|
| |
Vanderpump et al., Newcastle upon Tyne, UK, reported 20 a year follow-up
research on thyroid disorders in 1877 survivors of the original Whickham
survey comprising 2779 adults. The mean incidence of spontaneous hypothyroidism
in women was 3.5/1000 survivors/yr rising to 4.1/1000 survivors/yr for
all causes of hypothyroidism, and was in men 0.6/1000 survivors/yr. The
mean incidence of hyperthyroidism in women was 0.8/1000 survivors/yr and
was negligible in men. Similar incidence rates were calculated for the
deceased subjects. A positive family history of any form of thyroid disease,
presence of goiter, fasting cholesterol and triglyc e rid e levels, or
p a rity in wo me n, was not associated with an increased risk of hypothyroidism.
The increased risk for developing hypothyroidism when TSH was raised, was
8 in women and 44 in men, when thyroid antibodies were present 8 en 25
respectively, and when TSH was raised + positive antibodies, 38 and 173
respectively.
Laurberg et al., Aalborg, Denmark and Reykjavik, Iceland, studied goiter
rate and thyroid function in subjects of 68 years in East Jutland, Denmark
(n = 423, M/F 185/238) in which area mean iodine intake is 50 ug/day and
in Iceland (n= 100, M/F 46/54) with a high mean iodine intake of 300 ug/day.
Despite absence of significant goiter in young subjects, goiter rate in
the low iodine area was F/M: 12.2/2.7% and less common in the high iodine
area F/M: 1.9/2.2%. In the low iodine area subnormal TSH was F/M: 10.9/5.9%,
elevated T4 and/or T3 F/M: 3.8/1.1%. High TSH was present F/M: 3.4/1.1%.
In the high iodine area no low TSH was found, but high TSH was frequent,
F/M: 20.4/6.5%. The majority of these patients had positive TPOAb and/or
Tg-Ab. Despite this, using highly sensitive methods, antibodies against
TPO and TG were more frequent in the low iodine area than in the high iodine
area. (Comment: The high prevalence of borderline hyperthyroidism in the
low iodine area is probably caused by longstanding (nodular) goiter due
to iodine deficiency. Vice versa the high prevalence of subclinical hypothyroidism
in the high iodine area is not easily explained but may be related to the
high iodine intake in the presence of subclinical autoimmune thyroiditis,
leading to impaired organification of iodine in the thyroid gland.
|
|