet alone. There was no significant association between prevalence of DR and HbA_1c levels, systemic hypertension, or sex of patient. There was a lower overall prevalence of DR in comparison with earlier studies.
CONCLUSIONS—The prevalence of DR in these elderly type II diabetics is lower than that previously reported in patients with type II disease but a small percentage of patients had visually threatening retinopathy at presentation. Longer duration of diabetes and insulin use were associated with a significantly increased prevalence of DR. All elderly type II diabetic patients require thorough ophthalmic examination near to the time of first presentation and thereafter at regular intervals.

     

Detection of eicosanoids in epiretinal membranes of patients suffering from proliferative vitreoretinal diseases

AIM—Arachidonic acid is metabolised via lipoxygenase to 15-HETE (15-hydroxyeicosatetraenoic acid) and 15-HPETE (15-hydroperoxyeicosatetraenoic acid), which are believed to influence proliferation in tissue culture. 15-HETE is the reduction product of 15-HPETE. Cell proliferation is believed to be decreased by 15-HPETE and increased by 15-HETE. The aim of this study was to investigate epiretinal membranes for the presence of these lipoxygenase products and to compare membranes from different disease processes.
METHODS—Epiretinal membranes of 15 patients suffering from proliferative vitreoretinopathy (PVR, n=7) and proliferative diabetic retinopathy (PDR; n=8) were removed during vitrectomy and analysed by means of thin layer chromatography. The plates were evaluated by digital image analysis.
RESULTS—Both 15-HETE and 15-HPETE were identified in membranes from eyes of patients with PVR and PDR with HETE values significantly higher (p<0.05) than HPETE values (HETE/HPETE ratio = 5.2).
CONCLUSION—This study demonstrates that eicosanoids are present in the epiretinal membrane tissue of patients with PVR and PDR. Considering that HETE increases cell proliferation while HPETE inhibits it, it is conceivable that eicosanoids are an additional factor contributing to the regulation of membrane growth in proliferative retinal disorders. Thus, inhibition of lipoxygenase could be a therapeutic approach in these diseases.

     

Plasminogen in proliferative vitreoretinal disorders

OBJECTIVE—Intravitreal fibrin formation is a frequent observation after vitrectomy performed for a variety of vitreoretinal disorders including proliferative vitreoretinopathy (PVR), proliferative diabetic retinopathy (PDR), and endophthalmitis. Plasminogen activators (PA) have been used for the management of this postoperative complication. This approach requires the presence of plasminogen, the substrate for PA mediated fibrinolysis, in the vitreal cavity.
METHODS—Quantification of plasminogen in the vitreous of 60 patients with PVR, PDR, and macular pucker was performed by streptokinase mediated activation using a chromogenic substrate. The presence of immunoreactive plasminogen was confirmed by immunoblot analysis of vitreal proteins and immunocytochemistry of surgically removed epiretinal membranes.
RESULTS—Plasminogen levels were dramatically increased in the vitreous of PVR and PDR patients compared with macular pucker patients and normal controls. Staining for plasminogen in epiretinal membranes was confined to the extracellular matrix. Predominant staining of perivascular areas in PDR specimens indicated that breakdown of the blood-retinal barrier is an important source of intravitreal plasminogen in that condition.
CONCLUSION—Plasminogen may play a role in traction membrane formation in PVR and PDR. Our biochemical analysis of presurgical vitreous indicates that there may be abundant substrate for PA mediated fibrinolysis in the vitreous cavity after vitrectomy.

     

Use of eye care services by people with diabetes: the Melbourne Visual Impairment Project

AIM—The use of eye care services by people with and without diabetes was investigated in the Melbourne Visual Impairment Project (VIP), a population based study of eye disease in a representative sample of Melbourne residents 40 years of age and older.
METHODS—A comprehensive interview was employed to elicit information on history of diabetes, medication use, most recent visit to an ophthalmologist and optometrist, and basic demographic details. Presence and extent of diabetic retinopathy was determined by dilated fundus examination.
RESULTS—The Melbourne VIP comprised 3271 people who ranged in age from 40 to 98 years; 46.2% of them were male. Of 3189 people who had the fundus examination and knew their diabetes status, 162 (5.1%) reported having been previously diagnosed with diabetes and, of these, 37 (22.2%) were found to have diabetic retinopathy. Seven people (4.3%) had developed diabetes before age 30. The mean duration of diabetes was 9.2 years. People with diabetes were significantly more likely to have visited an ophthalmologist ever or in the past 2 years than people without diabetes. However, 31.8% of people with diabetes had never visited an ophthalmologist. The proportion of people who had never seen an ophthalmologist was 47.1% for people without diabetes, 34.2% for people with diabetes but without diabetic retinopathy, and 25% for people with diabetic retinopathy. Sixty one per cent of people with diabetic retinopathy had seen an ophthalmologist in the past year and a further 3% within the past 2 years. People with diabetes were not significantly more likely to have visited an optometrist than people without diabetes (p=0.51). Overall, 37.7% of people with diabetes and 32.9% of people without diabetes had visited an optometrist within the past year (χ²=2.25, 1 df, p=0.13). Information concerning retinal examinations was available for 135 individuals (83.3% of people with diabetes). Only 74 (54.8%) could recall ever having a dilated fundus examination; 10 (14%) by an optometrist, 62 (86%) by an ophthalmologist, and five (7%) by a general practitioner. Of those 68 people who had seen an ophthalmologist in the past 2 years, 48 (71%) reported a dilated fundus examination during that time. This compares with 28 (43%) reported dilated fundus examinations in the 65 people who had seen an optometrist in the past 2 years. This finding is statistically significant (χ²=10.2, 1 df, p<0.005).
CONCLUSION—These results indicate that nearly half of people with diabetes in Melbourne are not receiving adequate screening or follow up for diabetic retinopathy, despite universal health care.

Keywords: diabetes; diabetic retinopathy; screening guidelines     

Intravitreal growth factors in proliferative diabetic retinopathy: correlation with neovascular activity and glycaemic management

AIM—Many growth factors are implicated in proliferative diabetic retinopathy (PDR). It was decided to test the hypothesis that no one factor is predominant but that a regular profile of levels of different growth factors might be operating, and that the profile might differ according to whether or not insulin therapy was part of the patient's glycaemic management. The levels of several growth factors in vitrectomy samples were therefore determined from diabetic patients with tractional, non-haemorrhagic sequelae of PDR and these levels were correlated with (a) each other (growth factor profile), (b) neovascular activity, and (c) the method of glycaemic management (insulin treated (IT) or non-insulin treated (NIT)).
METHODS—72 samples of vitreous were obtained from either diabetic patients with PDR (n = 51) or non-diabetic (control) patients (n = 21). Levels of bFGF, IGF-I, EGF, and insulin were determined by radioimmunoassay; levels of TGF-β2 by ELISA; and levels of IGF-I binding protein by western ligand blotting. The data were analysed using appropriate statistics.
RESULTS—There was no regular growth factor profile. bFGF levels were significantly greater in vitreous from NIT patients compared with IT patients and controls. The highest levels of bFGF were found in NIT patients with actively vascularised membranes. TGF-β2 levels were significantly greater in vitreous from IT patients compared with NIT patients and controls The highest levels of TGF-β2 were found in IT patients with actively vascularised membranes. IGF-I levels were significantly greater in diabetics (irrespective of insulin treatment) than non-diabetics and the highest levels of IGF-I were found in IT patients with actively vascularised membranes. A 34 kDa IGFBP was the predominant IGFBP identified in vitreous and was found to be elevated in diabetics patients.
CONCLUSION—In PDR there is a correlation between intravitreal growth factor levels and both disease state (whether active or fibrotic) and method of glycaemic management.

     

Longer term visual outcome of eyes with retinopathy of prematurity treated with cryotherapy or diode laser

AIMS—Visual outcome of 66 eyes in 37 patients who had undergone treatment with either cryotherapy or diode laser for threshold retinopathy of prematurity was assessed.
METHODS—17 patients, representing 30 eyes treated with cryotherapy, were examined at between 56 and 98 months corrected age (median 68 months). 20 patients representing 36 eyes treated with diode laser, were examined at between 30 and 66 months corrected age (median 51 months). Structural outcome was categorised as: optimal—flat posterior pole; suboptimal—macular ectopia, optic nerve hypoplasia, retinal fold involving the macula, and retinal detachment involving the macula.
RESULTS—Optimal structural outcome was, in the absence of amblyopia, associated with optimal visual acuity (of 6/12 or better) in all cases, with most eyes achieving a visual acuity of 6/9 or 6/6. Suboptimal structural outcome was invariably associated with suboptimal visual acuity. Amblyopia was present in eight out of 20 cryotherapy treated eyes and in five out of 26 laser treated eyes with an optimal structural outcome. Refractive errors were significantly less in laser treated eyes as was the incidence of anisometropic amblyopia.
CONCLUSION—Eyes treated with either cryotherapy or diode laser for threshold retinopathy of prematurity with optimal structural outcome are associated with development of optimal visual acuity—that is, 6/12 or better. Treatment with either cryotherapy or laser does not in itself reduce the visual potential of these eyes.

Keywords: retinopathy of prematurity; cryotherapy; laser; visual acuity     

Partial reversal of protan and tritan colour defects with inhaled oxygen in insulin dependent diabetic subjects

AIMS—Abnormalities in colour perception occur early in the development of diabetic retinopathy. Whether these changes can be influenced by increasing circulating oxygen saturation was studied in comparison with non-diabetic controls.
METHODS—Protan and tritan colour thresholds were measured using a computer graphics system in 37 insulin dependent diabetic subjects, with no or minimal background retinopathy, and 27 matched controls. Colour thresholds were performed after subjects inhaled either gaseous air or 100% oxygen for a minimum of 5 minutes.
RESULTS—Diabetic subjects had higher colour vision thresholds when inhaling air when compared with controls (protan (mean 3.93 (SEM 0.39), v 2.36 (0.16), p<0.0002) and tritan (8.15 (0.62) v 5.42 (0.31), p <0.002)). The colour vision thresholds observed in diabetic subjects inhaling air fell when they inhaled oxygen (protan (3.93 (0.39) v 3.57 (0.33), p <0.025) and tritan (8.15 (0.62) v 7.35 (0.59), p<0.005)). No fall in colour thresholds was seen in non-diabetic controls who inhaled oxygen.
CONCLUSION—A small improvement in the colour vision thresholds was observed using computer graphics in diabetic subjects, with minimal or no retinopathy, who inhaled oxygen. This study supports a hypothesis that reduced retinal oxygenation contributes to the colour vision defects in diabetes.

     

Serotoninergic status in patients with hereditary vascular retinopathy syndrome

AIM/BACKGROUND—In a new autosomal dominant syndrome (which the authors called hereditary vascular retinopathy (HVR)) cerebral ischaemia, Raynaud's phenomenon, and migraine are the most striking features. As serotonin (5-HT) is known to play a role in vasospastic processes, Raynaud's phenomenon, and migraine they wondered whether the serotoninergic status in patients with HVR is different. Therefore, it was decided to investigate some serotoninergic variables in these patients.
METHODS—The study was conducted in 12 patients with HVR, 10 relatives, and 19 healthy controls. The levels of intraplatelet and plasma 5-HT were measured, as well as the plasma levels of its precursor amino acid tryptophan and the ratio of tryptophan to the large neutral amino acids, which compete with the transport of tryptophan through the blood-brain barrier.
RESULTS—In both the patients with HVR and in nine relatives the concentrations of 5-HT in plasma and platelets were significantly lower than in controls. The plasma levels of tryptophan and the tryptophan ratio were also found to be lower in the patient group compared with the control group, but not in the relatives.
CONCLUSION—The observed alterations in 5-HT and its precursor tryptophan strongly suggest the existence of a malfunctioning of the serotoninergic system in the HVR syndrome.

Keywords: vascular retinopathy; serotonin; tryptophan     

Absence of hypertensive retinopathy in a Turkish kindred with autosomal dominant hypertension and brachydactyly

BACKGROUND—A 60 member Turkish kindred with autosomal dominant hypertension, which cosegregates completely with brachydactyly and short stature, was studied. Affected people have severe hypertension and generally die of stroke by the age of 50. The hypertension closely resembles essential hypertension and, accordingly, the mechanisms of blood pressure elevation are unknown. The gene responsible was mapped to chromosome 12p.
METHODS—All 29 affected family members underwent a basic physical examination and funduscopy. Other than markedly elevated blood pressures and the residua of stroke in a few subjects, the apparent lack of end organ damage was striking, including the normal appearing fundi. Five affected individuals were studied in a clinical research unit study. All underwent a complete ophthalmological examination. Fluorescein angiograms were obtained in three subjects.
RESULTS—Systolic blood pressures ranged from 170 to 250 mm Hg, while diastolic blood pressures ranged from 100 to 150 mm Hg in affected individuals. In all affected subjects, the fundi were only minimally altered or clinically normal. All three fluorescein angiograms were normal. Despite severe hypertension since childhood the patients showed no signs of hypertensive retinopathy.
CONCLUSIONS—The absence of hypertensive retinopathy in this novel form of inherited hypertension is due to an altered structure of retinal arteriolar walls or some other protective mechanism. Since evidence of end organ damage is scarce in other organs as well, the protective mechanism appears to be generalised.

Keywords: hypertension; retinopathy; genetics; fundus, fluorescein angiography     

Anterior capsular contraction after cataract surgery in eyes of diabetic patients

AIM—To investigate change in the area of anterior capsular opening (ACO) after cataract surgery and its relation to the degree of postoperative anterior inflammation in patients with diabetes mellitus (DM).
METHODS—31 eyes of 31 patients with DM and 30 eyes of 30 normal controls scheduled to undergo cataract surgery were examined prospectively. The area of ACO was measured with an anterior eye segment analysis system (EAS-1000) on the day following surgery and 3, 6, and 12 months after surgery. Comparative analyses were made on the area of ACO relative to the presence of DM and diabetic retinopathy (DR). The percentage reduction of area of ACO was calculated from values 1 day and 12 months after surgery, and multiple regression analysis was performed on the presence of DM, patient age, ACO area on the first postoperative day, and aqueous flare intensity 1 day and 12 months after surgery.
RESULTS—The area was significantly smaller in the DM group at 3 (p=0.015, Student's t test), 6 (p=0.011), and 12 (p=0.010) months postoperatively. Patients having DR showed significantly smaller ACO area than the non-DR group 3 (p=0.039), 6 (p=0.033), and 12 (p=0.028) months after surgery. Multiple regression analysis revealed that presence of DM (p=0.003) and aqueous flare intensity 12 months after surgery (p=0.039) significantly correlated with the percentage reduction of area of ACO. Age, ACO area at 1 day postoperatively, and aqueous flare intensity immediately after surgery were not relevant to ACO contraction.
CONCLUSIONS—Anterior capsular contraction after cataract surgery was greater in eyes of DM patients, especially in those with DR and increased permeability of the blood-aqueous barrier.

     

Increased presence of Epstein-Barr virus DNA in ocular fluid samples from HIV negative immunocompromised patients with uveitis

AIMS—To investigate whether routine testing for Epstein-Barr virus (EBV) is necessary in the examination of a patient with uveitis.
METHODS—Intraocular EBV DNA was determined in 183 ocular fluid samples taken from patients with AIDS and uveitis, HIV negative immunocompromised uveitis, acute retinal necrosis, toxoplasma chorioretinitis, intraocular lymphoma, anterior uveitis, and miscellaneous uveitis of unknown cause. In 82 samples from this group of patients paired serum/ocular fluid analysis was performed to detect local antibody production against EBV. Controls (n=46) included ocular fluid samples taken during surgery for diabetic retinopathy, macular pucker, or cataract.
RESULTS—Serum antibody titres to EBV capsid antigen proved to be significantly increased in HIV negative immunocompromised patients with uveitis (p<0.01) compared with controls. Local antibody production revealed only three positive cases out of 82 patients tested, two results were borderline positive and one patient had uveitis caused by VZV. EBV DNA was detected in three out of 46 control ocular fluid samples. In the different uveitis groups EBV DNA was noted, but was not significantly higher than in the controls, except in six out of 11 HIV negative immunocompromised patients (p=0.0008). In four out of these six cases another infectious agent (VZV, HSV, CMV, or Toxoplasma gondii) had previously been identified as the cause of the uveitis.
CONCLUSIONS—When comparing various groups of uveitis patients, EBV DNA was found more often in HIV negative immunocompromised patients with uveitis. Testing for EBV does not have to be included in the routine management of patients with uveitis, since indications for an important role of this virus were not found in the pathogenesis of intraocular inflammation.

Keywords: Epstein-Barr virus; intraocular fluid; polymerase chain reaction; uveitis     

Ocular abnormalities in thin basement membrane disease

AIM/BACKGROUND—Alport syndrome is an X linked disease that results in renal failure, deafness, and ocular abnormalities including a dot and fleck retinopathy and anterior lenticonus. The ultrastructural appearance of the glomerular basement membrane in thin basement membrane disease (TBMD) resembles that seen in some patients with Alport syndrome, and in some cases this disease is inherited too. The aim of this study was to determine whether patients with TBMD have any ocular abnormalities.
METHODS—The eyes of 17 unrelated individuals with TBMD were studied by slit-lamp, including biomicroscopic fundus examination with a 78 D lens, by direct ophthalmoscopy, and by fundal photographs. The findings were compared with those in patients with IgA glomerulonephritis or Alport syndrome, and in normals.
RESULTS—No patient with TBMD had a dot and fleck retinopathy or anterior lenticonus. A corneal dystrophy (n = 2) or pigmentation (n = 1), and retinal pigment epithelial clumping and maculopathy (n = 1) were noted. Corneal, lens, and retinal dots were found in five (29%), three (18%), and 16 (94%) patients, respectively, but these were also demonstrated in individuals with other renal diseases and in normal individuals.
CONCLUSIONS—The dot and fleck retinopathy and anterior lenticonus typical of Alport syndrome do not occur in TBMD. The protein abnormality and genetic defect in TBMD are not known, but the lack of ocular lesions suggests that the abnormal protein in this disease is more sparsely distributed or less important in the basement membranes of the eye than of the kidney. Alternatively, the protein may be less affected by the mutations responsible for TBMD.

     

Retinal thickness variation in the diabetic patient measured by the retinal thickness analyser

AIM—To evaluate the potential of the retinal thickness analyser (RTA) as an objective tool for assessment and follow up of diabetic macular oedema.
METHODS—A prototype of the RTA that operates on the principle of laser slit biomicroscopy was used. Retinal thickness was obtained in 41 eyes of 41 diabetic patients. The clinical diagnosis was cystoid macular oedema (CMO) in 10 eyes, clinically significant macular oedema (CSMO) without retinal cysts in 21 eyes, and "dry" macula following grid pattern laser treatment in 10 eyes. The control group consisted of 46 eyes of age matched healthy volunteers.
RESULTS—In normal eyes (46 eyes), the foveal thickness measured was 178 (SD 44) µm and the macular thickness around the fovea was 311 (51) µm. The eyes with CMO displayed the largest foveal thickening, 875 (287) µm (390% increase compared with normal values). The average thickness of the fovea in the non-cystoid CSMO group was 427 (175) µm (144% increase compared with normal fovea). The average thickness of the foveal centre in eyes judged as having "dry" macula after laser treatment was 315 (71) µm (77% increase compared with normal value and a 26% decrease in thickness compared with the CSMO eyes). Statistically significant differences were found in central thickness between these four groups (p = 0.0001). The average thickness at 500 µm surrounding the fovea was 566 (202) µm in the CSMO eyes compared with 311 (51) µm in normal eyes (80% increase). The "dry" macula group (after undergoing laser treatments) had an average thickness of 414 (94) µm (27% decrease compared with CSMO eyes and a 33% increase compared with eyes of healthy controls).
CONCLUSIONS—RTA is a system for quantifying macular thickness and imaging of macular pathology. The system can be a useful tool for diagnosis of macular diseases and for evaluation of the effect of treatment modalities.

Keywords: diabetic retinopathy; retinal thickness; macular oedema; retinal imaging