MANAGEMENT OF DYSTHYROID EYE DISEASE

Once the diagnosis of thyroid eye disease has been made the doctor's problems begin because the management is long term with a condition that has many ramifications over a period of years. Short-term heroics to save vision by use of high-dose systemic steroids, orbital decompression or radiotherapy may have to be followed by control of diplopia by muscle surgery and prisms. Lid retraction, both upper and lower, may merit surgery, and even those patients who have come to terms with their facial appearance may still complain of lacrimation, irritation and grittiness. The advantages of a thyroid clinic, run jointly by a physician and an ophthalmologist, are presented and the patient is helped to live with this distressing condition.     

Platelet function in diabetes mellitus in relationship to complications, glycosylated haemoglobin and serum lipoproteins

Mean levels of beta-thromboglobulin and platelet factor 4 were highly significantly elevated in diabetes compared to controls (72.6 v. 36.3 ng/ml, P less than 0.0005; 48.5 v. 16.5 ng/ml, P less than 0.0005; respectively) as was malondialdehyde formation (12.4 v. 8.1 nmol/10(9) platelets, P less than 0.0005). Diabetes with retinopathy had significantly higher levels of beta-thromboglobulin than those without retinopathy (79 v. 70 ng/ml; P less than 0.042). However, those diabetics without clinical evidence of vascular disease had levels of beta-thromboglobulin and platelet factor 4 significantly higher than controls. beta-Thromboglobulin did not correlate with glycosylated haemoglobin but did correlate significantly with individual lipid and lipoprotein levels (beta-thromboglobulin v. total triglyceride, P less than 0.029; v. VLDL triglyceride, P less than 0.041; v. LDL cholesterol, P less than 0.042; v. HDL/total cholesterol ratio, P less than 0.02). Abnormal platelet function may contribute to the vascular complications of diabetes mellitus.     

IMMUNOGENETICS OF GRAVES'' OPHTHALMOPATHY

We have performed an immunogenetic analysis of 53 patients with severe Graves' ophthalmopathy, 51 patients with Graves' disease but little or no clinically apparent eye disease, and 90 controls. The distribution of restriction fragment length polymorphisms was analysed in the three groups, using probes for the HLA-DQ alpha and DR beta regions, the T-cell receptor C alpha, V alpha, C beta and J gamma genes and the immunoglobulin gene switch regions, S alpha and S mu. There was no abnormal distribution of these polymorphisms in either group of Graves' patients, or differences between the Graves' patients with or without eye disease. It was possible to assign HLA-DR types in most patients using the polymorphisms found after probing with DQ alpha and DR beta; there was no abnormal distribution of DR types (including HLA-DR3) assigned by restriction fragment polymorphisms in the two Graves' groups. These results fail to confirm the reported associations between ophthalmopathy and HLA-DR3 and between Graves' disease and the T-cell receptor C beta polymorphism; they also argue against a strong influence of Gm allotypes in Graves' disease since these genes are in linkage disequilibrium with the S alpha polymorphisms. The association of Graves' disease with HLA-DR3, defined hitherto using serological reagents, may be less strong than previously described.     

Effects of Chronic Left Vagal Stimulation on Visceral Vagal Function in Man

We examined the effects of chronic left vagal electrostimulation on afferent and efferent gastrointestinal vagal function in eight patients. Afferent function was assessed using cortical evoked responses to electrical stimulation of the esophagus and to direct vagal stimulation using the implanted left vagal electrode. Efferent gastrointestinal vagal function was measured by examining the basal, maximal, and sham fed stimuJated gastric acid output prior to and with chronic left vagal electrostimulation. Esophageal electro-stimulation produced a cortical evoked response consisting of three negative and three positive peaks within 400 msec after stimulation. Prior to vagal eJectrostimulation the mean conduction velocity of the afferent signal was measured at 8.72 ± 3.39 m/sec, compatible with A-delta fibers involvement. Basal, maximal, and sham fed acid output were 1.11, 21.87, and 9.37 mmol/hour, respectively. The evoked response to esophageal electrical stimulation was not changed with chronic left vagal electrostimulation. Direct vagal stimulation also produced evoked potentials that were comparable to those obtained with esophageal stimulation. The mean conduction velocity was 6.26 ± 2.72 m/sec (NS) so that there was no evidence of loss of myelinated fibers with chronic stimulation. No differences were detected in basal (1.29 mmol/h), maximal (21.64 mmol/h), or sham fed stimulated (8.03 mmol/h) acid output, showing that vagal electrostimulafion has no effect on either total or vagally mediated acid output, an efferent vagal function. In conclusion, chronic left vagal electrostimulation has no significant adverse effect on gastrointestinal vagal function.     

Cognitive evoked potentials to anticipated oesophageal stimulus in humans: quantitative assessment of the cognitive aspects of visceral perception

Evoked potential studies provide an objective measure of the neural pathways involved with perception. The effects of cognitive factors, such as anticipation or awareness, on evoked potentials are not known. The aim was to compare the evoked potential response to oesophageal stimulation with the cortical activity associated with anticipation of the same stimulus. In 12 healthy men (23.5 +/- 4 years), oesophageal electrical stimulation (15 mA, 0.2 Hz, 0.2 msec) was applied, and the evoked potentials recorded using scalp electrodes. A computerized model of randomly skipped stimuli (4:1 ratio) was used to separately record the evoked potentials associated with stimulation and those associated with an anticipated stimulus. The electrical stimulus represented the nontarget stimulus and the skipped impulse the target (anticipatory) stimulus. This anticipatory evoked potential was also compared to auditory P300 evoked potentials. Reproducible evoked potentials and auditory P300 responses were elicited in all subjects. Anticipatory evoked potentials (peak latency 282.1 +/- 7.9 msec, amplitude 8.2 +/- 0.7 microV, P < 0.05 vs auditory P300 evoked potential) were obtained with the skipped stimulus. This anticipatory evoked potential was located frontocentrally, while the auditory P300 potential was located in the centro-parietal cortex. The anticipatory evoked potential associated with expectation of an oesophageal stimulus, although of similar latency to that of the auditory P300 evoked response, originates from a different cortical location. The recording of cognitive evoked potentials to an expected oesophageal stimulus depends on attention to, and awareness of, the actual stimulus. Anticipatory evoked potentials to GI stimuli may provide an objective electrophysiological tool for the assessment of the cognitive factors associated with visceral perception.     

ISOLATION AND PROPERTIES OF A TRYPTOPHAN-CONTAINING PEPTIDE FROM BOVINE AND TURKEY BRAINS

A tryptophan-containing peptide has been isolated from bovine cerebral hemispheres. A similar peptide has also been isolated from the turkey brain. Isoelectric focusing on polyacrylamide gels shows the peptides to be essentially homogeneous. Both peptides consist of 67 amino acids with isoleucine at the COOH-terminus. The NH₂-terminal residues cannot be detected by end-group analysis. Both peptides exhibit 45–50%α-helix as revealed by circular dichroism spectra.