Creswell Eastman - Academia.edu (original) (raw)

Papers by Creswell Eastman

Research paper thumbnail of Contents Vol. 12, 1990

Developmental Neuroscience, 1990

Research paper thumbnail of Gestational Subclinical Hypothyroidism

Research paper thumbnail of Iodized salt in bread improves iodine nutrition in Australia

Background There has not been any regular, national surveillance program of iodine nutrition in A... more Background There has not been any regular, national surveillance program of iodine nutrition in Australia, but some States, such as Tasmania, have regularly surveyed schoolchildren by testing urinary iodine levels. It has generally been believed that the Australian population was iodine replete, with data showing average urinary iodine levels in excess of 200 μg/L in the early 1990s (1). Since then, we have reported the re-emergence of iodine deficiency in Australia (2). A similar situation pertains in New Zealand where iodine deficiency has also been reported in schoolchildren, infants, toddlers and pregnant women. In 2003-2004 we conducted the Australia National Iodine Nutrition Study (NINS), examining 2,000 schoolchildren across five mainland States and found that Australian children were mildly iodine deficient, with a weighted national median urinary iodine concentration (UIC) of 96 μg/L. The levels were lowest in the two most populated States on the eastern seaboard, Victoria and New South Wales (3). The UIE in schoolchildren is a proxy indicator of iodine nutrition status of the general population. The NINS results became the major driver for the development of new public policy on food fortification to correct iodine deficiency in Australia and New Zealand. In October 2008, the Australia Commonwealth Government gazetted a new mandatory iodine fortification policy, stating “iodised salt must be used for making bread where otherwise salt would be used” (4). This mandatory food fortification policy was fully implemented in October 2009. However, it was essential that the national program be monitored for its effectiveness.

Research paper thumbnail of Biochemistry of steroid hormones, 2nd edn

The Medical Journal of Australia, Sep 1, 1985

Research paper thumbnail of Mild to Moderate Iodine Deficiency

Springer eBooks, 2017

Measurement of iodine excretion in urine is the accepted surrogate marker for dietary iodine inta... more Measurement of iodine excretion in urine is the accepted surrogate marker for dietary iodine intake. Results of these measurements are used to classify and report the spectrum of iodine deficiency in a population as mild, moderate or severe, but the evidence supporting these definitions is imprecise and questionable. The current practice of describing a population as being iodine deficient is based on single spot urine iodine excretion measurements, rather than measuring habitual iodine intake. We examine and question current practices of extrapolating spot urine iodine results, obtained in school-age children, to other segments of a population as being representative of iodine deficiency in the population as a whole. We suggest that the time has come for a review of definitions and a revised classification system for iodine deficiency rather than repeating the historical imprecise descriptors of mild, moderate and severe iodine deficiency. While the crippling, adverse consequences of severe iodine deficiency are indisputable, the frequency and extent of damage-the iodine deficiency disorders (IDD)-caused by the currently accepted definitions of mild to moderate iodine deficiency remains uncertain. Enlargement of the thyroid gland in response to continuing iodine deficiency is a normal physiological adaptation designed to maintain normal secretion of thyroid hormones and prevent deficiency disorders. It only becomes a pathological entity when the body can no longer compensate for inadequate iodine intake and irreversible pathological changes occur. Underpinning our understanding of IDD is the assumption that all of the damage to the central nervous system and other organs occurring in association with iodine deficiency is a consequence of deficient thyroid hormone secretion and action. There is evidence for this assumption in populations suffering from severe iodine deficiency but a paucity of good evidence for any significant effect in mild to moderate iodine deficiency. Of particular interest is the recent findings, in the United Kingdom and Tasmania

Research paper thumbnail of Iodine deficiency in Australia: is iodine supplementation for pregnant and lactating women warranted?

The Medical Journal of Australia, Apr 1, 2010

Fortification, has been adopted in New Zealand, and P1003, Mandatory Iodine Fortification for Aus... more Fortification, has been adopted in New Zealand, and P1003, Mandatory Iodine Fortification for Australia, was implemented in Australia in October 2009. 15 Despite this measure, the most vulnerable groups, pregnant and lactating women, may not be protected. The voluntary Tasmanian Iodine Supplementation Program, which began in 2001, involved monitoring the effect of fortifying bread with iodised salt on the population' s iodine status. 4

Research paper thumbnail of doi:10.1155/2012/798963 Research Article Iodine Intake and Thyroid Function in Pregnant Women in a Private Clinical Practice in Northwestern Sydney before Mandatory Fortification of Bread with Iodised Salt

Copyright © 2012 Norman Blumenthal et al. This is an open access article distributed under the Cr... more Copyright © 2012 Norman Blumenthal et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Aim. The primary objective of the study was to assess the iodine nutritional status, and its effect on thyroid function, of pregnant women in a private obstetrical practice in Sydney. Methods. It was a cross-sectional study undertaken between November 2007 and March 2009. Blood samples were taken from 367 women at their first antenatal visit between 7 and 11 weeks gestation for measurement of thyroid stimulating hormone (TSH) and free thyroxine (FT4) levels and spot urine samples for urinary iodine excretion were taken at the same time as blood collection. Results. The median urinary iodine concentration (UIC) for all women was 81 µg/l (interquartile range 41–169 µg/l). 71.9 % of the women exhibited a UIC of <150 µg/l. 26 % of ...

Research paper thumbnail of Iodized salt in bread improves iodine nutrition in Australia

Background There has not been any regular, national surveillance program of iodine nutrition in A... more Background There has not been any regular, national surveillance program of iodine nutrition in Australia, but some States, such as Tasmania, have regularly surveyed schoolchildren by testing urinary iodine levels. It has generally been believed that the Australian population was iodine replete, with data showing average urinary iodine levels in excess of 200 μg/L in the early 1990s (1). Since then, we have reported the re-emergence of iodine deficiency in Australia (2). A similar situation pertains in New Zealand where iodine deficiency has also been reported in schoolchildren, infants, toddlers and pregnant women. In 2003-2004 we conducted the Australia National Iodine Nutrition Study (NINS), examining 2,000 schoolchildren across five mainland States and found that Australian children were mildly iodine deficient, with a weighted national median urinary iodine concentration (UIC) of 96 μg/L. The levels were lowest in the two most populated States on the eastern seaboard, Victoria ...

Research paper thumbnail of Mild to Moderate Iodine Deficiency

Iodine Deficiency Disorders and Their Elimination, 2017

Measurement of iodine excretion in urine is the accepted surrogate marker for dietary iodine inta... more Measurement of iodine excretion in urine is the accepted surrogate marker for dietary iodine intake. Results of these measurements are used to classify and report the spectrum of iodine deficiency in a population as mild, moderate or severe, but the evidence supporting these definitions is imprecise and questionable. The current practice of describing a population as being iodine deficient is based on single spot urine iodine excretion measurements, rather than measuring habitual iodine intake. We examine and question current practices of extrapolating spot urine iodine results, obtained in school-age children, to other segments of a population as being representative of iodine deficiency in the population as a whole. We suggest that the time has come for a review of definitions and a revised classification system for iodine deficiency rather than repeating the historical imprecise descriptors of mild, moderate and severe iodine deficiency. While the crippling, adverse consequences of severe iodine deficiency are indisputable, the frequency and extent of damage-the iodine deficiency disorders (IDD)-caused by the currently accepted definitions of mild to moderate iodine deficiency remains uncertain. Enlargement of the thyroid gland in response to continuing iodine deficiency is a normal physiological adaptation designed to maintain normal secretion of thyroid hormones and prevent deficiency disorders. It only becomes a pathological entity when the body can no longer compensate for inadequate iodine intake and irreversible pathological changes occur. Underpinning our understanding of IDD is the assumption that all of the damage to the central nervous system and other organs occurring in association with iodine deficiency is a consequence of deficient thyroid hormone secretion and action. There is evidence for this assumption in populations suffering from severe iodine deficiency but a paucity of good evidence for any significant effect in mild to moderate iodine deficiency. Of particular interest is the recent findings, in the United Kingdom and Tasmania

Research paper thumbnail of The Story of the ThyroMobil

Research paper thumbnail of The production of antisera for the radioimmunoassay of thyroxine

The Journal of endocrinology, 1973

Research paper thumbnail of Thyroid Hormone Binding to Putative Nuclear Receptors in Human Mononuclear Blood Cells

Australian Journal of Experimental Biology and Medical Science, 1982

Nuclear protein extracts from mononuclear cells in normal subjects, subjects with the clinical sy... more Nuclear protein extracts from mononuclear cells in normal subjects, subjects with the clinical syndrome of thyroid hormone resistance and cultured B lymphocytes bound thyroxine (T4) (Ka; 1-3-3 5 X lO^ m-i) and triiodothyronine (T3) (Ka; 1-2-3-9 X 10» m-i) with similar affinities. When an extra wash step was introduced, the maximum specific binding of T4 and T3 was reduced by 75% and binding was abolished by three washes. These data suggest binding is to a serum protein contaminant present in the mononuclear cell preparation.

Research paper thumbnail of Deiodination of Reverse 3,3′,5′-Triiodothyronine by Hepatic Nuclear Protein Preparations*

Endocrinology, Aug 1, 1984

A reassessment of the binding characteristics of [125I]rT3 to putative receptors in nuclear prote... more A reassessment of the binding characteristics of [125I]rT3 to putative receptors in nuclear protein extracts of rat and pig liver revealed that significant deiodination of radioligand occurred during incubation. When previously reported separation procedures are used, released radioiodine is included in the protein-bound [125I]rT3 fraction during separation of protein bound from free hormone by Sephadex G-25 chromatography. This misclassification produces artefacts in binding curves and Scatchard plots used to calculate binding affinity and capacity. Previously reported affinities and capacities derived by this methodology are therefore erroneous. Deiodination of rT3 in the nuclear protein extracts appears to be mediated by outer ring deiodinase. Whereas dithiothreitol markedly enhanced radioiodine generation, the enzyme inhibitors ipodate and salicylate reduced iodine production. These effects produced dramatic changes in apparent binding curves for the radioreceptor assay. When [125I]T3 was incubated with nuclear protein extract, no significant deiodination was detected. Whereas it is likely that the deiodinase is a microsomal contaminant of the nuclear preparation, as suggested by the presence of glucose-6-phosphatase in the nuclear protein preparation, the possibility of an intrinsic nuclear-linked deiodinase cannot be overlooked.

Research paper thumbnail of Radioimmunoassay of prolactin in blood spotted on filter paper

PubMed, May 1, 1986

In this method for estimating prolactin, 50 microL of whole blood obtained by finger puncture is ... more In this method for estimating prolactin, 50 microL of whole blood obtained by finger puncture is spotted onto filter paper and blood-spot samples are "punched out" with a 3-mm (diameter) paper punch. The blood is extracted with aqueous buffers and the prolactin measured in large batches by radioimmunoassay. Results were identical with those for prolactin in serum. Prolactin in blood spots is stable at room temperature for up to one week and for several months at -20 degrees C. This simple technique for obtaining blood samples for prolactin estimation has particular potential for field studies of lactating women.

Research paper thumbnail of Iodine deficiency in Australia: is iodine supplementation for pregnant and lactating women warranted?

The Medical Journal of Australia, Sep 1, 2010

Fortification, has been adopted in New Zealand, and P1003, Mandatory Iodine Fortification for Aus... more Fortification, has been adopted in New Zealand, and P1003, Mandatory Iodine Fortification for Australia, was implemented in Australia in October 2009. 15 Despite this measure, the most vulnerable groups, pregnant and lactating women, may not be protected. The voluntary Tasmanian Iodine Supplementation Program, which began in 2001, involved monitoring the effect of fortifying bread with iodised salt on the population' s iodine status. 4

Research paper thumbnail of Growth hormone release during sleep in growth retarded children

Archives of Disease in Childhood, Jul 1, 1973

Research paper thumbnail of Topical Iodine-Containing Antiseptics and Neonatal Hypothyroidism in Very-Low-Birthweight Infants

The Lancet, Sep 1, 1989

The thyroid function of very-low-birthweight (VLBW; below 1500 g) infants admitted to neonatal in... more The thyroid function of very-low-birthweight (VLBW; below 1500 g) infants admitted to neonatal intensive-care units was studied at two hospitals; one routinely used topical iodinated antiseptic agents and the other used chlorhexidine-containing antiseptics. Serial monitoring of urinary iodine excretion and serum thyrotropin and thyroxine levels was undertaken from birth for the first 4 weeks of life. Urinary iodine excretion rose dramatically in the 54 iodine-exposed infants and was up to fifty times greater than in the 29 non-exposed infants. Within 14 days, 25% (9 of 36) of the infants exposed to iodine had serum thyrotropin levels above 20 mIU/l, compared with none of the control group. The mean serum thyroxine level in these 9 infants (44.1 nmol/l) was significantly lower than that in exposed infants with normal thyrotropin levels (83.1 nmol/l) and in the non-exposed control group (83.0 nmol/l); thyroxine levels fell before serum thyrotropin rose. These disturbances in thyroid function correlated positively with urinary iodine excretion and hence iodine absorption. Thyroid function had returned to normal by the time of discharge from hospital. It is concluded that iodine absorption, from topical iodine-containing antiseptics, may cause hypothyroidism during a critical period of neurological development in the newborn infant. The routine use of iodine antisepsis in VLBW infants should be avoided because of this effect.

Research paper thumbnail of Table 3, Frequency distributions of urinary iodine concentrations in healthy term infants in 14 cities in Europe and in Toronto, Canada

Research paper thumbnail of Diagnosis and management of hyperthyroidism and hypothyroidism

The Medical Journal of Australia, May 1, 2004

Research paper thumbnail of The Effect of Iodized Oil on Goitre Size, Thyroid Function and the Development of the Jod Basedow Phenomenon

Clinical Endocrinology, Sep 1, 1982

SUMMARYIn the Lubok Antu district of Sarawak, Malaysia, 240 subjects with 75% prevalence of goitr... more SUMMARYIn the Lubok Antu district of Sarawak, Malaysia, 240 subjects with 75% prevalence of goitre were studied before and at intervals of 1 and 2 years following iodized oil injection. After 1 year the prevalence of goitre was reduced to 33%, but 2 years after injection, goitres had regrown in fourteen subjects (6%). The mean urinary iodine concentration was low initially at 0±17±0±08 (SD) μmol/l, consistent with iodine deficiency, and rose to a level of 2±6 ± 2±5 μmol/l at 1 year, before falling to 0±46 ± 0±38 μmol/l, again consistent with deficiency. Such a rapid depletion of iodine may be related to the high consumption of cassava. Before injection serum TSH concentrations showed a wide scatter from normal up to 62 mU/l and at 1 year, serum TSH concentrations were undetectable. At 2 years serum TSH was again detectable in 50% of subjects with levels up to 8±6 mu/l. During the 2 years, there was a progressive rise in the mean serum T4 concentration from 92 ± 22 (SD) nmol/l to 110 ± 22 nmol/l (P &lt; 0±05). Serum T3 concentrations rose serially in all subjects from a pre‐injection mean of 1±9 ± 0±3 nmol/l to 2±5 ± 0±9 nmol/l (P &lt; 0±001) and then fell significantly below the baseline level to a mean of 1±7 ± 0±6 nmol/l 2 years after injection (P &lt; 0±01). The mean serum rT3 levels followed the same trend. At 1 or 2 years following injection, eight subjects were clinically hyperthyroid. Four of these consented to venesection and hyperthyroidism was confirmed biochemically. These data reveal that: goitres decreased rapidly in size in response to iodized oil injection; 2 significant though incomplete depletion of the iodine stores occurred within 2 years of injection; the consistent increase in serum T3 was associated with a fall in serum TSH to undetectable levels; the prevalence of the Jod Basedow phenomenon was l±7%. These data suggest the need for closer biochemical monitoring of subjects receiving massive doses of iodine and a reappraisal of the use of iodized oil in the treatment of endemic goitre.

Research paper thumbnail of Contents Vol. 12, 1990

Developmental Neuroscience, 1990

Research paper thumbnail of Gestational Subclinical Hypothyroidism

Research paper thumbnail of Iodized salt in bread improves iodine nutrition in Australia

Background There has not been any regular, national surveillance program of iodine nutrition in A... more Background There has not been any regular, national surveillance program of iodine nutrition in Australia, but some States, such as Tasmania, have regularly surveyed schoolchildren by testing urinary iodine levels. It has generally been believed that the Australian population was iodine replete, with data showing average urinary iodine levels in excess of 200 μg/L in the early 1990s (1). Since then, we have reported the re-emergence of iodine deficiency in Australia (2). A similar situation pertains in New Zealand where iodine deficiency has also been reported in schoolchildren, infants, toddlers and pregnant women. In 2003-2004 we conducted the Australia National Iodine Nutrition Study (NINS), examining 2,000 schoolchildren across five mainland States and found that Australian children were mildly iodine deficient, with a weighted national median urinary iodine concentration (UIC) of 96 μg/L. The levels were lowest in the two most populated States on the eastern seaboard, Victoria and New South Wales (3). The UIE in schoolchildren is a proxy indicator of iodine nutrition status of the general population. The NINS results became the major driver for the development of new public policy on food fortification to correct iodine deficiency in Australia and New Zealand. In October 2008, the Australia Commonwealth Government gazetted a new mandatory iodine fortification policy, stating “iodised salt must be used for making bread where otherwise salt would be used” (4). This mandatory food fortification policy was fully implemented in October 2009. However, it was essential that the national program be monitored for its effectiveness.

Research paper thumbnail of Biochemistry of steroid hormones, 2nd edn

The Medical Journal of Australia, Sep 1, 1985

Research paper thumbnail of Mild to Moderate Iodine Deficiency

Springer eBooks, 2017

Measurement of iodine excretion in urine is the accepted surrogate marker for dietary iodine inta... more Measurement of iodine excretion in urine is the accepted surrogate marker for dietary iodine intake. Results of these measurements are used to classify and report the spectrum of iodine deficiency in a population as mild, moderate or severe, but the evidence supporting these definitions is imprecise and questionable. The current practice of describing a population as being iodine deficient is based on single spot urine iodine excretion measurements, rather than measuring habitual iodine intake. We examine and question current practices of extrapolating spot urine iodine results, obtained in school-age children, to other segments of a population as being representative of iodine deficiency in the population as a whole. We suggest that the time has come for a review of definitions and a revised classification system for iodine deficiency rather than repeating the historical imprecise descriptors of mild, moderate and severe iodine deficiency. While the crippling, adverse consequences of severe iodine deficiency are indisputable, the frequency and extent of damage-the iodine deficiency disorders (IDD)-caused by the currently accepted definitions of mild to moderate iodine deficiency remains uncertain. Enlargement of the thyroid gland in response to continuing iodine deficiency is a normal physiological adaptation designed to maintain normal secretion of thyroid hormones and prevent deficiency disorders. It only becomes a pathological entity when the body can no longer compensate for inadequate iodine intake and irreversible pathological changes occur. Underpinning our understanding of IDD is the assumption that all of the damage to the central nervous system and other organs occurring in association with iodine deficiency is a consequence of deficient thyroid hormone secretion and action. There is evidence for this assumption in populations suffering from severe iodine deficiency but a paucity of good evidence for any significant effect in mild to moderate iodine deficiency. Of particular interest is the recent findings, in the United Kingdom and Tasmania

Research paper thumbnail of Iodine deficiency in Australia: is iodine supplementation for pregnant and lactating women warranted?

The Medical Journal of Australia, Apr 1, 2010

Fortification, has been adopted in New Zealand, and P1003, Mandatory Iodine Fortification for Aus... more Fortification, has been adopted in New Zealand, and P1003, Mandatory Iodine Fortification for Australia, was implemented in Australia in October 2009. 15 Despite this measure, the most vulnerable groups, pregnant and lactating women, may not be protected. The voluntary Tasmanian Iodine Supplementation Program, which began in 2001, involved monitoring the effect of fortifying bread with iodised salt on the population' s iodine status. 4

Research paper thumbnail of doi:10.1155/2012/798963 Research Article Iodine Intake and Thyroid Function in Pregnant Women in a Private Clinical Practice in Northwestern Sydney before Mandatory Fortification of Bread with Iodised Salt

Copyright © 2012 Norman Blumenthal et al. This is an open access article distributed under the Cr... more Copyright © 2012 Norman Blumenthal et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Aim. The primary objective of the study was to assess the iodine nutritional status, and its effect on thyroid function, of pregnant women in a private obstetrical practice in Sydney. Methods. It was a cross-sectional study undertaken between November 2007 and March 2009. Blood samples were taken from 367 women at their first antenatal visit between 7 and 11 weeks gestation for measurement of thyroid stimulating hormone (TSH) and free thyroxine (FT4) levels and spot urine samples for urinary iodine excretion were taken at the same time as blood collection. Results. The median urinary iodine concentration (UIC) for all women was 81 µg/l (interquartile range 41–169 µg/l). 71.9 % of the women exhibited a UIC of <150 µg/l. 26 % of ...

Research paper thumbnail of Iodized salt in bread improves iodine nutrition in Australia

Background There has not been any regular, national surveillance program of iodine nutrition in A... more Background There has not been any regular, national surveillance program of iodine nutrition in Australia, but some States, such as Tasmania, have regularly surveyed schoolchildren by testing urinary iodine levels. It has generally been believed that the Australian population was iodine replete, with data showing average urinary iodine levels in excess of 200 μg/L in the early 1990s (1). Since then, we have reported the re-emergence of iodine deficiency in Australia (2). A similar situation pertains in New Zealand where iodine deficiency has also been reported in schoolchildren, infants, toddlers and pregnant women. In 2003-2004 we conducted the Australia National Iodine Nutrition Study (NINS), examining 2,000 schoolchildren across five mainland States and found that Australian children were mildly iodine deficient, with a weighted national median urinary iodine concentration (UIC) of 96 μg/L. The levels were lowest in the two most populated States on the eastern seaboard, Victoria ...

Research paper thumbnail of Mild to Moderate Iodine Deficiency

Iodine Deficiency Disorders and Their Elimination, 2017

Measurement of iodine excretion in urine is the accepted surrogate marker for dietary iodine inta... more Measurement of iodine excretion in urine is the accepted surrogate marker for dietary iodine intake. Results of these measurements are used to classify and report the spectrum of iodine deficiency in a population as mild, moderate or severe, but the evidence supporting these definitions is imprecise and questionable. The current practice of describing a population as being iodine deficient is based on single spot urine iodine excretion measurements, rather than measuring habitual iodine intake. We examine and question current practices of extrapolating spot urine iodine results, obtained in school-age children, to other segments of a population as being representative of iodine deficiency in the population as a whole. We suggest that the time has come for a review of definitions and a revised classification system for iodine deficiency rather than repeating the historical imprecise descriptors of mild, moderate and severe iodine deficiency. While the crippling, adverse consequences of severe iodine deficiency are indisputable, the frequency and extent of damage-the iodine deficiency disorders (IDD)-caused by the currently accepted definitions of mild to moderate iodine deficiency remains uncertain. Enlargement of the thyroid gland in response to continuing iodine deficiency is a normal physiological adaptation designed to maintain normal secretion of thyroid hormones and prevent deficiency disorders. It only becomes a pathological entity when the body can no longer compensate for inadequate iodine intake and irreversible pathological changes occur. Underpinning our understanding of IDD is the assumption that all of the damage to the central nervous system and other organs occurring in association with iodine deficiency is a consequence of deficient thyroid hormone secretion and action. There is evidence for this assumption in populations suffering from severe iodine deficiency but a paucity of good evidence for any significant effect in mild to moderate iodine deficiency. Of particular interest is the recent findings, in the United Kingdom and Tasmania

Research paper thumbnail of The Story of the ThyroMobil

Research paper thumbnail of The production of antisera for the radioimmunoassay of thyroxine

The Journal of endocrinology, 1973

Research paper thumbnail of Thyroid Hormone Binding to Putative Nuclear Receptors in Human Mononuclear Blood Cells

Australian Journal of Experimental Biology and Medical Science, 1982

Nuclear protein extracts from mononuclear cells in normal subjects, subjects with the clinical sy... more Nuclear protein extracts from mononuclear cells in normal subjects, subjects with the clinical syndrome of thyroid hormone resistance and cultured B lymphocytes bound thyroxine (T4) (Ka; 1-3-3 5 X lO^ m-i) and triiodothyronine (T3) (Ka; 1-2-3-9 X 10» m-i) with similar affinities. When an extra wash step was introduced, the maximum specific binding of T4 and T3 was reduced by 75% and binding was abolished by three washes. These data suggest binding is to a serum protein contaminant present in the mononuclear cell preparation.

Research paper thumbnail of Deiodination of Reverse 3,3′,5′-Triiodothyronine by Hepatic Nuclear Protein Preparations*

Endocrinology, Aug 1, 1984

A reassessment of the binding characteristics of [125I]rT3 to putative receptors in nuclear prote... more A reassessment of the binding characteristics of [125I]rT3 to putative receptors in nuclear protein extracts of rat and pig liver revealed that significant deiodination of radioligand occurred during incubation. When previously reported separation procedures are used, released radioiodine is included in the protein-bound [125I]rT3 fraction during separation of protein bound from free hormone by Sephadex G-25 chromatography. This misclassification produces artefacts in binding curves and Scatchard plots used to calculate binding affinity and capacity. Previously reported affinities and capacities derived by this methodology are therefore erroneous. Deiodination of rT3 in the nuclear protein extracts appears to be mediated by outer ring deiodinase. Whereas dithiothreitol markedly enhanced radioiodine generation, the enzyme inhibitors ipodate and salicylate reduced iodine production. These effects produced dramatic changes in apparent binding curves for the radioreceptor assay. When [125I]T3 was incubated with nuclear protein extract, no significant deiodination was detected. Whereas it is likely that the deiodinase is a microsomal contaminant of the nuclear preparation, as suggested by the presence of glucose-6-phosphatase in the nuclear protein preparation, the possibility of an intrinsic nuclear-linked deiodinase cannot be overlooked.

Research paper thumbnail of Radioimmunoassay of prolactin in blood spotted on filter paper

PubMed, May 1, 1986

In this method for estimating prolactin, 50 microL of whole blood obtained by finger puncture is ... more In this method for estimating prolactin, 50 microL of whole blood obtained by finger puncture is spotted onto filter paper and blood-spot samples are "punched out" with a 3-mm (diameter) paper punch. The blood is extracted with aqueous buffers and the prolactin measured in large batches by radioimmunoassay. Results were identical with those for prolactin in serum. Prolactin in blood spots is stable at room temperature for up to one week and for several months at -20 degrees C. This simple technique for obtaining blood samples for prolactin estimation has particular potential for field studies of lactating women.

Research paper thumbnail of Iodine deficiency in Australia: is iodine supplementation for pregnant and lactating women warranted?

The Medical Journal of Australia, Sep 1, 2010

Fortification, has been adopted in New Zealand, and P1003, Mandatory Iodine Fortification for Aus... more Fortification, has been adopted in New Zealand, and P1003, Mandatory Iodine Fortification for Australia, was implemented in Australia in October 2009. 15 Despite this measure, the most vulnerable groups, pregnant and lactating women, may not be protected. The voluntary Tasmanian Iodine Supplementation Program, which began in 2001, involved monitoring the effect of fortifying bread with iodised salt on the population' s iodine status. 4

Research paper thumbnail of Growth hormone release during sleep in growth retarded children

Archives of Disease in Childhood, Jul 1, 1973

Research paper thumbnail of Topical Iodine-Containing Antiseptics and Neonatal Hypothyroidism in Very-Low-Birthweight Infants

The Lancet, Sep 1, 1989

The thyroid function of very-low-birthweight (VLBW; below 1500 g) infants admitted to neonatal in... more The thyroid function of very-low-birthweight (VLBW; below 1500 g) infants admitted to neonatal intensive-care units was studied at two hospitals; one routinely used topical iodinated antiseptic agents and the other used chlorhexidine-containing antiseptics. Serial monitoring of urinary iodine excretion and serum thyrotropin and thyroxine levels was undertaken from birth for the first 4 weeks of life. Urinary iodine excretion rose dramatically in the 54 iodine-exposed infants and was up to fifty times greater than in the 29 non-exposed infants. Within 14 days, 25% (9 of 36) of the infants exposed to iodine had serum thyrotropin levels above 20 mIU/l, compared with none of the control group. The mean serum thyroxine level in these 9 infants (44.1 nmol/l) was significantly lower than that in exposed infants with normal thyrotropin levels (83.1 nmol/l) and in the non-exposed control group (83.0 nmol/l); thyroxine levels fell before serum thyrotropin rose. These disturbances in thyroid function correlated positively with urinary iodine excretion and hence iodine absorption. Thyroid function had returned to normal by the time of discharge from hospital. It is concluded that iodine absorption, from topical iodine-containing antiseptics, may cause hypothyroidism during a critical period of neurological development in the newborn infant. The routine use of iodine antisepsis in VLBW infants should be avoided because of this effect.

Research paper thumbnail of Table 3, Frequency distributions of urinary iodine concentrations in healthy term infants in 14 cities in Europe and in Toronto, Canada

Research paper thumbnail of Diagnosis and management of hyperthyroidism and hypothyroidism

The Medical Journal of Australia, May 1, 2004

Research paper thumbnail of The Effect of Iodized Oil on Goitre Size, Thyroid Function and the Development of the Jod Basedow Phenomenon

Clinical Endocrinology, Sep 1, 1982

SUMMARYIn the Lubok Antu district of Sarawak, Malaysia, 240 subjects with 75% prevalence of goitr... more SUMMARYIn the Lubok Antu district of Sarawak, Malaysia, 240 subjects with 75% prevalence of goitre were studied before and at intervals of 1 and 2 years following iodized oil injection. After 1 year the prevalence of goitre was reduced to 33%, but 2 years after injection, goitres had regrown in fourteen subjects (6%). The mean urinary iodine concentration was low initially at 0±17±0±08 (SD) μmol/l, consistent with iodine deficiency, and rose to a level of 2±6 ± 2±5 μmol/l at 1 year, before falling to 0±46 ± 0±38 μmol/l, again consistent with deficiency. Such a rapid depletion of iodine may be related to the high consumption of cassava. Before injection serum TSH concentrations showed a wide scatter from normal up to 62 mU/l and at 1 year, serum TSH concentrations were undetectable. At 2 years serum TSH was again detectable in 50% of subjects with levels up to 8±6 mu/l. During the 2 years, there was a progressive rise in the mean serum T4 concentration from 92 ± 22 (SD) nmol/l to 110 ± 22 nmol/l (P &lt; 0±05). Serum T3 concentrations rose serially in all subjects from a pre‐injection mean of 1±9 ± 0±3 nmol/l to 2±5 ± 0±9 nmol/l (P &lt; 0±001) and then fell significantly below the baseline level to a mean of 1±7 ± 0±6 nmol/l 2 years after injection (P &lt; 0±01). The mean serum rT3 levels followed the same trend. At 1 or 2 years following injection, eight subjects were clinically hyperthyroid. Four of these consented to venesection and hyperthyroidism was confirmed biochemically. These data reveal that: goitres decreased rapidly in size in response to iodized oil injection; 2 significant though incomplete depletion of the iodine stores occurred within 2 years of injection; the consistent increase in serum T3 was associated with a fall in serum TSH to undetectable levels; the prevalence of the Jod Basedow phenomenon was l±7%. These data suggest the need for closer biochemical monitoring of subjects receiving massive doses of iodine and a reappraisal of the use of iodized oil in the treatment of endemic goitre.