Biotin induced biochemical hyperthyroidism: a case report and review of the literature.

BACKGROUND: Biotin is a commonly used supplement for hair, nail, and skin. Recent literature suggests that high-dose biotin therapy for neurological diseases like Multiple sclerosis can interfere with lab results that use biotin/streptavidin immunoassay, called biotin interference. Biotin interference can affect thyroid lab results, giving biochemical hyperthyroidism. CASE PRESENTATION: Our patient, a 64-year-old white man with a known history of multiple sclerosis, presented with elevated free T3, free T4, and low TSH that resembled hyperthyroidism. He had no symptoms of hyperthyroidism except some fatigue and tachycardia on the first encounter. He was started on anti-thyroid medications. He was then re-evaluated since his lab results remained the same after two months of anti-thyroid medications. It was found that he was on biotin, 10000mcg/day, for his multiple sclerosis. Biotin was discontinued, and five days later his lab results returned to normal values. CONCLUSION: The lack of knowledge of biotin use by patients can lead to misdiagnosis of patients' thyroid lab results and improper management. Awareness about biotin interference and abnormal thyroid lab values should be a priority among clinicians and the public. If the biotin is discontinued on time, such misdiagnosis can be avoided.

Postoperative Hypocalcemia in Hyperthyroid Patients: The Parathyroids Aren't Always to Blame.

INTRODUCTION: Hypocalcemia is commonly reported after thyroidectomy and has multiple possible etiologies including: parathyroid devascularization, reactive hypoparathyroidism from relative hypercalcemia in thyrotoxicosis, and abrupt reversal of thyrotoxic osteodystrophy. In patients that are actively hyperthyroid and undergoing thyroidectomy, it is not known how many experience hypocalcemia from nonhypoparathyroidism etiologies. Therefore, our aim was to examine the relationship among thyrotoxicosis, hypocalcemia, and hypoparathyroidism. METHODS: A retrospective review was performed of prospectively-collected data from all patients undergoing thyroidectomy for hyperthyroidism by 4 surgeons from 2016 to 2020. All patients carried a diagnosis of Graves' disease or toxic multinodular goiter. Patient demographics, preoperative medications, laboratory reports, and postoperative medications were reviewed. Hypocalcemia within the first month of surgery despite a normal parathyroid hormone (PTH) level was the primary outcome of interest and was compared between patients with and without thyrotoxicosis. Secondary outcomes were duration of postoperative calcium use and the relationship between preoperative calcium supplementation and postoperative calcium supplementation. Descriptive statistics, Wilcoxon rank-sum, and chi-square tests were used for bivariate analysis, as appropriate. RESULTS: A total of 191 patients were identified, with mean age of 40.5 y (range 6-86). Most patients were female (80%) and had Graves' disease (80%). At the time of surgery, 116 (61%) had uncontrolled hyperthyroidism (thyrotoxic group, Free Thyroxine >1.64 ng/dL or Free Triiodothyronine > 4.4 ng/dL), with the remaining 75 (39%) considered euthyroid. Postoperative hypocalcemia (calcium < 8.4 mg/dL) developed in 27 (14%), while hypoparathyroidism (PTH < 12 pg/mL) was observed in 39 (26%). Thyrotoxic patients comprised a majority of those with hypocalcemia (n = 22, 81%, P = 0.01) and hypoparathyroidism immediately following surgery (n = 14, 77%, P = 0.04). However, a majority of initially hypocalcemic, thyrotoxic patients had normal PTH values within the first month after surgery (n = 17, 85%), pointing to a potential nonparathyroid etiology. On bivariate analysis, no significant relationship was found for thyrotoxic patients with initial postoperative hypocalcemia (18%) and hypoparathyroidism <1-month after surgery (29%, P = 0.29) or between 1 and 6 mo after surgery (2%, P = 0.24). Of the 19 patients in the nonhypoparathyroidism group, 17 (89%) were off all calcium supplements by 6 mo postop. CONCLUSIONS: In patients with hyperthyroidism, those in active thyrotoxicosis at time of surgery have a higher rate of postoperative hypocalcemia compared to euthyroid patients. When hypocalcemia lasts >1 mo postoperatively, data from this study suggest that hypoparathyroidism may not be the primary etiology in many of these patients, who typically require calcium supplementation no more than 6 mo postoperatively.

Factitious thyrotoxicosis and thyroid hormone misuse or abuse.

Factitious thyrotoxicosis (FTT) is a common form of thyroid hormone (TH) abuse involving voluntary but concealed intake of an excessive amount of TH. In most cases, FTT seeks to improve body composition with a decrease in body fat and weight while maintaining apparent fitness. It is frequent in Munchausen syndrome, to attract attention for care. It can involve excessive intake either of thyroxine (T4) or of thyroid extracts or liothyronine (T3). In addition, several dietary supplements available on-line were shown to contain clinically relevant amounts of T4 and T3. TH abuse also occurs in elite athletes and bodybuilders, to reach the appropriate weight and prioritize fat loss. Diagnosis should be suspected whenever the typical features of hyperthyroidism or endogenous thyrotoxicosis are not present, as prolonged overlooked TH abuse can lead to severe consequences, including life-threatening events.

The Perspective of Unani Medicine in Understanding Hyperthyroidism.

Context: Hyperthyroidism, Kasrat-e-Ifraz-e-Darqiyya in Unani medicine, is a condition in which the thyroid gland produces an excessive amount of the thyroid hormone thyroxine. Its clinical features are excessive sweating, heat intolerance, increased bowel movements, a voracious appetite, insomnia, tremors, palpitations, and a rapid pulse. Objective: This review intended to investigate the observations in ancient Unani literature, Traditional Chinese Medicine (TCM), and Ayurveda that correspond to the clinical presentation of hyperthyroidism as well as to identify probable treatments in Unani medicine. Design: The research team performed a narrative review to evaluate the concept of hyperthyroidism using classical Unani Medicine books, such as Firdaus-Ul-Hikmat (Wisdom of Paradise), Al-Havi Fit Tib (Liber Continence), Kamil- Us- Sana (Liber Regius), Al-Qanoon (The Canon of Medicine), and Zakheera Khvarazm Shahi (The Treasure of Medicine) to assess the perception of hyperthyroidism. The team also searched internet sources, such as Pubmed, Medline, Scopus, Web of Science, Publons, and Google Scholar. using keywords such as Su-e-Mizaj Ha'ar Maddi, Ghair Tabayi Safra, Yang-Yin, Pitta, hyperthyroidism. The study was undertaken at National Institute of Unani medicine, Bengaluru, India. Results: In TCM, a dominant Yang Qi is considered as cause of hyperthyroidism; in Ayurveda, excessive Pitta production is considered as its cause, and in Unani Medicine it is due to an excess of abnormal bile (Ghair Tabayi Safra). Thus, the traditional systems all view the disease as a manifestation of excessive energy production. Conclusions: The clinical symptoms of the hot temperament of bile (Su-e-Mizaj Ha'ar Maddi) and hyperthyroidism are similar in the literature. The resemblance may help medical practitioners to recommend a better approach for preventing, treating, and reducing the condition's devastating complications using the treatment approach of Unani medicine. It approaches hyperthyroidism with recommendations for reducing excessive energy production, with the help of restoration of the imbalance in temperament (Mizaj).

How to manage Graves' disease in women of childbearing potential.

The management of Graves' disease (GD) in women of childbearing potential has multiple specific complexities. Many factors are involved, which differ at the various stages from preconception, conception, first trimester, later pregnancy, postpartum and lactation, with both maternal and foetal considerations. The incidence and significance of the risks incurred from antithyroid drugs (ATDs) in pregnancy have been re-evaluated recently and must be balanced against the risks of uncontrolled hyperthyroidism during childbearing years. Contraception is advised until hyperthyroidism is controlled. ATD cessation should be considered in those who are well controlled on low dose therapy before conception and in early pregnancy. Advice on iodine supplementation does not generally differ in those with GD. Radioiodine (RAI) is contraindicated from 6 months preconception until completion of breastfeeding. In all women who have a history of GD, monitoring of TSH receptor antibodies (TRAb) is strongly recommended during pregnancy, and if elevated, foetal monitoring and assessment of thyroid function in the neonate are required. Of note, RAI increases TRAb for up to a year, making this treatment option even less attractive in this patient group. A small amount of ATD is transferred into breast milk but low doses are safe during lactation. Routine periodic thyroid function testing is recommended in remission to detect postpartum GD recurrence. We present our approach to the Clinical Question 'How to manage GD in women of childbearing potential?'

[Factitious hyperthyroidism due to intake of herbal supplements for weight reduction]. / Hipertiroidismo facticio por ingesta de suplementos herbales para reducción de peso.

Factitious thyrotoxicosis is characterized by the intentional or accidental intake of excess thyroid hormones or their derivatives. We describe 6 cases of patients who developed thyrotoxicosis and adverse effects by weight-reducing herbal medicines. Currently there is a lot of publicity about supplements that "help to lose weight", which are over-the-counter and widely distributed in health food stores or online, which is why it is common to have patients who consume them, without many noticing their possible risks. If factitious hyperthyroidism is suspected, we should request thyroglobulin and anti-thyroglobulin tests, as well as a thyroid scan or uptake curve. To make the differential diagnosis between intake of thyroxine (T4) or triiodothyronine (T3) or its derivatives, we must request the measurement of T4 and T3. In case of ingestion of T4, T4 and T3 will be elevated, but in case of ingestion of triodothyronine or its derivatives, T4 will be decreased with elevated T3.

La tirotoxicosis facticia se caracteriza por la ingesta de un exceso de hormonas tiroideas o derivados de las mismas de forma intencional o accidental. Describimos 6 casos clínicos de pacientes que desarrollaron tirotoxicosis y efectos adversos con la ingesta de suplementos de herbales de venta libre para descenso de peso. Actualmente existe mucha publicidad sobre suplementos que "ayudan al descenso de peso", los cuales son de venta libre y distribuidos ampliamente en tiendas de dietéticas o por internet por lo cual es habitual tener pacientes que los consumen, sin que muchos reparen en sus posibles riesgos. En caso de sospechar un hipertiroidismo facticio debemos solicitar tiroglobulina y anticuerpos anti tiroglobulina así como centellograma tiroideo o curva de captación. Para realizar el diagnóstico diferencial entre ingesta de tiroxina (T4) o triiodotironina (T3) o sus derivados debemos solicitar medición de T4 y T3. En caso de ingesta de T4, la T4 y T3 se encontrarán elevadas, pero en caso de ingesta de triodotironina o sus derivados la T4 se encontrará descendida con una T3 elevada.

Follow-Up of Thyroid Function in Children With Neonatal Hyperthyroidism.

Introduction: Neonatal hyperthyroidism mainly occurring in the children born to mothers with Graves' disease (GD). The influence of maternal GD on the newborn's thyroid function includes not only hyperthyroidism, but also various forms of hypothyroidism. Maternally transferred thyrotropin receptor antibodies (TRAb), the antithyroid drug (ATD) administration during pregnancy and previous definitive treatment of GD (radioactive iodine therapy or thyroidectomy) in the mother impact the function of the fetal/neonatal thyroid. Some newborns born to mothers with GD may present central hypothyroidism (CeH) due to impaired regulation of the fetal hypothalamic-pituitary-thyroid axis. The aim of this study was to evaluate different types of thyroid dysfunction in babies with neonatal hyperthyroidism. Materials and Methods: Medical records of 14 infants with neonatal hyperthyroidism (13 born to mothers with GD, and one born to mother with Hashimoto thyroiditis) were analyzed. Results: Transient hyperthyroidism was the main thyroid dysfunction in our study group. Overt hyperthyroidism with highly increased TRAb levels (mean 13.0 ± 7.0 IU/L) was diagnosed in 6 (43%) neonates. Another 6 (43%) babies presented hyperthyroidism with slightly increased fT4 and/or fT3 levels and TSH levels in the lower limit of the normal range coinciding with positive TRAb levels (mean 3.8 ± 1.6 IU/L). Normal thyroid hormone levels with TSH levels below the lower limit of the range were observed in 2 (14%) neonates. Four babies in the study group (28.5%) required further levothyroxine (L-T4) supplementation due to CeH or, in one case, due to primary hypothyroidism. Conclusion: Our study highlights the need for prolonged monitoring of thyroid function in children born to mothers with GD. Diagnosis of CeH could be delayed due to its masking by transient hyperthyroidism. Prolonged thyroid-stimulating hormone suppression after TRAb elimination should be considered as a signal announcing CeH.

Thyrotoxic periodic paralysis in two sexagenarian men: A case report.

RATIONALE: Thyrotoxic periodic paralysis (TPP) characterized by the triad of muscle paralysis, acute hypokalemia, and the presence of hyperthyroidism is often reported in young adults but rarely reported in age >60 year-old. PATIENT CONCERNS: Two sexagenarian males (age 61 and 62) presenting to the emergency department with progressive muscle paralysis for hours. There was symmetrical flaccid paralysis with areflexia of lower extremities. Both of them did not have the obvious precipitating factors and take any drugs. DIAGNOSIS: Their Wayne scores, as an objective index of symptoms and signs associated with thyrotoxicosis, were <19 (7 and 14, respectively). Their blood pressure stood 162/78 and 170/82 mm Hg, respectively. Their thyroid glands were slightly enlarged. Both of them had severe hypokalemia (1.8 and 2.0 mmol/L). Their presumptive diagnosis of mineralocorticoid excess disorders with severe potassium (K+) deficit were made. However, low urine K+ excretion and relatively normal blood acid-base status were suggestive of an intracellular shift of K+ rather than K+ deficit. Hormone studies confirmed hyperthyroidism due to Graves disease. INTERVENTIONS: A smaller dose of K+ supplementation (only a total of 50 and 70 mmol K+, respectively) were prescribed for the patient. OUTCOMES: After treatment, their serum K+ levels became normal with a full recovery of muscle strength. LESSONS: Our 2 cases highlight the fact that thyrotoxic periodic paralysis must be still kept in mind as the underlying cause of hypokalemia with paralysis and hypertension in elderly patients to avoid missing curable disorders.

Lithium carbonate as add-on therapy to radioiodine in the treatment on hyperthyroidism: a systematic review and meta-analysis.

BACKGROUND: The main purpose is to investigate the effect of LiCO3 as an add-on therapy with radioactive iodine in increasing the cure and decreasing the T4 level compared to radioactive iodine alone. The primary outcome is the cure rate as defined by the number of hyperthyroid patients who became euthyroid or hypothyroid. The secondary outcome is the T4 level. METHODS: Four databases were searched (PubMed, Scopus, Web of Science, and Cochrane central library). The inclusion criteria were randomized and non-randomized clinical trials of hyperthyroidism patients receiving LiCO3 with radioiodine compared with hyperthyroidism patients receiving radioactive iodine alone. Included studies were appraised with the risk of bias version 2 tool, according to the Cochrane Handbook for Systematic Reviews of Interventions 5.1.0. RESULTS: Nine studies were eligible for inclusion in the study, six randomized control trials and three non-randomized control trials. There were 477 patients in the intervention group and 451 patients in the control group. The cure rate was not significantly different between the two groups, while it was significantly increased with 5000 to 6500 mg optimized cumulative dose of LiCO3 compared with the control group, P = 0.0001. The T4 level showed no significant difference between the two groups, P = 0.13. CONCLUSIONS: LiCO3 adjunct to radioactive iodine did not show significant differences compared with radioactive iodine alone in terms of cure rate or decreasing T4 level. However, the dose of 5000 to 6000 mg of LiCO3 may increase the cure rate.

At the origin of "Endocrinology and Art": Woman's Head (third century BCE).

In 1911, the Danish physician Hans Christian Gram (1853-1938) sustained to have found signs of hyperthyroidism in a marble head of a Roman woman that he observed in the Ny Carlsberg Glyptotek in Copenhagen. It could be one of the first examples of a clinical diagnosis of an endocrine disease in an ancient statue.

[Intake of high dose biotin: A cause of artificial hyperthyroidism]. / La prise de biotine à fortes doses : une cause d'hyperthyroïdie biologique factice.

INTRODUCTION: Many hormone immunoassays use the biotin streptavidin interaction to immobilize immune complexes. The intake of high dose biotin can interfere with immunoassays using the biotin streptavidin interaction. The biotin-immunoassay interference generates falsely low or falsely high tests of hormones according to the type of immunoassay used. CASE REPORT: A 70-year-old patient, with progressive multiple sclerosis, was referred to our hospital for thyrotoxicosis. She was found to have markedly elevated thyroid hormones level (T3-T4) and decreased thyrotropin (TSH) level but she had no symptoms of hyperthyroidism. An ingestion of biotin, that is more and more frequent in patients with progressive multiple sclerosis, was found. Thyroid function tests normalized after discontinuation of biotin treatment. CONCLUSION: The discrepancy between a clinical exam which is not indicative of thyrotoxicosis and markedly abnormal thyroid function tests should lead to a search for biotin intake, which can interfere with thyroid function tests.

Monitoring of Thyroid Malfunction and Therapies in Pregnancy and the Postpartum Period: A Systematic Updated Critical Review of the Literature.

PURPOSE: From the very beginning of pregnancy, the maternal thyroid has to adapt to increased thyroid hormone secretion of up to 50%. This is paralleled by changes in thyroid-stimulating hormone secretion and by the thyroid-topic action of human chorionic gonadotropin. Thus, hypothyroidism and hyperthyroidism may occur. Many women exhibit preexisting thyroid diseases. This review tries to add the most recently published approaches to diagnosing thyroid malfunction in pregnancy to existing guidelines. METHODS: Different literature-based approaches to diagnosing thyroid malfunction during pregnancy and the postpartum period were applied. To diagnose thyroid malfunction in pregnancy, trimester-specific reference ranges for thyroid-stimulating hormone and T4 are used. RESULTS: Definitions of thyroid malfunction are given. Treatment schedules for various thyroid diseases were reviewed and, on the basis of recent findings, were revised where necessary. For a daily clinical workup, this outline not only suggests diagnostic and therapeutic steps but also refers to frequent pitfalls and misinterpretations of laboratory data. CONCLUSIONS: Although the body of knowledge is increasing rapidly, the authors believe that this review is able to present new ideas concerning diagnostic and therapeutic tools for thyroid malfunction in pregnancy and the postpartum period. Nevertheless, there seems to remain room for individual approaches based on the personal experience of physicians who deal with these issues regularly.

Unraveling the Molecular Basis for Successful Thyroid Hormone Replacement Therapy: The Need for New Thyroid Tissue- and Pathway-Specific Biomarkers.

Thyroid function is conventionally assessed by measurement of thyroid-stimulating hormone (TSH) and free circulating thyroid hormones, which is in most cases sufficient for correct diagnosis and monitoring of treatment efficiency. However, several conditions exist, in which these parameters may be insufficient or even misleading. For instance, both, a TSH-secreting pituitary adenoma and a mutation of thyroid hormone receptor ß present with high levels of TSH and circulating hormones, but the optimal treatment is substantially different. Likewise, changes in thyroid hormone receptor α signaling are not captured by routine assessment of thyroid status, as serum parameters are usually inconspicuous. Therefore, new biomarkers are urgently needed to improve the diagnostic management and monitor treatment efficiency for e. g., replacement therapy in hypothyroidism or thyroid hormone resistance. By comparing animal models to human data, the present minireview summarizes the status of this search for new tissue- and pathway-specific biomarkers of thyroid hormone action.

Transient Hyperthyroidism following the ingestion of complementary medications containing kelp seaweed: A case-report.

RATIONALE: The prevalence of obesity has increased over the past few years, becoming a public health problem. Generally, the primary therapeutic remedies are diet, physical exercise, medication, and bariatric surgery. However, an increased number of obese and overweight people are using complementary and herbal slimming supplements. PATIENT CONCERNS: A 70-years-old Caucasian woman presented to the outpatient clinic with tachycardia (>100 bpm), insomnia, anxiety, and recent weight loss (6 kilos in 3 months). She had no previous thyroid disease, but she presented transient hyperthyroidism at 3 months after ingestion of tablets containing kelp seaweeds. DIAGNOSES: Hypertensive and obese patient, without previous thyroid disease, presented with transient hyperthyroidism at 3 months following ingestion of tablets containing kelp seaweed. INTERVENTIONS: The kelp-containing tablets were discontinued, and antithyroid therapy with Methimazole was initiated as follows: Methimazole at 15 mg/day for 1 month, at 10 mg/day in the second month, and 5 mg/day for the third month. OUTCOMES: After 3 months of antithyroid therapy and without the consumption of kelp - containing tablets, normal thyroid function was regained. Further analysis revealed normal thyroid function, so the hyperthyroidism reversed completely. LESSONS: Adults who consume complementary medication based on kelp seaweed should be informed of the risk of developing thyroid dysfunction also in the absence of any pre-existing thyroid disease. Due to the high iodine content, supplements containing kelp should be taken with the supervision of a physician and with monitoring of thyroid function.

Excess iodine intake: sources, assessment, and effects on thyroid function.

Iodine is essential for thyroid hormone synthesis. High iodine intakes are well tolerated by most healthy individuals, but in some people, excess iodine intakes may precipitate hyperthyroidism, hypothyroidism, goiter, and/or thyroid autoimmunity. Individuals with preexisting thyroid disease or those previously exposed to iodine deficiency may be more susceptible to thyroid disorders due to an increase in iodine intake, in some cases at intakes only slightly above physiological needs. Thyroid dysfunction due to excess iodine intake is usually mild and transient, but iodine-induced hyperthyroidism can be life-threatening in some individuals. At the population level, excess iodine intakes may arise from consumption of overiodized salt, drinking water, animal milk rich in iodine, certain seaweeds, iodine-containing dietary supplements, and from a combination of these sources. The median urinary iodine concentration (UIC) of a population reflects the total iodine intake from all sources and can accurately identify populations with excessive iodine intakes. Our review describes the association between excess iodine intake and thyroid function. We outline potential sources of excess iodine intake and the physiological responses and consequences of excess iodine intakes. We provide guidance on choice of biomarkers to assess iodine intake, with an emphasis on the UIC and thyroglobulin.

Interference of High Dose Biotin Supplementation with Thyroid Parameters in Immunoassays Utilizing the Interaction between Streptavidin and Biotin: a Case Report and Review of Current Literature.

BACKGROUND: Automated immunoassays utilizing the interaction between streptavidin and biotin are widely used. Nonetheless, biotin remains an often overlooked confounder. METHODS: We report the case of a 54-year-old female patient with progressive multiple sclerosis and Hashimoto's thyroiditis who presented herself for a follow-up. Measurements on Roche's cobas® 8000 modular analyzer series suggested severe hyperthyroidism. Initially, no relevant confounders could be identified. RESULTS: All requested thyroid parameters were measured with alternative methods, yielding plausible results. CONCLUSIONS: Biotin is a significant confounder in many immunoassays. Alternative measurement methods or methods of biotin neutralization need to be implemented for certain situations.

An unsuspected complication with immune checkpoint blockade: a case report.

BACKGROUND: Immunotherapy treatment with immune-checkpoint blockade has become a new paradigm in cancer treatment. Despite its efficacy, it has also given rise to a new class of adverse events, immune-related adverse events, which may affect any organ, including the thyroid and the pituitary. CASE PRESENTATION: We present a case of a 77-year-old Caucasian man with metastatic renal cell carcinoma on immunotherapy treatment who was admitted to our hospital with a severe persistent headache of sudden onset. He had been on corticosteroid therapy for 10 days for suspected immune-related thyroiditis. The patient had tachycardia and mild diarrhea, and his thyroid function tests were compatible with subclinical hyperthyroidism with a suppressed thyroid-stimulating hormone level of 0.01 µIU/ml (0.4-4.5), a raised free T4 level of 2.17 ng/dl (0.7-1.9), and a free T3 level of 4.66 pg/ml (2.27-5). Computed tomography and magnetic resonance imaging revealed an enlargement of the pituitary gland compatible with macroadenoma. In the face of a probable immune-related hypophysitis, high-dose corticosteroid treatment was started. A posterior hormonal evaluation revealed secondary hypothyroidism with a suppressed thyroid-stimulating hormone level of 0.11 µIU/ml (0.4-4.5) and low thyroid hormones, a normal free T4 level of 1.02 ng/dl (0.7-1.9), and a low free T3 level of 1.53 pg/ml (2.27-5). These new findings suggested central hypothyroidism possibly due to pituitary apoplexy as a complication of the macroadenoma. Therefore, levothyroxine substitution was started along with the previously started corticosteroid therapy. The patient's headache and asthenia gradually resolved, and after a few days, he was released from the hospital with levothyroxine substitution and corticosteroid tapering. CONCLUSIONS: This case emphasizes the importance of the differential diagnosis when dealing with patients on immune checkpoint inhibitors because other non-immune-related events may present. Our patient was finally diagnosed with immune-related hyperthyroidism and a concurrent pituitary macroadenoma. This case also highlights the importance of a prompt start of corticosteroid therapy once immune-related adverse events such as hypophysitis are suspected, because otherwise the outcome would be fatal.

An atypical presentation of high potassium renal secretion rate in a patient with thyrotoxic periodic paralysis: a case report.

BACKGROUND: Hypokalemia is one of the most common clinical electrolyte imbalance problems, and thyrotoxic periodic paralysis (TPP) is a leading cause of presentation to the emergency department. Low renal potassium secretion rates, a normal acid-base balance in the blood, and hyperthyroidism are the hallmarks of suspected TPP. CASE PRESENTATION: Here we report the case of a 36-year-old man who presented to the emergency department with a sudden onset of acute muscle weakness at 5 h prior to admission. Biochemistry tests revealed hypokalemia with hyperthyroidism and renal potassium wasting. TPP was initially not favored due to the presence of renal potassium wasting. However, his serum potassium level rebounded rapidly within several hours after potassium supplementation, indicating that the intracellular shifting of potassium ions was the main etiology for his hypokalemia. The early stage of TPP development may have contributed to this paradox. CONCLUSION: Therefore, it is premature to rule out TPP based on the presentation of high renal potassium secretion rates alone. This finding may result in an incorrect impression being made in the early stage of TTP and may consequently lead to an inappropriate potassium supplementation policy.

[Thyroid and pregnancy]. / Schilddrüse und Schwangerschaft.

During pregnancy thyroid hormones have profound effects on embryonal/fetal development and maternal health. Therefore, thyroid gland disorders should be immediately diagnosed and adequately treated. Pregnancy-specific physiological alterations during pregnancy cause changes in the reference interval for thyroid-stimulating hormone levels and trimester-specific thresholds must be taken into account. This article summarizes the most important diagnostic and therapeutic aspects before, during and after pregnancy. With reference to the period prior to pregnancy, the article discusses iodide supplementation, preconceptional examination of thyroid gland metabolism and the importance of thyroid gland functional disorders for fertility and fulfilling the desire to have children. With a view to the period during pregnancy, the effect of hypothyroxinemia, hypothyroidism, and hyperthyroidism as well as the effects of their treatment on the development of the child are explained. Finally, a description is given of what must be paid attention to in the breast-feeding period and in postpartum thyroiditis.

Leptin, neuropeptide Y (NPY), melatonin and zinc levels in experimental hypothyroidism and hyperthyroidism: relation with melatonin and the pineal gland.

Background Melatonin, an important neurohormone released from the pineal gland, is generally accepted to exercise an inhibitor effect on the thyroid gland. Zinc mediates the effects of many hormones and is found in the structure of numerous hormone receptors. Aim The present study aims to examine the effect of melatonin supplementation and pinealectomy on leptin, neuropeptide Y (NPY), melatonin and zinc levels in rats with hypothyroidism and hyperthyroidism. Methods This study was performed on the 70 male rats. Experimental animals in the study were grouped as follows: control (C); hypothyroidism (PTU); hypothyroidism + melatonin (PTU + M); hypothyroidism + pinealectomy (PTU + Pnx); hyperthyroidism (H); hyperthyroidism + melatonin (H + M) and hyperthyroidism + pinealectomy (H + Pnx). Blood samples collected at the end of 4-week procedures were analyzed to determine melatonin, leptin, NPY and zinc levels. Results It was found that thyroid parameters thyroid stimulating hormone (TSH), free triiodthyronine (FT3), free thyroxine (FT4), total T3 (TT3) and total T4 (TT4) decreased in hypothyroidism groups and increased in the groups with hyperthyroidism. The changes in these hormones remained unaffected by melatonin supplementation and pinealectomy. Melatonin levels rose in hyperthyroidism and fell in hypothyroidism. Leptin and NPY levels increased in both hypothyroidism and hyperthyroidism. Zinc levels, on the other hand, decreased in hypothyroidism and pinealectomy, but increased in hyperthyroidism. Conclusion The results of the study demonstrate that hypothyroidism and hyperthyroidism affect leptin, NPY, melatonin and zinc values in different ways in rats. However, melatonin supplementation and pinealectomy do not have any significant influence on the changes occurring in leptin, NPY and zinc levels in thyroid dysfunction.