| Gunji et al., Naples, Italy, Pittsburg, PA and San Francisco, CA, USA tested the presence of circulating antibodies against the flavoprotein (Fp) subunit of mitochondrial succinate dehydrogenase. This eye muscle protein has been suggested to play a central role in the development of TAO. Sera were screened of 20 patients with Graves’ disease during 12 months of antithyroid drug treatment. Patients were with or without TAO and/or eye muscle dysfunction. The authors reported the presence of anti-Fp subunit antibodies in 73% of patients with active ophthalmopathy and eye muscle involvement, but in only 25% of patients with active ophthalmopathy if there was no eye muscle involvement. In chronic TAO these values were respectively 0 and 11%. Positive antibodies were present in 14% of patients with Graves’disease without TAO and in 12% of normal subjects. (Comment: There is still controversy with regard to the question if Fp subunits play a central role in the development of TAO or that antibodies against this protein are an epiphenomenon of this autoimmune condition. The fact that in no less than 14% of healthy controls antibodies are present, is somewhat disturbing.) The same group of investigators tested the presence of circulating antibodies against a 55 kDa protein, also suggested to be a key autoantigen in TAO. This antigen resembles the calcium binding proteins and was found to be present in eye muscle and other skeletal muscle and thyroid but not in other tissues. Antibodies were present in 92% of patients with TAO and eye muscle dysfunction compared to 52% of patients with TAO but no apparent eye muscle involvement. Antibodies were also detected in 36% of patients with Graves’ hyperthyroidism without TAO, in 17% with Hashimoto’s disease, in 23% of patients with type I diabetes and in 16% of normal subjects. Antibodies against this antigen were detected earlier in the course of disease than against the Fp subunit. (Comment: The results of this study are very similar to those of the previous report in that the distribution of the antibodies over the different patients group seemed to be about the same. An interesting question is if there is structure homology between the two antigens to explain this similarity.) Benker et al., Essen, Germany, reported the results of a multicentered study comprising 313 patients with Graves’disease who were treated with either 10 or 40 mg methimazole daily supplemented if necessary with T4, with regard to the effect of these two regimens on TAO. TAO was present in 42% of patients with equal distribution of numbers and grades of severity over the two regimens. The results showed that there was no different effect with regard to the course of TAO between the two groups. Taken the results of these regimen groups together during the first two years of treatment, TAO developed or worsened in 63 patients while in 69 patients TAO signs improved. Inzerillo et al., New York, NY, USA, investigated the environmental versus genetic influences on the development of severe (at least class IIIa-nospecs) TAO in 52 consecutive patients, of whom 69% were Caucasians, 23% African Americans, 3% Hispanic, and 2% Asian. Treatment consisted of antithyroid medication alone in 23%, radioactive iodine in 71%, and surgery in 6% of patients. Seventy-five percent of patients were on T4 replacement, 60% were smokers and 38% had a family history of autoimmune thyroid disease. The segregation ratio for autoimmune thyroid disease was 0.114 overall and 0.156 in females. Only 2 of 52 patients had a family history of severe TAO. From the presented data it was concluded that environmental factors rather than major genetic influences are more likely to predispose for severe TAO. (Comment: This conclusion does not suggest however that in the autoimmune process per se, but rather in the severity of TAO, environmental factors are more important than genetic factors.) Quadbeck et al., Essen, Germany, assessed the influence of smoking on the course of TAO under antiinflammatory therapy. They divided smokers in three groups: light (1–10 cigarettes per day, n = 9), moderate (10–20 cigarettes per day, n = 20), and heavy (more than 20 cigarettes per day, n = 3). The results were compared with a group of 54 non-smokers. At initial presentation smokers showed more often edema (64/66 eyes) than non-smokers (93/108 eyes, p < 0.02). There was no difference with respect to other eye symptoms and improvement of eye signs was independent of cigarette consumption, indicating that smoking ultimately does not adversely affect treatment outcome. (Comment: Apparently smokers present with little more edema than non-smokers but differences disappear during treatment. Isn’t smoking after all that bad for eyes in Graves’ disease?) |
