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HB Shahbazian, F Sarvghadi, and F Azizi

OBJECTIVE: To determine the prevalence of postpartum thyroiditis (PPT), one of the autoimmune disorders of the thyroid which usually occurs in women in the first year after parturition. PPT presents with periods of transient thyrotoxicosis and hypothyroidism, in many cases resulting in permanent hypothyroidism. DESIGN: The study involved 1040 mothers who had contacted five health centers in Tehran for vaccination of their children. METHODS: Signs and symptoms of hypothyroidism and thyrotoxicosis, and the presence of goiter (using the World Health Organization classification), were sought. Serum T3, T4, TSH, anti-TPO and anti-Tg antibodies were measured at 3, 4.5, 6 and 9 months after parturition. In those with hypothyroidism or thyrotoxicosis and a matched group of normal women, thyroid sonography was performed. RESULTS: The prevalence of thyroiditis was 11.4%. Hypothyroidism and thyrotoxicosis occurred in 68 and 42 mothers respectively. Nine had thyrotoxicosis followed by hypothyroidism. There was one case of Graves' disease. Out of 68 hypothyroid patients, 33 women underwent treatment with levothyroxine (because of the severity of symptoms) for 12 months. Six women showed increased TSH at 6 weeks after discontinuation of thyroxine. Stage II goiter (World Health Organization classification) were observed in 21.8% of patients and in 6.7% of pospartum euthyroid women (P<0.001). Positive anti-TPO was found in 61.5% of patients and in 19% of the control group; positive anti-Tg was found in 58% of patients and in 6% of the control group (P<0.001). Sonographic changes were observed in 96% of the patients and in 7% of the control group (P<0.001). There was no significant correlation between the occurrence of thyroiditis and parity, the age of the mother, a previous history of thyroid disease in the patient or family, breast-feeding, or the gender of the child. CONCLUSION: The results of this study show a high prevalence of PPT in Tehranian women. This may be due to the length and frequency of follow-up and/or the transition from low to adequate iodine intake. The major difference with respect to other studies is the low frequency of the biphasic form of PPT.

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N. J. B. Christiansen, K. Siersbæk-Nielsen, J. E.M. Hansen, and L. Korsgaard Christensen


Serum thyroxine (T4) and other thyroid function tests were studied in 14 patients with subacute thyroiditis and compared with the same parameters in 32 patients with untreated thyrotoxicosis. The mean values of serum T4 and protein-bound iodine (PBI) were found to be elevated to the same extent in the two groups and the calculated T4 iodine did not differ significantly from the PBI in any of the groups. The resin-T3-test and the basal metabolic rate (BMR) mean values were significantly lower in patients with subacute thyroiditis than in patients with thyrotoxicosis. The serum T4 determination based on competitive protein-binding was not influenced by other organic iodinated products, and our results indicate that the elevated serum PBI in subacute thyroiditis is largely due to T4. The lower BMR in patients with subacute thyroiditis is possibly explained by a difference in the thyroxine binding protein (TBP) binding capacity and free T4 in the serum between patients with subacute thyroiditis and those with thyrotoxicosis.

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Allan Carlé, Nils Knudsen, Inge Bülow Pedersen, Hans Perrild, Lars Ovesen, Lone Banke Rasmussen, and Peter Laurberg


To characterize thyroid hormone levels at the time of diagnosis in the nosological types of thyrotoxicosis diagnosed in the population and to analyze determinants for serum thyroxine (T4) and tri-iodothyronine (T3).


Population-based study of thyrotoxicosis at disease onset.


In the period 1997–2000, we prospectively identified all patients diagnosed with incident primary overt thyrotoxicosis in a Danish population cohort and classified patients into ten well-defined nosological types of disease (n=1082). Untreated levels of serum T3, T4, and T3:T4 ratio were compared and related to sex, age, level of iodine deficiency, smoking status, alcohol intake, iodine supplement use, co-morbidity, and TSH receptor antibodies (TRAbs) in multivariate models.


Graves' disease (GD) patients had much higher levels of T3 and higher T3:T4 ratio at diagnosis compared with other thyrotoxic patients, but with a profound negative association between hormone levels and age. In GD, patients diagnosed in the area with more severe iodine deficiency had lower levels of T3 and T4. TRAb-negative GD patients had biochemically mild thyrotoxicosis. Higher age was also associated with lower degree of biochemical thyrotoxicosis in nodular toxic goiter. We found no association between serum T3 and T4 and sex, smoking habits, iodine supplements, alcohol intake, or co-morbidity in any type of thyrotoxicosis.


The study gives new insight into the hormonal presentation of thyrotoxicosis and showed that young age, positive TRAb levels, but also residency in the area with higher iodine intake was positively associated with biochemical disruption in GD.

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Per Anders Dahlberg and Rolf Jansson

Abstract. During a 4 year period 19 women with post-partum onset of thyroid dysfunction have been seen in our clinic. Five women had high radioiodine uptake thyrotoxicosis (Graves' disease). Twelve women had hypothyroid symptoms starting within 3–6 months of delivery. All of these women had thyroid microsomal and/or cytoplasmic autoantibodies and thyroid lymphocytic infiltration suggesting aggravation of pre-existing subclinical autoimmune thyroiditis (Hashimoto's disease). At follow-up thyroid function gradually improved in all but signs of persistent thyroid hypofunction remained in seven. Thus women developing symptomatic postpartum hypothyroidism should be followed regularly and when thyroxine treatment is commenced in the post-partum period, it has to be continued indefinitely in many cases.

Two women presented with transient low radioiodine uptake thyrotoxicosis and a small painless goitre. Thyroid cytology revealed thyroiditis but they had no thyroid autoantibodies. When followed after a succeeding delivery none of these women developed post-partum thyroid dysfunction in contrast to women in the autoimmune group. Probably the aetiology of thyroid dysfunction in these 2 women was different.

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Issac Sachmechi and George C Schussler

Sachmechi I, Schussler GC. Familial dysalbuminemic hyperthyroxinemia in pregnancy. Eur J Endocrinol 1995;133:729–31. ISSN 0804–4643

A 16-year-old pregnant Puerto Rican woman who had been treated for thyrotoxicosis previously was evaluated for goiter, increased total thyroxine (T4) and triiodothyronine (T3) and free T4 estimate, despite a normal thyroid-stimulating hormone (TSH) concentration. These findings are consistent with a TSH-producing pituitary adenoma or the syndrome of generalized thyroid hormone resistance. However, sera from the patient, her mother and subsequently her newborn daughter demonstrated the increased albumin binding of T4 but not T3 that is characteristic of familial dysalbuminemic hyperthyroxinemia (FDH). The free T4 estimate had been elevated artefactually by the increased affinity of FDH albumin for the analog in a one-step assay. The T3 and T4 concentrations were increased by pregnancy and T4 was increased further by FDH. This first report of FDH recognized during pregnancy emphasizes that the effects of pregnancy on thyroid hormone and TSH concentrations complicate the diagnosis of FDH. It is particularly important to distinguish this benign condition from thyrotoxicosis during pregnancy, because inappropriate treatment may affect fetal development.

Issac Sachmechi, Dept. of Medicine, Queens Hospital Center, 82-68 164th Street, Queens, New York, USA

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Harry R. Maxon, Kenneth D. Burman, Bhartur N. Premachandra, I-Wen Chen, Albert Burger, Phillip Levy, and Leon P. Georges


Elevations of serum thyroxine without thyrotoxicosis or binding protein abnormalities have been documented in 8 of 13 family members, representing 4 generations. This syndrome appears to represent an elevated threshold for the amount of free thyroxine substrate required to maintain adequate T3 production form the peripheral monodeiodination of T4. It reiterates the need for a prudent re-evaluation of all clinically euthyroid patients with elevated serum thyroxine concentrations before concluding that they are indeed thyrotoxic.

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C.J. Pearce and R. L. Himsworth

Abstract. Serum concentrations of total thyroxine (T4) and total triiodothyronine (T3) were measured in a group of patients (n = 113) presenting with untreated hyperthyroidism due to Graves' disease and in subjects receiving oral T4 replacement (n = 93) in whom the total T4 concentration was supraphysiological (> 150 nmol/l). The mean total T4 concentration in the hyperthyroid group was 226 nmol/l, sd 59, range 151–420, and the mean total T3 concentration was 6.8 nmol/l, sd 2.73, range 3.1–17.5. For the group receiving T4 the mean total T4 concentration was 175 nmol/l, sd 25, range 150–258, and the mean total T3 concentration was 2.66 nmol/l, sd 0.45, range 1.7–4.2. In the hyperthyroid group a highly significant linear correlation was found between total T4 and total T3, T3 = 0.0354 T4 – 1.21, r = 0.761, P ⪡0.001, while in the patients taking T4 this correlation was less close, T3 = 0.0073 T4 + 1.39, r = 0.398, P⪡0.001. The two groups are readily distinguished by expressing total T4 as a molar ratio of total T3. In the hyperthyroid group the mean T4:T3 ratio was 35.6, sd 7.8, range 19.9–56.1, compared to the patients on T4 where the mean T4:T3 ratio was 67.0, sd 11.7, range 44.3–114 (t = 22.5, P⪡0.0001). An arbitrarily chosen value of 50 for the T4:T3 ratio affords a simple and convenient means of distinguishing the two categories: in only 3 patients with Graves' disease (2.6%) was the ratio above this, and it was below in only 5 patients (5.4%) taking T4. Where there is doubt as to the aetiology of hyperthyroxinaemia this simple operation will differentiate between hyperthyroidism caused by Graves' disease and surreptitious ingestion of T4. In other clinical situations where symptoms of hyperthyroidism are associated with a T4:T3 ratio greater than 50 the combination may suggest subacute thyroiditis or iodide-induced thyroid dysfunction.

Free access

J Rojano, S Sasian, I Gavilan, M Aguilar, L Escobar, and JA Giron

The distribution of peripheral blood CD16/56 cytotoxic T and natural killer (NK) cells in Graves' disease patients is analyzed in order to correlate them with disease activity and with prognosis. Eighteen patients with Graves' disease, twenty-four patients with Hashimoto's thyroiditis and thirty-two sex- and age-matched healthy control subjects were studied. Peripheral blood CD16/56 (cytotoxic T and NK) cells were analyzed by cytofluorometry. A decreased proportion of CD16/56+ and CD16/ 56+CD3+ cells were detected in Graves' disease patients when compared with thyroiditis patients and healthy control groups. No correlation was detected with serum free thyroxine. On diagnosis, patients who would require a radical treatment for thyrotoxicosis control showed a significant decrease of cytotoxic CD56+ T (CD3+) and NK (CD3-) cells compared with those who would maintain the euthyroid state after methimazole. These results suggest that the cytotoxic compartment, both T and NK cells, of the immune system is altered in patients with Graves' disease, independently of the functional thyroid status. Changes in peripheral blood lymphocytes in Graves' disease patients could be useful as predictive markers of an unfavorable outcome.

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Bernhard E. Schreiber, Hugo M. Ortner, Georg Leb, and Otto Eber


An assay of stable 3,5,3′-triiodo-L-thyronine (T3) in serum of 54 patients was performed, using a new simple chromatographic procedure. With samples of 5 ml serum, the lower detection limit was 0.04 μg/100 ml. The total time required for a complete analysis was less than 3 hours, which was accomplished by partial automatization of the procedure. The range of the T3-concentration was 0.22 ± 0.05 (sd) μg/100 ml in 18 normal subjects, 0.67 ± 0.3 in 15 thyrotoxic patients and 0.08 ± 0.04 in 8 patients with hypothyroidism. Among 13 patients with normal serum thyroxine (T4) levels after thyroid surgery owing to thyrotoxicosis, there were 3 with marked increases in serum T3. In spite of normal T4-levels, symptoms of hyperthyroidism were still present in these patients. It is concluded, that serum T3-determinations may be useful for diagnosing cases of hyperthyroidism where clinical findings do not correspond with serum T4 or PBI-findings.

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J. Chakravarty, A. R. Guansing, S. Chakravarty, and C. V. Hughes


Systolic time intervals consisting of indices of electromechanical systole (QS2-I), left ventricular ejection time (LVET-I) and pre-ejection period (PEP-I) were calculated serially during therapy in 12 euthyroid, 9 hypothyroid and 9 hyperthyroid individuals. These parameters were analyzed sequentially together with the changes in serum thyroxine (T4), triiodothyronine (T3) and thyrotrophin (TSH) in order to determine the sensitivity of these non-invasive procedures in monitoring peripheral thyroid hormone effect. The results are expreseed in mean ± sem. QS2-I (506.3 ± 8.2 ms) and PEP-I (102.9 ± 4.2) were shortened (P < 0.02 and P < 0.001, respectively) in hyperthyroidism and prolonged (579.3 ± 7.3 and 169.6 ± 3.6 ms) in hypothyroidism (P < 0.01 and P < 0.001, respectively) compared to euthyroid controls (538.1 ± 8.8 and 130.3 ± 5.3 ms), while LVET-I did not change significantly in either condition. Simultaneous determinations of circulating T4, T3 and TSH showed changes appropriate to both hypo- and hyperthyroid states. In 2 patients with T3-thyrotoxicosis, PEP-I was decreased to an average of 103.1 ms, while in 2 patients with compensated hypothyroidism (normal T4 but elevated TSH) this was prolonged to 163.7 ms (average) compared to euthyroid controls. During treatment the hypothyroid group showed significant sequential correlation of TSH and PEP-I. In the hyperthyroid individuals, PEP-I correlated significantly with T4 and T3. PEP-I may be a useful, sensitive, quantitative biologic indicator of thyroid hormone effect on myocardial function.