Steven C. Boyages

The thyroid gland in acromegaly: an ultrasonographic study

OBJECTIVEAn association between acromegaly and goitre is well recognized. We have studied the incidence and morphology of goitre in acromegaly, and examined the role of IGF‐I and TSH in goitre pathogenesis.

Relationship of Type 2 diabetes to the prevalence, incidence and progression of age-related hearing loss

Aims  Type 2 diabetes and associated microvascular abnormalities are postulated to affect hearing. Our study reports on the relationship between Type 2 diabetes and the prevalence, 5‐year incidence and progression of hearing impairment in a representative, older, Australian population.

Increased incidence of neoplasia in females with acromegaly

Some studies have indicated an increased incidence of neoplasia, particularly breast and colon, in acromegaly. We have determined the incidence of benign and malignant neoplasms in an Australian population of patients with acromegaly.

Effect of prehospital triage on revascularization times, left ventricular function, and survival in patients with ST-elevation myocardial infarction.

Shorter reperfusion times lead to better outcomes in patients with ST-elevation myocardial infarction (STEMI). We assessed the efficacy of prehospital triage with bypass of community hospitals and early activation of the cardiac catheterization team on revascularization times, left ventricular (LV) ejection fraction, and survival. Patients with STEMI (624) were divided into 3 groups determined by site of triage: ambulance field triage (163), interventional center emergency department (202), and 3 community hospital emergency departments (259). Compared with community hospital and interventional center triages, ambulance field triage resulted in a significant median decrease in door-to-balloon times of 68 and 27 minutes, respectively (p <0.001). LV ejection fraction was highest in the field triage group (52 +/- 13%) compared with the interventional center (49 +/- 12%) and community hospital (48 +/- 12%, p = 0.017) groups. Thirty-day mortality was lowest in the ambulance field group (3%) compared with the interventional facility (11%) and community hospital (4%, p = 0.007) groups. There was a significant difference in long-term survival with up to 30-month follow-up among the 3 triage groups (p = 0.041). With time-dependent Cox regression modeling the difference in survival was significant only during the first week after STEMI (p = 0.020). Every extra minute of symptom onset to reperfusion time was associated with a relative risk of long-term mortality of 1.003 (95% confidence interval 1.000 to 1.006, p = 0.027). In conclusion, field triage of patient with STEMI decreased revascularization times, which preserved LV function, and improved early survival.

THYROID AUTOIMMUNITY IN ENDEMIC GOITRE CAUSED BY EXCESSIVE IODINE INTAKE

The pathophysiology of endemic goitre caused by excessive iodine intake is not well defined. By interacting with the immune system, iodine excess may trigger the development of autoimmune thyroid disease such as lymphocytic Hashimotos thyroiditis (LT). In an attempt to examine this further, we compared the presence of thyroid autoantibodies in 29 goitrous children, from an iodine excess area, and in 26 healthy children, from an iodine sufficient area, of north central China. Serum was tested for antimicrosomal (MAb), anti‐thyroglobulin (TgAb), second colloid antigen antibodies (CA2‐Ab) and TSH binding inhibitory immunoglobulins (TBII). Affinity chromatographically purified IgG was tested for thyroid growth‐stimulating activity (TGI) by two different methods: a sensitive cytochemical bioassay (CBA) using guinea‐pig thyroid explants and a mitotic arrest assay (MAA) employing a continuous rat thyroid cell line (FRTL‐5). We found no increased prevalence of LT in patients with endemic iodine goitre. The levels of MAb, TgAb and CA2‐Ab did not differ significantly between the two groups of children. Further, TBII were not present in either group. Thyroid growth‐stimulating immunoglobulins (TGI) were the major autoantibodies found in children with goitres caused by iodine excess. In the CBA, 12 of 20 (60%) goitrous children and 0 of 12 (0% P<0.05) healthy children were positive for TGI. Similar results were found in the MAA, and a good correlation between results of the CBA and MAA was found (P = 0.003). Maximal TGI activity in dose‐response CBA showed a good relation with clinical goitre size (r = 0.63; P < 0.05) indicating a possible pathophysiological role for these antibodies. We conclude that endemic iodine goitre is not associated with Hashimotos lymphocytic thyroiditis. Nevertheless, autoimmune growth factors such as TGI may play a primary role in the pathogenesis of thyroid growth in this condition.

Iodide induced lymphocytic thyroiditis in the BB/W rat : evidence of direct toxic effects of iodide on thyroid subcellular structure

A high dietary iodine intake accelerates the development of lymphocytic thyroiditis (LT) in the BB/W rat. Our previous studies have defined the temporal sequence of the immunological events triggered by excess iodide intake in these animals. It was still not clear, however, whether these observed immunological changes were a direct effect on immune effector cells, or whether they represented a secondary response to a toxic effect of iodine on thyroid tissue. In the present study, the effect of excessive iodine intake on the subcellular structure of the BB/W rat thyroid gland, particularly, whether iodide had a toxic effect independent of its immune response has been examined. BB/W rats were exposed, prenatally through maternal drinking water, to excessive iodide at two doses (Moderate 3 x 10(-6) M iodide/l; High 3 x 10(-3) M iodide/l); a third group of BB/W rats was given tap water; till 12 weeks postnatal age. Two groups of Wistar rats received high dose iodide water or tap water for the same period of time and served as controls. Thyroid gland ultrastructure was determined by electron microscopic (EM) examination. Thyroid 125I uptake and perchlorate discharge tests were also performed in separate experiments. We found that thyroid glands of non-iodine supplemented Wistar rats were morphlogically normal under EM. There were no overt changes in the iodide treated Wistar rats. By contrast, iodide treated BB/W rats exhibited marked accumulation of secondary lysosomes and lipid droplets; markedly swollen and disrupted mitochondria and extreme dilatation of rough endoplasmic reticulum (RER).(ABSTRACT TRUNCATED AT 250 WORDS)

The rising cost of vitamin D testing in Australia: time to establish guidelines for testing.

TO THE EDITOR: A rising awareness of the prevalence of 25hydroxyvitamin D (25OHD) deficiency over the past decade is likely to have led to a surge in the number of individuals who undergo 25OHD testing.1 United States data indicate that testing for 25OHD has increased by 80%–90% annually,2 yet there are no reports that investigate the cost of 25OHD testing in Australia. We analysed the Medicare Benefits Schedule (MBS) to determine the economic impact of vitamin D testing in Australia from 1 January 2000 to 31 December 2010. We found that the annual benefit for 25OHD testing subsidised by the MBS increased from

Iodine Induced Lymphocytic Thyroiditis in the Bb/W Rat: Early and Late Immune Phenomena

1.02 million in 2000 to

The rise and rise of vitamin D testing

96.7 million in 2010, an average increase of approximately 59% per year (Box). This increase in 25OHD testing has risen above the general trend of other common pathology tests such as full blood count. Benefits paid by state resemble the population distribution, whereby most benefits in 2010 were paid in New South Wales (

Does mitochondrial genome mutation in subjects with maternally inherited diabetes and deafness decrease severity of diabetic retinopathy

35.3 million) and Victoria (