Thirty-two rabbits were immunized by subcutaneous human serum albumin in Freund's adjuvant and challenged after four weeks by intracorneal injection in both eyes. On a random and blind basis, one of the eyes in each animal received three consecutive injections of antilymphocyte serum obtained from rats and the other eye the same dose of normal rat serum. Statistical analysis of results showed no significant difference between both treatments. Two eyes treated with antilymphocyte serum had limbal necrosis with uveal prolapse.
Purpose: Are central corneal thicknes values in ocular hypertensive patients comparable to that of non‐diabetic patients?. Is there some influence of diabetic disease on these values? Methods: A samle of 271 patients has been distributed in 4 groups: 77 normal control patients (N), 74 ocular hypertensive (OHT), 59 diabetic patients without ocular hypertension (DM) and 61ocular hypertensive type II diabetic patients (DMOHT). Time from diagnosis and diabetes treatment are recorded. Also central corneal thickness (CCT), intraocular pressure (IOP) and diabetic retinopathy stage are also recorded. SPSS 14.0 statistical program was used and one‐factor ANOVA, Kruskal‐Wallis and chi‐square tests, and Pearson calculation have been applied. Results: Mean CCT in N group (536,50±38,1μ), and mean CCT in DM group (545,49±29,06μ) are not statistically different. Mean CCT in DMOHT group (570,45±33,59μ) and mean CCT for OHT group (570,51±38,26μ) are not statistically different. Mean ECC difference between diabetic and non‐diabetic subgroups is not statistically significant. However, the mean ECC difference between ocular hypertensives and ocular normotensives subgroups is highly significant in both eyes (P < 0,000). Diabetes treatment has not influence on mean CCT intergroup comparisons. CCT and IOP correlate significantly in the whole sample for both eyes (P < 0,000). There was no linear correlation between mean CCT and age, nor between mean CCT and time of diagnosis. Conclusions: Like OHT patients, DMOHT patients showed thick corneas. DM patients have normal CCT. Neither diabetes treatment, nor time of diagnosis are correlated to CCT. Corneal thickness is probably not related to the disease in DMOHT patients.
Purpose: Goldmann applanation tonometry readings are affected by central corneal thickness. We have determined the level of pachymetric and tonometric asymmetry in normal, diabetic, ocular hypertensives and diabetic ocular hypertensive patients, and the relationship between both asymmetries. Methods: Four groups, one of 77 normal patients (N), one of 59 type II diabetic patients (DM), one of 74 patients with ocular hypertension (OHT), and one group of 61 type II diabetic ocular hypertensive patients (DMOHT) have been included. Ocular exploration, including ultrasound pachymetry, has been performed in all of them. Time from diagnosis and current treatment are also recorded. Interocular differences are analyzed by the SPSS 14.0 program using ANOVA and Pearson tests. Results: The pachymetric asymmetry between groups is not significant (ANOVA P < 0,072). The difference between pachymetric assymetry in diabetic patients (DM+DMOHT) 6,83±5,45μ and non‐diabetic patients (N+OHT) 5,50±5,01μ is statistically significant (P < 0.037). This difference is not significant between ocular hypertensives (OHT+DMOHT) and ocular normotensives (N+DM) (P < 0,982). There is not linear correlation between pachymetric and tonometric asymmetry in the whole sample (r = 0,003). Pachymetric asymmetry correlates with time from diagnosis, and asymmetry is bigger under treatment with insuline, and in retinal proliferative stages. IOP asymmetry correlates with time from diagnosis, is bigger for insuline treated patients and is similar through the different stages of retinopathy. Conclusions: Pachymetric asymmetry is not related to tonometric asymmetry in this study. Diabetic patients showed bigger pachymetric asymmetry than non diabetic patients, but is not related to tonometric asymmetry.
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