Transient hypothyroidism after iodine‐131 therapy for Graves' disease

We studied 355patients withGrave's disease tocharacterize transient hypothyroidism andits prognostic valuefollowing 1311 therapy. Methods:Thepatients received therapeutic 1311 treat mentasfollows:333received a dose 10mCi(12.8Â± 2.9mCi).Diagnosis of transienthypothyroidism wasbasedon lowT4, regardless of TSHwithinthefirstyearafter1311 followed byrecovery ofT4and normalTSH.Results:Afteradministration of 10 mCi)of 1311. lodine-131 uptake >70% at 2 hr before treatment was a risk factorfor developing transienthypothyroidism (Oddsratio2.8, 95%confidence interval0.9â€”9.4). At diagnosis of transient hy pothyroidism, basalTSHlevelswerehigh(51%),normal(35%) or low (14%);therefore, thetransienthypothyroidism wasnot Centralized. If hypothyroidism developed duringthefirst6 mo afterbasalTSH>45mUiliter ruledouttran&ent hypothyrokfism. Conclusion:Thedevelopment oftransient hypothyroidism and itshormonal pattern didnotinfiuenoe long-term thyroid function. Sincenoprognostic factorsreliably predicted transient hypothy roidism before1311 oratthetimeof diagnosis, Ifhypothyroidism appearswithin the first monthsafter 1311, the reevaluationof thyroidfunctionlateriswarranted to avoidunnecessary chronic re@acement therapy.

Sirs, We read the paper by Bülow et al. (1997) where an increased cerebrovascular mortality was found in patients with hypopituitarism, with much interest. This is in agreement with our previous finding (Rosén & Bengtsson, 1990), although premature death from cardiovascular disease was more pronounced in our study.
We have hypothesized that untreated growth hormone deficiency (GPD) is the principal factor behind this increased cardiovascular mortality. Further studies have linked several cardiovascular risk factors such as hyperlipidaemia, hypertension, overweight, truncal obesity (Rosén et al., 1993), insulin resistance (Johansson et al., 1995), elevated fibrinogen levels and decreased fibrinolysis (Johansson et al., 1994), but not smoking (Rosén et al., 1993), to the adult GHD syndrome. However, it is unclear to what extent the individual risk factors explain the premature cardiovascular mortality. The major risk factors for coronary heart disease (CHD) are hyperlipidaemia, smoking and hypertension. The increased prevalence of treated hypertension noted among our hypopituitary patients with GHD (Rosén et al., 1993) was counterbalanced by decreased smoking.
Serum total cholesterol concentrations were not elevated among the GHD patients (6·16 mmol/l; males and 6·48 mmol/l; females compared with the general population (6·17 mmol/l;

525
᭧ 1998 Blackwell Science Ltd males and 6·22 mmol/l; females). To study the role of increased triglycerides and decreased HDL cholesterol concentrations noted among the GHD patients, we have used data obtained from the Framingham Study, which predicts the risk of CHD from triglyceride and HDL cholesterol levels (Castelli, 1986). The mean serum concentrations of triglycerides and HDL cholesterol in both GHD patients and controls (MONICA-Study, Göteborg, Sweden, N ¼ 1019; age groups 35-64 years) in a previous study (Rosén et al., 1993) are shown in Table 1.
According to the Framingham model (Fig. 1a, b) the male GHD patients had 'low' HDL cholesterol and 'high' triglycerides levels, in contrast to the 'high' HDL cholesterol and 'medium' triglycerides levels noted in the male controls. The female GHD patients had 'medium' levels of both HDL cholesterol and triglycerides, while the female controls had 'high' HDL cholesterol and 'medium' triglyceride levels. The triglycerides-HDL cholesterol results for both male and female GHD patients and controls were then placed into the appropriate Framingham 'boxes', which thus predict the incidence of CHD by the level of HDL cholesterol and triglycerides.
The male GHD patients had an estimated CHD incidence of about 130 events/1000 individuals, compared with the incidence of 40 events/1000 individuals among the male controls. The CHD incidences for the female GHD patients and controls were 47 events/1000 individuals and about 10 events/ 1000 individuals, respectively. According to these calculations both male and female GHD patients had at least a twofold increase in the CHD risk compared with healthy controls. As the calculations are based upon an American risk function and used in Swedish GHD patients, the absolute risks may be somewhat biased, but the estimations of relative risk are less open to criticism. Thus, our data indicate that the disturbed lipid pattern plays a major role in the premature cardiovascular mortality among adult hypopituitary patients with GHD.

Transient hypothyroidism after iodine-131 therapy for Graves' disease
Sirs, We read with interest the article by Aizawa et al. (1997) dealing with the finding of transient hypothyroidism after iodine-131 therapy for Graves' disease. The authors report transient hypothyroidism in 15% of patients treated, which is similar to values reported previously (Dorfman et al., 1977;Sawers et al., 1980;Connell et al., 1983;Gómez et al., 1995).
In the study of Aizawa et al. (1997) the prevalence of permanent hypothyroidism 1 year after iodine-131 therapy was 11% compared with 33% in our experience with individualized dose of iodine-131 and their prevalence of hyperthyroidism at 1 year was 42·3% vs. 26·1% in our study (Gómez et al., 1995). This important difference in the outcome between the two studies may be due to deficient iodine intake in our country (Serra-Majem et al., 1993).
Their results suggest that measurement of TSAb activity at the onset of hypothyroidism may differentiate transient for permanent hypothyroidism. In our experience basal TSH levels were high at the onset of transient hypothyroidism in 51% of cases, normal TSH in 35% and low TSH in 14% and no patient with basal TSH higher than 45 mU/l had transient hypothyroidism. Thus TSH plays some role in the recovery of hypothyroidism.
Our results and the results of Aizawa et al. (1997) do not support the hypothesis that transient hypothyroidism is a central hypothyroid phase during recovery of the hypothalamic axis after iodine-131 treatment, as suggested by Uy et al. (1995). A slow decrease in thyroid function in the first months due to imbalance between radiation damage and higher TSAb and TSH activity is presumably relevant in these patients and in some of them a sluggish response of the pituitary thyrotrophs to the presence of low serum thyroid hormone levels might therefore be expected.
The final outcome in our patients showed that thyroid function did not differ from that of patients without previous transient hypothyroidism and was independent of TSH levels during the transient hypothyroid phase.
Although the mechanisms underlying transient hypothyroidism are not homogeneous and its occurrence was not a prognostic indicator of future thyroid function, its clinical significance lies in accurate diagnosis.