Orbital phlebography in the diagnosis of painful ophthalmoplegia

Three cases of painful ophthalmoplegia have been described in which symptoms suggesting a tumor of the orbit justified neuroradiological assessment. Phlebography in each case revealed stenosis of the superior ophthalmic vein in its third portion, and non-opicification of the cavernous sinus. Hirtz incidences revealed contralateral cavernous sinus opacification and venous drainage through the coronary sinus. These neuradiological findings helped to differentiate this syndrome from other affections which have similar signs and symptoms.     

Lack of relationship between 11beta-hydroxysteroid dehydrogenase setpoint and insulin sensitivity in the basal state and after 24h of insulin infusion in healthy subjects and type 2 diabetic patients

OBJECTIVES: To test whether insulin resistance in type 2 diabetes mellitus is associated with an altered overall setpoint of the 11beta-hydroxysteroid dehydrogenase (11betaHSD) mediated cortisol to cortisone interconversion towards cortisol, and to evaluate whether changes in insulin sensitivity induced by antecedent hyperinsulinaemia are related to changes in the 11betaHSD setpoint. PATIENTS AND MEASUREMENTS: The urinary ratio of (tetrahydrocortisol + allo-tetrahydrocortisol)/tetrahydrocortisone ((THF + allo-THF)/THE) and of free cortisol/free cortisone (UFF/UFE), as well as the plasma cortisol/cortisone ratio were measured in 8 male type 2 diabetic patients and 8 healthy male subjects without and after 24 h of insulin infusion. Insulin was infused at a rate of 30 mU/kg/h with blood glucose being clamped at euglycaemic levels in healthy subjects and at isoglycaemic levels in diabetic patients. Insulin sensitivity was assessed by measurement of whole body glucose uptake (M-value) during a 3-4 h euglycaemic clamp, directly after the 24 h insulin infusion and compared to the M-value on a control day, at least 1 week apart from the 24 h insulin infusion. RESULTS: Despite impaired insulin sensitivity (M-value, 11.6 +/- 7.7 vs. 28.5 +/- 11.6 micromol/kg/minutes, in type 2 diabetic and healthy subjects, respectively, P < 0.05), urinary (THF + allo-THF)/THE ratio and baseline plasma cortisol/cortisone ratio at 0800 h were similar in type 2 diabetic patients (0.82 +/- 0.07 and 3. 77 +/- 0.70, respectively) and healthy subjects (0.76 +/- 0.14 and 3. 81 +/- 0.88, respectively, ns). Insulin sensitivity was not correlated with urinary (THF + allo-THF)/THE ratio nor with baseline plasma cortisol/ cortisone. In type 2 diabetic patients, insulin sensitivity was further impaired by antecedent hyperinsulinaemia (P < 0.05), but the urinary (THF + allo-THF)/THE ratio (0.80 +/- 0.14, ns) and the plasma cortisol/cortisone at 0800 h (3.66 +/- 0.72, ns) did not change. In healthy subjects, insulin sensitivity did not change significantly (M-value, 22.5 +/- 9.7 micromol/kg/minutes, ns), although the urinary (THF + allo-THF)/THE ratio (0.92 +/- 0.25, P < 0.05) and the plasma cortisol/cortisone (4.59 +/- 0.63, P < 0.05) increased. Insulin did not affect the UFF/UFE ratio in either group. CONCLUSION: The present study does not support the hypothesis that insulin resistance in type 2 diabetes mellitus is associated with an overall change in the 11betaHSD set point towards cortisol. In view of the stimulatory effects of insulin and cortisol on adipogenesis, long-term stimulation of 11betaHSD reductase activity by insulin could aggravate visceral obesity.     

Plasma cholesteryl ester transfer and hepatic lipase activity are related to high-density lipoprotein cholesterol in association with insulin resistance in type 2 diabetic and non-diabetic subjects

We evaluated the hypothesis that plasma cholesteryl ester transfer (CET) and lipase activities are influenced by insulin sensitivity and contribute to the low high-density lipoprotein (HDL) cholesterol observed in type 2 diabetic patients and insulin-resistant non-diabetic subjects. Sixteen type 2 diabetic and 16 non-diabetic subjects participated. Diabetic and non-diabetic subjects were divided in equal groups of eight subjects with low or high insulin sensitivity, which was documented as the glucose infusion rate (M-value) during the last hour of a 3-h euglycaemic hyperinsulinaemic clamp (150 mU kg(-1) h(-1), blood glucose target 4.6 mmol L(-1)). Post-heparin plasma lipoprotein lipase (LPL) and hepatic lipase (HL) activities were measured in samples obtained 1-2 weeks before the clamp. Plasma CET was measured by a radioisotope method. Compared to non-diabetic men with high insulin sensitivity (n = 8) HDL cholesterol was lower in type 2 diabetic men (n=8, p<0.01) and non-diabetic men (n=8, p <0.05) with low insulin sensitivity, and the HDL cholesterylester content was lower in type 2 diabetic men with high insulin sensitivity (n=8, p<0.05). In non-diabetic subjects with high insulin sensitivity, plasma CET was lower than in the other groups (p<0.05 for all). Multiple regression analysis showed that plasma CET (p=0.001) and HL activity (p=0.02) were independently and negatively associated with the M-value. No association between the M-value and LPL activity was observed. Independent negative relationships of HDL cholesterol with plasma CET (p = 0.04) and HL activity (p=0.03) were observed. This study supports the hypothesis that a low HDL cholesterol associated with insulin resistance in type 2 diabetic and non-diabetic subjects is related to a high plasma CET and a high HL activity.     

Impact of ocular graft‐versus‐host disease on visual quality of life in patients after allogeneic stem cell transplantation: questionnaire study

Purpose: To determine the influence of ocular complications on quality of life (QoL) 3 years after allogeneic stem cell transplantation (allo‐SCT). Methods: All 54 adult patients that underwent and survived allo‐SCT in 2006/2007 in our centre received two questionnaires (VFQ‐25: visual function questionnaire‐25 and OSDI: ocular surface disease index). In addition, the following data were included: gender, age, underlying disease, presence of chronic and/or ocular graft‐versus‐host disease (GVHD), number of visits to an ophthalmologist, manifestations of dry eye disease, the duration of follow‐up and treatment for ocular GVHD. Results: Ocular GVHD developed in 26% (14 of 54) of patients and 71% (10 of 14) received treatment for ocular GVHD. The presence of ocular GVHD correlated with the severity of systemic GVHD (correlation coefficient: 0.52, p = 0.00). The Karnofsky scores were significantly lower in the patients with ocular GVHD compared to the patients with no ocular GVHD (p = 0.001). Karnofsky scores were weakly correlated with the severity of systemic GVHD (correlation coefficient: 0.25, p = 0.03. Three years after the all‐SCT, OSDI and VFQ‐25 scores were significantly impaired in patients with ocular GVHD [mean: 76.5; range (46.1–100) and mean: 31.1; range (0–72.9)] compared to patients with no ocular GVHD [mean: 89.4; range (45.2–100) and mean: 12.9; range (0–58.3); p = 0.02]. The scores of the VFQ‐25 were significantly lower in the domains of general health, ocular pain, social functioning and role difficulties. Conclusion: The long‐term vision‐related QoL measured by the OSDI and VFQ‐25 was impaired in patients with ocular GVHD.     

Plasma phospholipid transfer protein activity is lowered by 24-h insulin and acipimox administration: blunted response to insulin in type 2 diabetic patients.

Cholesteryl ester transfer protein (CETP) transfers cholesteryl esters from HDL to VLDL and LDL. Phospholipid transfer protein (PLTP) transfers phospholipids between lipoproteins, converts HDL3 into larger and smaller particles, and is involved in pre-beta-HDL generation. We examined the effects of 24-h hyperinsulinemia (30 mU x kg(-1) x h(-1)) and 24-h Acipimox (250 mg/4 h) on plasma lipids as well as CETP and PLTP activities (measured with exogenous substrate assays) in eight healthy and eight type 2 diabetic subjects. After 24 h of insulin, plasma free fatty acids (FFAs), HDL cholesterol, and plasma apolipoprotein AI decreased in healthy subjects and type 2 diabetic patients (P < 0.05). Plasma triglycerides did not significantly change in either group. After 24 h of Acipimox, all parameters, including plasma triglycerides, decreased in both groups (P < 0.05). Insulin decreased plasma PLTP activity by 17.6% after 24 h in healthy subjects (P < 0.05) and 10.2% in diabetic patients (P < 0.05 vs. baseline; P < 0.05 vs. healthy subjects). Acipimox lowered PLTP activity by 10.3% in healthy subjects (P < 0.05) and 11.3% in diabetic patients (P < 0.05). When insulin was infused for 3 h after Acipimox, a further decrease was found only in healthy subjects. Plasma CETP activity decreased by 9.5% after 24 h of insulin in healthy subjects (P < 0.05), but not in diabetic patients. Acipimox did not decrease plasma CETP activity in either group. In healthy subjects, the PLTP responses with insulin and Acipimox were larger than the changes in CETP activity (P < 0.05). These findings suggest that there is a metabolic link between the regulation of plasma FFA and PLTP, but not CETP. The PLTP response to insulin is blunted in type 2 diabetes.