Thyroid Diseases: Lazarus JH

Bartalena L, Baldeschi L, Dickinson AJ, Eckstein A, Kendall-Taylor P, Marcocci C, Mourits MP, Perros P, Boboridis K, Boschi A, Currò N, Daumerie C, Kahaly GJ, Krassas G, Lane CM, Lazarus JH, Marinò M, Nardi M, Neoh C, Orgiazzi J, Pearce S, Pinchera A, Pitz S, Salvi M, Sivelli P, Stahl M, von Arx G, Wiersinga WM. · Department of Clinical Medicine, University of Insubria, Varese, Italy. · Thyroid. · Pubmed #18341379 No free full text.

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Owen PJ, Lazarus JH. · No affiliation provided · J Endocrinol Invest. · Pubmed #12841533 No free full text.

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Okosieme OE, Marx H, Lazarus JH. · Prince Charles Hospital, Department of Endocrinology and Diabetes, Cwm Taff NHS Trust Merthyr Tydfil, Mid Glamorgan CF479DT, UK. · Expert Opin Pharmacother. · Pubmed #18710353 No free full text.

Abstract: BACKGROUND: Uncontrolled thyroid dysfunction in pregnancy is associated with adverse fetal and maternal outcomes. OBJECTIVES: To review relevant literature and developments in the medical management of thyroid dysfunction in pregnancy. RESULTS: Hyperthyroidism in pregnancy requires careful control of maternal disease whilst avoiding fetal hypothyroidism. Propylthiouracil is the preferred antithyroid drug in pregnancy although thiamazole can be used where propylthiouracil is unavailable. Synthetic levothyroxine is the treatment of choice in hypothyroidism. Patients with pre-existing hypothyroidism will generally require an increase in thyroxine dose in pregnancy. Most patients with postpartum thyroiditis will require treatment during the hypothyroid phase. Long-term follow-up of patients with this syndrome is essential owing to the risk of permanent hypothyroidism. CONCLUSION: Excellent maternal and fetal outcomes can be achieved with appropriate management of thyroid dysfunction in pregnancy.

Marx H, Amin P, Lazarus JH. · Department of Obstetrics, University Hospital of Wales, Cardiff CF14 4XN. · BMJ. · Pubmed #18356235 No free full text.

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Lazarus JH, Kaklamanou M. · Centre for Endocrine and Diabetes Sciences, University Hospital of Wales, Cardiff University, Heath Park, Cardiff, UK. · Curr Opin Endocrinol Diabetes Obes. · Pubmed #17940469 No free full text.

Abstract: PURPOSE OF REVIEW: To describe the significance of low thyroid-stimulating hormone in pregnancy. RECENT FINDINGS: Interpretation of thyroid function in pregnancy must be seen in the context of changes in thyroid economy associated with gestation. Improvements in thyroid-stimulating hormone assay methodology have resulted in accurate identification of low and suppressed thyroid-stimulating hormone in pregnancy, and recent studies of screening thyroid function in pregnancy have found an incidence of low thyroid-stimulating hormone in up to 18% of women. Normative gestational-related reference ranges for thyroid hormones, particularly thyroid-stimulating hormone and thyroxine, should be established to identify the higher as well as the lower limits of these analytes. The adverse obstetric and neonatal outcomes associated with hyperthyroidism due to Graves' disease mean that this must be differentiated from the more common cause of suppressed thyroid-stimulating hormone, i.e. gestational transient thyrotoxicosis. It is suggested that estimation of thyroid peroxidase antibodies may be a useful initial diagnostic strategy in the evaluation of women with a low or suppressed thyroid-stimulating hormone. SUMMARY: In addition to identifying women with high thyroid-stimulating hormone levels at screening (with implications for child intelligence), establishing the cause of low thyroid-stimulating hormone will improve obstetric outcome in a number of pregnant women.

Owen PJ, Sabit R, Lazarus JH. · Centre for Endocrine and Diabetes Sciences, School of Medicine, Cardiff University, Wales, United Kingdom. · Thyroid. · Pubmed #17614771 No free full text.

Abstract: Altered cardiac function in thyroid disease is well recognized and has been extensively investigated, vascular function has however been less well studied in those with thyroid dysfunction. Thyroid hormones, thyroxine (T(4)) and triiodothyronine (T(3)) are important regulators of cardiac function and cardiovascular hemodynamics. The cardiovascular system responds to minimal but persistent changes in circulating thyroid hormone levels producing changes in vascular reactivity and endothelial function. The detection of endothelial dysfunction and/or arterial stiffness allows early identification of individuals at risk as these occur in both patients with risk factors for coronary artery disease and in those with established disease. This may allow treatment to be targeted at high risk individuals with the aim of slowing the progression of vascular disease. The various methods used to assess arterial function are reviewed and the changes demonstrated in human and animal models of thyroid dysfunction.

Lazarus JH. · Centre for Endocrine and Diabetes Sciences, University Hospital of Wales, Wales, United Kingdom. · Thyroid. · Pubmed #17465860 No free full text.

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Premawardhana LD, Lazarus JH. · Department of Medicine, Caerphilly Miners' Hospital, Caerphilly, UK. · Postgrad Med J. · Pubmed #16954449 No free full text.

Abstract: Autoimmune thyroid disease is the predominant form of thyroid dysfunction in the developed world. Although its precise cause is currently unclear, principles of management have been established. There is a vigorous debate about the management of the increasingly commonly recognised subclinical forms of thyroid dysfunction despite recent recommendations. Nodular thyroid disease and thyroid carcinoma have received wide attention. The effects of drugs and pregnancy on thyroid function have also been investigated widely. This short review attempts to give an overview and clarify the current management of common thyroid disorders.

Anonymous00251, Wiersinga WM, Perros P, Kahaly GJ, Mourits MP, Baldeschi L, Boboridis K, Boschi A, Dickinson AJ, Kendall-Taylor P, Krassas GE, Lane CM, Lazarus JH, Marcocci C, Marino M, Nardi M, Neoh C, Orgiazzi J, Pinchera A, Pitz S, Prummel MF, Sartini MS, Stahl M, von Arx G. · Department of Endocrinology, Academic Medical Centre, Amsterdam, The Netherlands. · Eur J Endocrinol. · Pubmed #16914591 links to  free full text

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Lazarus JH. · Cardiff University School of Medicine, Centre for Endocrine and Diabetes Sciences, Academic Centre, Llandough Hospital, Llandough, Cardiff, UK. · Minerva Endocrinol. · Pubmed #15988403 No free full text.

Abstract: The subject of thyroid disease in pregnancy is receiving increasing attention from many scientific disciplines. Thyroid function in pregnancy is characterised by a T4 surge at 12 weeks declining thereafter. Serum thyroid hormone concentrations fall in the second half of pregnancy but there are few data on normal reference ranges. Fetal brain development depends on T4 transport into the fetus which in turn depends on sufficient maternal iodine supply. There is current concern that adequate iodisation is not present in large parts of Europe. There is increasing evidence that thyroid autoimmunity is associated with fetal loss but the mechanism is unclear and therapy requires carefully conducted studies. While hyperthyroidism in pregnancy is uncommon, effects on both mother and child are critical if untreated. The use of propylthiouracil is recommended together with measurement of TSH receptor antibodies at 36 weeks gestation. Women receiving thyroxine therapy for hypothyroidism or as suppressive therapy should have their dose increased by up to 50% during pregnancy. There are now substantial data to show deleterious effects on child IQ resulting from low maternal T4 (or high TSH) during gestation. Major advances in molecular biology have contributed to elucidation of many genetic causes of congenital hypothyroidism. However, the aetiology of the majority of cases is still unclear and further research is required. The presence of TPO antibodies in about 10% of pregnant women in early gestation is a predictor of an increased incidence of subclinical hypothyroidism during pregnancy and also of postpartum thyroid dysfunction. The latter condition occurs in 5-9% of women and 25-30% progress to permanent hypothyroidism. This review suggests that screening for thyroid function in early pregnancy and levothyroxine intervention therapy for maternal subclinical hypothyroidism should be considered but evidence is awaited. Screening for both thyroid dysfunction and thyroid antibodies ideally at a preconception clinic but certainly in early gestation is recommended.

Lazarus JH, Premawardhana LD. · Centre for Endocrine and Diabetes Sciences, Cardiff University, Cardiff CF14 4XN, Wales, UK. · J Clin Pathol. · Pubmed #15858112 links to  free full text

Abstract: Although gestational hyperthyroidism is uncommon (0.2%), hypothyroidism (autoimmune disease or suboptimal iodine intake) occurs in 2.5% of women and is predictive of reduced neonatal and child neuropsychological development and maternal obstetric complications. Postpartum thyroid dysfunction (PPTD) occurs in 5-9% of women and is associated with antithyroid peroxidase antibodies (antiTPOAb) in 10% of women in early pregnancy. Therefore, screening for thyroid dysfunction in pregnancy should be considered. T4 and thyroid stimulating hormone measurements could be used to screen for hypothyroidism, which would require levothyroxine intervention treatment. T4 supply is crucial to fetal nervous system maturation; currently, the recommended daily iodine intake is 200 microg, and this is not always achieved, even in the UK. At present, a randomised prospective trial is ongoing to provide the evidence base for this screening strategy. Meanwhile, it is reasonable to (a) optimise iodine nutrition during pregnancy; (b) ascertain women with known thyroid disease; (c) identify women at increased risk of thyroid disease-for example, those with other autoimmune diseases. PPTD can be predicted by measurement of antiTPOAb in early gestation.

Lazarus JH. · Department of Medicine, University of Wales College of Medicine, Cardiff, Wales, UK. · Treat Endocrinol. · Pubmed #15649099 No free full text.

Abstract: Pregnancy has an effect on thyroid economy with significant changes in iodine metabolism, serum thyroid binding proteins, and the development of maternal goiter especially in iodine-deficient areas. Pregnancy is also accompanied by immunologic changes, mainly characterized by a shift from a T helper-1 (Th1) lymphocyte to a Th2 lymphocyte state. Thyroid peroxidase antibodies are present in 10% of women at 14 weeks' gestation, and are associated with (i) an increased pregnancy failure (i.e. abortion), (ii) an increased incidence of gestational thyroid dysfunction, and (iii) a predisposition to postpartum thyroiditis. Thyroid function should be measured in women with severe hyperemesis gravidarum but not in every patient with nausea and vomiting during pregnancy. Graves hyperthyroidism during pregnancy is best managed with propylthiouracil administered throughout gestation. Thyroid-stimulating hormone-receptor antibody measurements at 36 weeks' gestation are predictive of transient neonatal hyperthyroidism, and should be checked even in previously treated patients receiving thyroxine. Postpartum exacerbation of hyperthyroidism is common, and should be evaluated in women with Graves disease not on treatment. Radioiodine therapy in pregnancy is absolutely contraindicated. Hypothyroidism (including subclinical hypothyroidism) occurs in about 2.5% of pregnancies, and may lead to obstetric and neonatal complications as well as being a cause of infertility. During the last few decades, evidence has been presented to underpin the critical importance of adequate fetal thyroid hormone levels in order to ensure normal central and peripheral nervous system maturation. In iodine-deficient and iodine-sufficient areas, low maternal circulating thyroxine levels have been associated with a significant decrement in child IQ and development. These data suggest the advisability of further evaluation for a screening program early in pregnancy to identify women with hypothyroxinemia, and the initiation of prompt treatment for its correction. Hypothyroidism in pregnancy is treated with a larger dose of thyroxine than in the nonpregnant state. Postpartum thyroid dysfunction (PPTD) occurs in 50% of women found to have thyroid peroxidase antibodies in early pregnancy. The hypothyroid phase of PPTD is symptomatic and requires thyroxine therapy. A high incidence (25-30%) of permanent hypothyroidism has been noted in these women. Women having transient PPTD with hypothyroidism should be monitored frequently, as there is a 50% chance of these patients developing hypothyroidism during the next 7 years.

Owen PJ, Lazarus JH. · Dept Medicine, University of Wales College of Medicine, Llandough Hospital, Penarth CF64 2XX, Wales, UK. · Trends Endocrinol Metab. · Pubmed #12890589 No free full text.

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Lazarus JH. · Department of Medicine, University of Wales College of Medicine, Cardiff, United Kingdom. · Semin Reprod Med. · Pubmed #12536361 No free full text.

Abstract: Thyroid function during pregnancy is characterized by changes in circulating thyroid hormone concentrations related to alterations in thyroxine binding globulin (TBG), human chorionic gonadotropin (hCG), and iodine status. The immunology of normal pregnancy shows a reduction in antibody titer during gestation and an increase in T helper-2 (TH2) immune responses. Thyroid dysfunction may cause menstrual disturbances in hyper- and hypothyroidism but less marked disturbances of sexual function in men. Fertility is reduced in hypo- and hyperthyroid females. Accumulating evidence suggests a strong association between the presence of thyroid antibodies and fetal loss, although the data relating to recurrent abortion are not so convincing. Asymptomatic maternal gestational hypothyroidism may occur in up to 2.5% of women; studies have shown a significant impact of this condition in causing a decrease of child IQ, suggesting that screening for maternal hypothyroidism with intervention may be justified. Postpartum thyroid disease occurs in 5 to 9% of women and thyroid dysfunction postpartum is seen in 50% of thyroid peroxidase antibody positive (TPO Ab+ve) women. There is a significant rate of hypothyroidism in long-term follow-up of women who have transient postpartum thyroid dysfunction.

Lazarus JH, Parkes AB, Premawardhana LD. · · Autoimmunity. · Pubmed #12389641 No free full text.

Abstract: Post partum thyroiditis occurs in 50% of TPO AB+ve women and is characterised by transient hyperthyroidism followed by transient hypothyroidism during the first six months, post partum. A third of the latter group develop permanent hypothyroidism. The syndrome is seen in 5-9% of women and post partum thyroid dysfunction (PPTD) reoccurs in 75% of women in a subsequent pregnancy. An increase in depressive symptomatology is seen in women with PPTD as well as in ante TPO Ab+ve women without PPTD. The immunology of PPT is associated with the presence of TPO antiboides with those IgG subclasses best able to activate the complement cascade. The HLA-DR frequencies seen in PPT suggest that PPT may be related to Hashimoto's thyroiditis. TPO Ab driven complement fixation is seen in PPT and complement activation relates to the extent and progression of thyroid damage. Recent studies have shown an increase in both Th2 and Th1 cytokine release from lymphocytes in ante partum women destined to develop PPTD. More data are required on the cellular immune changes both ante partum and post partum in PPT.

Lazarus JH, Kokandi A. · Department of Medicine, University of Wales College of Medicine, Cardiff, UK. · Clin Endocrinol (Oxf). · Pubmed #10971442 No free full text.

Abstract: Inspection of the references cited in this review indicates that much work has occurred in the area of thyroid and pregnancy during the last decade. Significant advances in our understanding of the immunology of pregnancy and the effect of thyroid disease on this process have taken place. The role of hCG in the physiology of pregnancy and its relevance to thyroid function has been an emerging theme. There is still no clear explanation for the association between thyroid antibodies and infertility or miscarriage. During the last decade a general concensus has developed in relation to the management of hyperthyroidism in pregnancy although there are still variations in antithyroid drug use at this time. The aetiological classification of congenital hyper- and hypothyroidism utilizing new technologies has opened up a new perspective on these disorders. Attention has been drawn to the importance of treating maternal hypothyroidism with adequate thyroid replacement therapy and to the possibility of impaired child neuropsychological development consequent on low maternal thyroid hormone concentration in early gestation in non iodine deficient areas. Significant advances have been made during the last decade in the description of the clinical features and in our understanding of the pathogenesis of postpartum thyroid disease. The importance of long-term follow up of selected patient groups has also been emphasized.

Lazarus JH, Obuobie K. · Department of Medicine, University of Wales College of Medicine, Llandough Hospital, Cardiff, UK. · Postgrad Med J. · Pubmed #10964113 links to  free full text

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Hanna FW, Lazarus JH, Scanlon MF. · Department of Medicine, Prince Charles Hospital, Merthyr Tydfill, Cardiff CF47 9DT. · BMJ. · Pubmed #10506049 links to  free full text

This publication has no abstract.

Lazarus JH. · Department of Medicine, University of Wales College of Medicine, Cardiff, United Kingdom. · Thyroid. · Pubmed #10447015 No free full text.

Abstract: Postpartum thyroiditis (PPT) occurs in 5%-9% of unselected postpartum women; hyperthyroidism and hypothyroidism develop, the latter being permanent, in up to 25 %-30% of women. PPT is strongly associated with antithyroid peroxidase (anti-TPO) antibodies, but 50% of anti-TPO positive women do not develop thyroid dysfunction. Symptom analysis has shown that lack of energy and irritability were the most frequent hyperthyroid symptoms whereas lack of energy, aches and pains, poor memory, dry skin, and cold intolerance were the significant hypothyroid features. Some of these symptoms were more frequently observed than in antibody-negative controls even when these patients were euthyroid and in anti-TPOAb positive women who did not develop PPT at all. The diagnosis of PPT is based on the observation of abnormal thyroid function tests in a postpartum anti-TPOAb-positive woman: transient hyperthyroidism occurs at 14 weeks and hypothyroidism at 19 weeks postpartum. Diffuse or multifocal hypoechogenicity of the thyroid is seen on echography and a thyroid destructive process is evidenced by an increase in serum thyroglobulin and urinary iodine excretion. In addition to the 25%-30% of women who develop permanent hypothyroidism at 3 years, recent data indicate that 50% of women who have developed PPT will be hypothyroid 7-9 years later. The long-term risk is only 5% for those anti-TPOAb positive women not developing thyroid dysfunction postpartum. The risk of recurrent PPT is 70% if previous PPT was experienced and 25% if the patient was euthyroid after the first pregnancy.

Lazarus JH. · Department of Medicine, University of Wales College of Medicine, Cardiff, United Kingdom. · Thyroid. · Pubmed #10447010 No free full text.

Abstract: Cretinism, which is characterized by marked intellectual impairment and is associated with severe iodine deficiency, has been appreciated for many years. Advances in the knowledge of thyroid physiology and its changes in normal pregnancy have now led to the realization of the potential importance of minor changes in maternal thyroxine (T4) concentrations in relation to brain maturation and development. Mild and subclinical neuropsychomotor deficits have been observed in neonates both in mildly iodine-deficient areas and in iodine-sufficient areas where maternal T4 concentrations are in the low normal range. Recent data from Holland suggest that children born to mothers known to have circulating antithyroid peroxidase antibodies or from mothers with low normal free T4 concentrations measured at 12 weeks gestation have significant development impairment. There are important implications for possible screening for thyroid dysfunction during pregnancy arising from these studies.

Gullu S, Emral R, Bastemir M, Parkes AB, Lazarus JH. · Ankara University, School of Medicine, Department of Endocrinology and Metabolic Diseases, Ibn-i Sina Hospital, 10th floor, D-Block, 06100 Sihhiye, Ankara, Turkey. · Eur J Endocrinol. · Pubmed #15994744 links to  free full text

Abstract: BACKGROUND: Statins have apoptotic effects on many cell types. Hashimoto's thyroiditis (HT) is an autoimmune disease in which cell-mediated autoimmune mechanisms are pathogenetically involved. OBJECTIVE: The aim of this study was to evaluate the in vivo effects of Simvastatin on thyroid function, lymphocyte subtypes and also to investigate the apoptotic effects of Simvastatin, Mevastatin, Pravastatin and Cerivastatin on lymphocytes from patients with HT. METHODS: In the first part of the study, 11 patients with HT and subclinical hypothyroidism (SH) were given Simvastatin (20 mg/day) for 8 weeks. Ten patients with SH and HT served as the control group. No treatment was given to controls. Thyroid function, C-reactive protein (CRP) levels and lymphocyte subtypes of both groups were determined before the study and after 8 weeks. In the second part of the study, the apoptotic effects of statins on lymphocytes were evaluated in patients with HT (n = 10) and normal subjects (n = 10) in vitro. Apoptosis was investigated by using Annexin-V and propidium iodide. Lymphocytes from patients and controls were incubated with different concentrations of Simvastatin, Cerivastatin, Mevastatin and Pravastatin. RESULTS: An increase in serum free tri-iodothyronine and free thyroxine levels and a decrease in TSH levels were observed (P < 0.05) with Simvastatin treatment. CD4+ cells and B lymphocytes increased whilst CD8+ cells, natural killer cells and activated T lymphocytes decreased significantly in the treatment group (P < 0.05). The CRP level of the group also decreased with Simvastatin but it did not reach significance (P = 0.057). None of parameters was found to be different from the baseline in the control group. In in vitro experiments, apoptosis was observed in CD3 + (both in CD8+ and CD4+ cells) with all statins in both patient and control samples. Mevalonate, which was used in experiments, reversed apoptosis in some but not all samples. CONCLUSIONS: The results of this study suggested that Simvastatin is an immune modulatory agent and improves thyroid function in patients with HT. This effect is probably mediated via lymphocyte apoptosis as demonstrated with in vitro experiments and is not confined to Simvastatin since Mevastatin, Pravastatin and Cerivastatin also induced apoptosis in lymphocytes.

Syed AA, Evans C, Ludgate M, Lazarus JH. · Department of Medical Biochemistry, University Hospital of Wales and University of Wales College of Medicine, Cardiff, UK. · Med Princ Pract. · Pubmed #12966202 No free full text.

Abstract: OBJECTIVE: The aim of this study was to determine whether or not the titre of thyroid-stimulating hormone receptor antibody with stimulating (TRAb-S) activity changes in patients with Graves' disease (GD) or toxic multinodular goitres (TMNG) 3 months after treatment with sodium iodide ((131)I). SUBJECTS AND METHODS: Serum specimens were obtained from 21 hyperthyroid patients (15 with GD and 6 with TMNG) at a median 0.5 months before and 3 months after (131)I treatment using a standard ablative dose of 555 MBq. TRAb-S activity was measured in a sensitive and specific luminescent bioassay employing the lulu cell line and expressed as a stimulation index (SI; normal </=1.5). RESULTS: The mean TRAb-S in the GD patients was 2.72 SI (95% CI: 1.51-4.03) 0.5 months before administration of (131)I and 3.98 SI (95% CI: 1.20-6.76) 3 months after administration of (131)I. The difference was not statistically significant at p LT; 0.8. It was not elevated in the TMNG patients before (0.57 SI; 95% CI: 0.41- 0.73) and after (1.00 SI; 95% CI: 0.74-1.26) treatment either. CONCLUSIONS: Radioiodine therapy for GD or TMNG did not induce a significant change in TRAb-S activity at 3 months after treatment with (131)I, probably due to effective antithyroid therapy or the timing of samples.

Mazziotti G, Premawardhana LD, Parkes AB, Adams H, Smyth PP, Smith DF, Kaluarachi WN, Wijeyaratne CN, Jayasinghe A, de Silva DG, Lazarus JH. · Department of Medicine, University of Wales College of Medicine, Cardiff, UK. · Eur J Endocrinol. · Pubmed #12887286 links to  free full text

Abstract: OBJECTIVE: To study the evolution of thyroid autoimmunity, in relation to the change in goitre prevalence, during 3 Years of iodine prophylaxis in Sri Lanka. METHODS: Two groups of Sri Lankan schoolgirls between the ages of 10.8 and 17.5 Years were studied in 1998 (401 girls) and 2001 (282 girls). A prospective study was performed in 42 schoolgirls who were thyroid autoantibody (Ab)-positive (+ve) in 1998. Anthropometric measures, urinary iodine excretion (UIE), thyroid Volume, free thyroxine, free tri-iodothyronine, TSH, and thyroglobulin (Tg) and thyroid peroxidase (TPO) Ab were evaluated in all 683 girls. RESULTS: Goitre prevalence was significantly lower in 2001 compared with 1998 related to age (2.9% compared with 20.2%) and body surface area (11.6% compared with 40.8%), although UIE was unchanged. Prevalence of thyroid Ab in 2001 was also lower (23.4% compared with 49.9%); among those with the Ab, 34.8% had TgAb alone and 46.9% had a combination of TgAb+TPOAb, compared with 82.0% TgAb alone in 1998. In 2001, subclinical hypothyroidism was more frequent in Ab+ve (6.3%) than Ab-negative girls (1.0%). A cohort of 42 Ab+ve schoolgirls in 1998 (34 with TgAb alone, eight with TgAb+TPOAb) were evaluated again in 2001. Only 10 of them (23.8%) remained Ab+ve (mostly TPOAb+/-TgAb) in 2001. CONCLUSIONS: This study demonstrates that: (1) in 2001, goitre prevalence and thyroid autoimmunity rates were significantly lower than in 1998; (2) the pattern of thyroid Ab was different in the two surveys; (3) in 2001 alone, the occurrence of hypothyroidism was correlated with the presence of thyroid autoimmunity. These results indicate an evolution of thyroid autoimmune markers during the course of iodine prophylaxis, which has not been described before.

Premawardhana LD, Parkes AB, Ammari F, John R, Darke C, Adams H, Lazarus JH. · Department of Medicine, University of Wales College of Medicine, Cardiff, United Kingdom. · J Clin Endocrinol Metab. · Pubmed #10634366 links to  free full text

Abstract: Postpartum thyroid dysfunction (PPTD) occurs in 5% of women, with hypothyroidism developing in 23% of these after 3-5 yr. We have determined the prognostic significance of thyroid peroxidase antibody (TPOAb), thyroid ultrasound morphology (U/S), human leukocyte antigen haplotype, and postpartum thyroid status on the development of thyroid dysfunction 77-81 months after PPTD. Ninety-eight TPOAb-positive [48 who had developed PPTD (group 1) and 50 without PPTD (group 2)] and 70 TPOAb-negative (group 3) women (derived from 145 TPOAb-positive and 229 TPOAb-negative cohorts at the index pregnancy), with comparable ages, parity, pregnancies after index pregnancy, and follow-up duration, were studied. Thyroid dysfunction occurred in 46% of group 1 vs. 4% of group 2 (P<0.001) and 24.5% of groups 1 and 2 vs. 1.4% of group 3 (P<0.001). Factors predictive of thyroid dysfunction included a hypothyroid form of PPTD, TSH more than 20 mU/L, and higher TPOAb levels (213.8 kIU/L in group 1 vs. 131.8 kIU/L in group 2; P<0.002) during the postpartum period. Although TPOAb was higher in group 1 than in group 2 at follow-up (166 vs. 97.7 kIU/L; P<0.03), there was no significant fall in TPOAb levels within either group during the period of follow-up. The prevalence of ultrasound hypoechogenicity was higher in group 1 than in group 2 at follow-up (76% vs. 52%; P<0.006), but U/S improved in 62.5% of group 1 during the period of follow-up. Human leukocyte antigen DR10 was lower in those who developed late thyroid dysfunction. These data, representing the longest follow-up of PPTD women, clearly show that the hypothyroid form of PPTD, high TPOAb levels, and a hypoechogenic U/S pattern lead to a high risk (relative risk, 32) of long term thyroid dysfunction. This compares with a relative risk of 12.9 for TPOAb- and PPTD-positive women, who remained euthyroid at the end of the first postpartum year, and 2.8 for TPOAb-positive but PPTD-negative women, all compared to TPOAb-negative women. Therefore, long term surveillance of TPOAb- and PPTD-positive women (group 1) is indicated.

Manetti L, Parkes AB, Lupi I, Di Cianni G, Bogazzi F, Albertini S, Morselli LL, Raffaelli V, Russo D, Rossi G, Gasperi M, Lazarus JH, Martino E. · Department of Endocrinology, University of Pisa, Ospedale Cisanello, Via Paradisa 2, 56124 Pisa, Italy. · Eur J Endocrinol. · Pubmed #18787047 No free full text.

Abstract: OBJECTIVES: The aim of this study was to evaluate antipituitary antibody (APA) prevalence in a series of patients with postpartum thyroiditis (PPT) during pregnancy and in the postpartum. DESIGN: We conducted a nested case-control study on consecutive PPT and normal pregnant women at the Centre for Endocrine and Diabetes Sciences in Cardiff and at the Department of Endocrinology in Pisa. METHODS: We enrolled 30 women with PPT: 17 were hypothyroid (Hypo), 7 with hyperthyroidism (Hyper) and 6 with a transient hyperthyroidism followed by hypothyroidism (Biphasic). Twenty-one healthy pregnant women served as controls. APA (measured using indirect immunofluorescence), free thyroxine, free triiodothyronine, TSH, antithyroid autoantibodies, and thyroid ultrasound were performed during pregnancy and postpartum. The stored sera have been sent to Pisa, where serum APA, IGF1, and cortisol were measured. RESULTS: APA were found in 8 out of the 30 PPT patients (26.7%) and in one normal pregnancy (4.7%, P=0.063). Three out of the seventeen Hypo with PPT (17.6%), three out of the seven Hyper PPT (42.8%), and two out of the six Biphasic PPT (33.3%) were positive for APA. APA prevalence was not significantly different in the PPT subgroups (P=0.453). With one exception, APA all increased in the postpartum period (87.5%, P<0.016). Basal serum IGF1 and cortisol were in the normal range with the exception of two patients with positive APA who presented low serum IGF1 levels (36 and 45 ng/ml). CONCLUSIONS: APA are frequently present in the postpartum period in patients affected by PPT. Further studies are necessary to evaluate whether APA in PPT patients are associated with pituitary function impairment.