Prediction-based prompt levothyroxine replacement to prevent a hypothyroid state after immune-related adverse events involving the thyroid gland.

Immune checkpoint inhibitors (ICIs) are used for various malignancies, although they frequently cause immune-related adverse events involving the thyroid gland (thyroid irAEs). We conducted a retrospective cohort study to elucidate thyroid function outcomes. Fifty of 639 patients who received PD-1 blockade therapy met criteria and were divided into the following groups: thyrotoxicosis with subsequent hypothyroidism (Toxic-Hypo, n = 21); thyrotoxicosis without subsequent hypothyroidism (Toxic, n = 9); and hypothyroidism without prior thyrotoxicosis (Hypo, n = 20). The Toxic-Hypo group developed thyroid irAEs earlier than the Toxic group (26 vs. 91 days; p < 0.001), and had higher serum free T4 levels (3.210 vs. 1.880 ng/dL; p = 0.011). In addition, positive anti-thyroglobulin antibodies (TgAbs) at thyroid irAE onset were more common in the Toxic-Hypo group (93.3%) than in the Toxic group (0.0%; p = 0.005) and Hypo group (44.4%; p = 0.007). The Toxic-Hypo group developed severe hypothyroidism and required larger levothyroxine (LT4) doses than the Hypo group (75 vs. 25 µg/day; p = 0.007). We predicted that patients with positive TgAbs who developed severe thyrotoxicosis within 4 weeks after the first ICI administration would develop subsequent hypothyroidism. We treated 4 such patients with prompt LT4 replacement, characterized by LT4 initiation after thyrotoxicosis improvement and quick dose titration. Their euthyroid state was successfully maintained, in contrast with patients receiving conventional replacement. In conclusion, rapid-onset severe thyrotoxicosis in patients with TgAbs correlated with a high likelihood of subsequent hypothyroidism. Accordingly, prompt LT4 replacement is suggested to prevent a severely hypothyroid state.

Concurrent Subacute Thyroiditis and Graves' Disease After COVID-19: A Case Report.

There are many reports of subacute thyroiditis (SAT) that occurred after the coronavirus disease 2019 (COVID-19), but no such case has been reported in Korea. Moreover, the simultaneous occurrence of SAT and Graves' disease (GD) is rare. Here, we describe a patient who developed SAT and GD after the second episode of COVID-19. A 27-year-old woman with no known history of thyroid disease presented with fever, upper respiratory tract symptoms, and painful neck swelling. Thyroid function tests revealed thyrotoxicosis, and thyroid ultrasound showed heterogeneous echogenicity of enlarged thyroid glands. Her initial clinical presentation was consistent with SAT after viral infection, with typical neck tenderness and spontaneous improvement of thyrotoxicosis without antithyroid drug use. However, this case had some atypical features, such as an elevated thyroid-stimulating immunoglobulin level, relapse of thyrotoxicosis in short-term follow-up, and increased Tc-99m pertechnetate uptake, suggesting the coexistence of GD. About two months after methimazole (15 mg/day) was prescribed, she was lost to follow up again. We report the first case of unusual co-occurrence of SAT and GD following COVID-19.

Audit of long-term treatment outcomes of thyrotoxicosis in a single-centre virtual clinic: The utility of long-term antithyroid drugs.

OBJECTIVE: To investigate the long-term outcomes and prognosis of thyrotoxicosis in a large number of patients in a single UK county (Leicestershire). DESIGN: Retrospective cohort analysis of 56,741 thyroid function test (TFT) results, treatment modalities and outcomes in a well-established virtual thyrotoxicosis clinic database. PATIENTS: One thousand four hundred and eighty-nine patients were included with a median length of follow-up of 10.9 years. The aetiology of thyrotoxicosis was autoimmune (85.9%), nodular (9.1%) and mixed (5.0%). Treatment modalities included antithyroid drugs (ATDs), radioiodine (RAI; 555 MBq fixed dose) and thyroidectomy. METHODS: We analysed both individual TFTs and groups of sequential TFTs on or after the same thyroid treatment(s), which we describe as 'phase of thyroid care' (POTC). Patients studied entered the virtual clinic between 1 January 1995 and 1 January 2010; we exported data on every TFT sample up to April 2020. RESULTS: ATD had been used in 99.2% (median 2, maximum seven courses) with long-term ATD (>2 years) in 48%. RAI and thyroidectomy were used more commonly with nodular and mixed aetiology. Overall, T4 was more often controlled than thyroid-stimulating hormone (TSH), and at the latest follow-up, T4 was normal in >96%, TSH in >79% and both in >76% of different aetiologies. The mean percentage control of T4 was 85% and TSH 50%; in long-term ATD courses, this improved to 89% and 62%, respectively. In the latest POTC, control of T4 and TSH was best in cases off treatment (95%/87%) and on T4 without ablative therapy (94%/72%), but was broadly similar in patients on long-term ATD (90%/68%), after RAI (92%/60%) or after thyroidectomy (91%/58%). After the first course of ATD, remission or hypothyroidism was seen in 47.3% autoimmune, 20.9% nodular and 32.5% mixed, with 90% relapses seen within 4 years. Relapse was more common in patients with ophthalmopathy, but there was no difference between the sexes. CONCLUSIONS: Thyrotoxicosis can be well controlled with minimal specialist clinic attendance using a software-supported virtual shared-care scheme. Long-term ATD appears to be a valid patient choice achieving TFT control comparable to that seen after RAI or surgery. In patients with autoimmune disease, relapse is more common in patients with ophthalmopathy, and hypothyroidism is common after RAI. In nodular disease, we found that spontaneous remission may occur.

Diagnosis and Management of Fetal and Neonatal Thyrotoxicosis.

Background and Objectives: Clinical fetal thyrotoxicosis is a rare disorder occurring in 1-5% of pregnancies with Graves' disease. Although transplacental passage of maternal TSH receptor stimulating autoantibodies (TRAb) to the fetus occurs early in gestation, their concentration in the fetus is reduced until the late second trimester, and reaches maternal levels in the last period of pregnancy. The mortality of fetal thyrotoxicosis is 12-20%, mainly due to heart failure. Case report: We present a case of fetal and neonatal thyrotoxicosis with favorable evolution under proper treatment in a 37-year-old woman. From her surgical history, we noted a thyroidectomy performed 12 years ago for Graves' disease with orbitopathy and ophthalmopathy; the patient was hormonally balanced under substitution treatment for post-surgical hypothyroidism and hypoparathyroidism. From her obstetrical history, we remarked a untreated pregnancy complicated with fetal anasarca, premature birth, and neonatal death. The current pregnancy began with maternal euthyroid status and persistently increased TRAb, the value of which reached 101 IU/L at 20 weeks gestational age and decreased rapidly within 1 month to 7.5 IU/L, probably due to the placental passage, and occurred simultaneously with the development of fetal tachycardia, without any other fetal thyrotoxicosis signs. In order to treat fetal thyrotoxicosis, the patient was administered methimazole, in addition to her routine substitution of 137.5 ug L-Thyroxine daily, with good control of thyroid function in both mother and fetus. Conclusions: Monitoring for fetal thyrotoxicosis signs and maternal TRAb concentration may successfully guide the course of a pregnancy associated with Graves' disease. An experienced team should be involved in the management.

Medical treatment of thyrotoxicosis.

Medical treatment is the primary therapeutic option for thyrotoxicosis/hyperthyroidism. Two groups of causes of thyrotoxicosis (i.e. thyrotoxicosis with hyperthyroidism and thyrotoxicosis without hyperthyroidism) need to be considered for therapeutic reasons. Herein we provide an updated review on the role of conventional medical therapies (i.e. ß-blockers, antithyroid drugs [ATDs], corticosteroids, inorganic iodide, perchlorate, cholecystographic agents, lithium, cholestyramine) in the main causes of thyrotoxicosis, starting from the rationale subtending their clinical application.

Two Cases of Thyrotoxicosis due to Redotex Ingestion, a Mexican Weight Loss Drug.

BACKGROUND: Redotex™ is a Mexican weight-loss supplement that is not U.S. Food and Drug Administration-approved. It consists of the following five ingredients: tri-iodothyronine 75 µg, atropine 0.36 mg, diazepam 8 mg, aloin 16 mg, and d-norpseudoephedrine 50 mg per tablet. There are few case reports with clinically severe ingestions. We report two cases of clinical thyrotoxicosis due to use of Redotex. CASE REPORTS: A 29-year-old woman presented to the emergency department (ED) with anxiety and palpitations. She reported taking Redotex daily for 1 week. Her temperature was 37.1°C, blood pressure (BP) was 166/104 mm Hg, and heart rate (HR) was 140 beats/min. Laboratory analysis was significant for a bicarbonate level of 20 mmol/L (reference 22-29 mmol/L), free T4 0.75 ng/dL (reference 0.93-1.70 ng/dL), and thyroid-stimulating hormone (TSH) 0.05 uIU/mL (reference 0.27-4.20 uIU/mL). She was treated with 2 mg i.v. lorazepam and 20 mg oral propranolol. A 37-year-old woman presented with chest pain, palpitations, and nausea after taking Redotex 1 to 2 tablets daily for 6 weeks. Her HR was 134 beats/min and BP was 130/66 mm Hg. Thyroid function tests on initial presentation showed a TSH of 0.013 uU/mL, free T4 of 0.24 ng/dL, and free T3 of >30 pg/mL. She was treated with propranolol 1 mg i.v. twice per day and 2 doses of lorazepam 1 mg. Both patients had resolution of their symptoms. WHY SHOULD AN EMERGENCY PHYSICIAN BE AWARE OF THIS?: When taken chronically and at recommended doses, Redotex can present with clinically significant T3 thyrotoxicosis. This has not been seen in prior reports.

Amiodarone-induced thyrotoxicosis. / Amiodaronindusert tyreotoksikose.

We see an increasing number of patients with amiodarone-induced thyrotoxicosis. This condition can be treated pharmacologically, but treatment over several months may give rise to adverse reactions. In most cases we recommend that amiodarone therapy be continued despite newly detected thyrotoxicosis. Particularly in cases of heart failure, one should not wait too long before considering thyroidectomy. Treatment of amiodarone-induced thyrotoxicosis must be delivered with close collaboration between endocrinologist and cardiologist.

Heart failure from thyrotoxicosis due to Graves' disease.

A 30-year-old female patient with a past medical history of pernicious anaemia presented with pleuritic chest pain, palpitations, fatigue, coryzal symptoms and a high temperature. She was hypoxic and tachycardic and was extensively investigated as well as aggressively treated. A type 1 'gut feeling' assessment by the admitting medical registrar made the diagnosis possible as thyroid function tests were grossly deranged and pointed to Graves' disease causing heart failure, complicated by pneumonia. The patient was discharged on carbimazole, antibiotics and beta blockers. Due to a resultant thrombocytopaenia, she has now been swapped onto propylthiouracil and is under active follow up.

Effect of high-dose intravenous glucocorticoid therapy on serum thyroid hormone concentrations in type 2 amiodarone-induced thyrotoxicosis: an exploratory study.

PURPOSE: Type 2 amiodarone-induced thyrotoxicosis (AIT2) is a form of drug-induced destructive thyroiditis, usually treated with oral glucocorticoids (oGCs). Our objective was to investigate the short-term effects of intravenous glucocorticoids (ivGCs) on serum thyroid hormone concentrations in patients with AIT2. METHODS: Exploratory study of three naive AIT2 patients treated with iv methylprednisolone (two pulses of 400 mg with no interpulse oGCs), followed by oGCs, matched 1:3 with AIT2 patients treated with oGCs alone. Changes in serum thyroid hormone concentrations were evaluated in the short-term period (24 h and 7 days) and after a cumulative dosage of 400 and 800 mg equivalents of methylprednisolone; in addition, healing time and duration of exposure to GCs were calculated. RESULTS: During the first 24 h of treatment, serum FT4 concentrations increased in ivGCs patients, and decreased in oGCs patients (+ 3.3% vs - 10.7%, respectively, p = 0.025). After 7 days, serum FT4 and FT3 concentrations decreased significantly in both groups, with no statistical difference between them (p = 0.439 for FT4 and p = 0.071 for FT3), even though the cumulative GCs dose was higher in ivGCs than in oGCs patients (800 mg vs 280 mg, p = 0.008). Furthermore, the iv administration of single 400 mg pulses of methylprednisolone resulted in a less significant decrease in serum thyroid hormone concentrations when compared to equivalent GCs doses fractionated in several consecutive days (p = 0.021 for FT4 and p = 0.052 for FT3). There were no significant differences in the healing time (p = 0.239) and duration of exposure to GCs (p = 0.099). CONCLUSIONS: High-dose ivGCs therapy does not offer advantages over standard oGCs therapy in the rapid, short-term control of AIT2.

A pregnant woman with an autonomously functioning thyroid nodule: a case report.

BACKGROUND: The epidemiology and natural history of autonomously functioning thyroid nodules (AFTNs) have not been elucidated. Here we report the pregnant Japanese woman with an AFTN. CASE PRESENTATION: The patient was a 31-year-old woman who was hospitalized due to the placenta previa associated with threatened abortion at the 16 weeks of her third pregnancy. At her second pregnancy, she was euthyroid but had a single, 2.3 cm nodule on her right thyroid lobe. Her thyroid hormone level was trended increased with her pregnancy progression, and the thyrotoxic state was remained after delivery. Before her third pregnancy, her hyper-vascular nodule enlarged to 3.4 cm at regular monitoring. When she visited our hospital, she was at 16 weeks of pregnancy and had thyrotoxicosis with negative TSH-receptor antibody. She delivered a baby weighing 2615 g without hypothyroidism at 39 weeks of pregnancy by natural delivery. After delivery, a 99mTc scintigram showed a hot spot in her right thyroid lobe. She was diagnosed with AFTN and treated with methimazole while nursing. CONCLUSIONS: This case showed that hCG stimulation during pregnancy caused thyroid nodule enlargement and enhanced thyroid hormone production. The pregnancy could be the pathological stimulus and provides chance to diagnosis for AFTNs.

Atypical hemolytic uremic syndrome precipitated by thyrotoxicosis: a case report.

BACKGROUND: Autoimmune thyroid disease (AITD) has a complex pathogenesis and is associated with the development of autoimmunity against the thyroid. Graves' disease and Hashimoto's thyroiditis are the two main types of AITD, and they are characterized by thyrotoxicosis and hypothyroidism, respectively. Atypical hemolytic uremic syndrome (aHUS) is a rare disease, presenting with microangiopathic hemolytic anemia, thrombocytopenia, and acute kidney injury. aHUS is caused by dysregulation of the alternative complement pathway, and its co-existence with AITD is rare. CASE PRESENTATION: We report the case of a 12-year-old girl with recent onset thyrotoxicosis. She was first treated with propylthiouracil for 2 months and then developed AITD presenting as abrupt-onset thrombocytopenia, acute kidney injury, and microangiopathic hemolytic anemia. Thyroid function tests favored hyperthyroidism, with increased free T4 and free T3 levels and a very low level of thyroid-stimulating hormone (TSH). We suspected aHUS, and the patient's condition responded dramatically to therapeutic plasma exchange (TPE) with disease remission. She experienced recurrent aHUS after subsequently receiving methimazole for 1 month, and in the recurrent episode, her condition responded again to TPE and concomitant glucocorticoids. She achieved euthyroidism with thiamazole ointment treatment, without aHUS recurrence during the 6-month follow-up. Mycophenolate mofetil was administered to manage proteinuria after 3 months of treatment with the steroid and angiotensin-converting enzyme inhibitor. CONCLUSIONS: The coexistence of aHUS and AITD in this case is likely more than coincidence, because both are autoimmune in origin. aHUS is associated with a high mortality without appropriate therapy, and treatment with TPE and adjunct immunosuppressants can be helpful.

Outcomes After Urgent Thyroidectomy Following Rapid Control of Thyrotoxicosis in Graves' Disease are Similar to Those After Elective Surgery in Well-Controlled Disease.

BACKGROUND: Surgery for Graves' disease (GD) is usually performed after adequate control with medical treatment. Occasionally, rapid pre-operative optimization is required. The primary objective was to compare the outcomes of patients undergoing elective surgery for well-controlled GD with those undergoing rapid pre-operative treatment. We also propose a formal treatment protocol for future use. METHODS: A retrospective cohort study in a tertiary referral centre included 247 patients with well-controlled GD undergoing elective surgery and 19 patients with poorly controlled disease undergoing surgery after rapid optimization. The latter group did not respond well to thionamides (carbimazole and/or propylthiouracil) or had intolerance or side effects to thionamides and were treated with a range of non-thionamide drugs, including Lugol's iodine, cholestyramine, beta blockers and steroids (with or without thionamides), and closely monitored for 1-2 weeks before surgery. Outcome measures included thyroid storm, hypoparathyroidism and recurrent laryngeal nerve palsy. RESULTS: In total, 266 patients with male-to-female ratio of 1:6 and median (interquartile range) age of 39 (31-51) were included. Overall, long-term recurrent laryngeal palsy and hypoparathyroidism occurred in 1 (0.38%) and 13 (4.9%) patients, respectively. No patient had thyroid storm. There was no significant difference in hypoparathyroidism (p = 1), vocal cord palsy (p = 0.803) and post-operative bleeding (p = 0.362), between elective surgery and rapid optimization groups. CONCLUSION: Rapid pre-operative treatment is effective, safe and is associated with similar outcomes compared to usual treatment. A rapid pre-operative optimization protocol is proposed.

Thyrotoxicosis: an unusual cause of syncope.

Syncope is a common emergency department (ED) chief complaint, with many known but also unknown causes. Here we present a novel ED presentation of a young woman with new-onset hyperthyroidism that masqueraded as a syncopal event with head trauma. A 21-year-old woman arrived in the ED with head trauma as the result of seemingly unprovoked syncope, due to her history as well as the nature of her trauma. Persistent tachycardia during her ED course after an unremarkable full trauma evaluation prompted ordering of additional lab testing, which revealed evidence of thyrotoxicosis. Here we consider the possibility of thyroid dysfunction resulting in syncope.

Treatment choice, satisfaction and quality of life in patients with Graves' disease.

BACKGROUND: Thyrotoxicosis, most often caused by Graves' disease (GD), when treated inadequately may result in premature mortality. There is little consensus as to which of the 3 treatment options available - antithyroid drugs (ATD), radioactive iodine (RAI) and surgery, is better. AIMS: (i) To assess factors involved in treatment choice and treatment satisfaction in patients treated for Graves' disease; (ii) To assess quality of life (QoL) following treatment of Graves' disease. METHOD: Participants were selected from a prospective study cohort assessing thyrotoxicosis incidence and severity. Of the 172 eligible patients with Graves' disease, 123 treated patients participated (64% had received ATD only, 11% RAI and 25% total thyroidectomy, the latter 2 usually after a period of ATD), along with 18 untreated patients with newly diagnosed Graves' disease (overall participation rate, 73%). Consented patients completed a questionnaire detailing factors involved in treatment choice, QoL and satisfaction with treatment. RESULTS: Participants reported that the most important factors in choosing a treatment were the following: the effects on activities of daily living, concern about use of radioiodine, possibility of depression or anxiety, and doctor's recommendations. Satisfaction levels were high across all 3 treatment types. QoL 1-year following treatment was higher than in untreated patients, and comparable with other international studies. CONCLUSIONS: Patient satisfaction with therapy and QoL does not differ by treatment type. Therefore, clinical and social factors, in combination with patient choice and resource availability, should determine which treatment modality patients with Graves' disease should receive.

Diabetic Ketoacidosis Associated with Thyroxine (T4) Toxicosis and Thyrotoxic Cardiomyopathy.

Thyrotoxicosis and diabetic ketoacidosis (DKA) both may present as endocrine emergencies and may have devastating consequences if not diagnosed and managed promptly and effectively. The combination of diabetes mellitus (DM) with thyrotoxicosis is well known, and one condition usually precedes the other. Furthermore, thyrotoxicosis is complicated by some degree of cardiomyopathy in at least 5% de patients; but the coexistence of DKA, thyroxin (T4) toxicosis, and acute cardiomyopathy is extremely rare. We describe a case of a man, previously diagnosed with DM but with no past history of thyroid disease, who presented with shock and severe DKA that did not improve despite optimal therapy. The patient evolved with acute pulmonary edema, elevated troponin levels, severe left ventricular systolic dysfunction, and clinical and laboratory evidence of thyroxin (T4) toxicosis and thyrotoxic cardiomyopathy. Subsequently, the patient evolved favorably with general support and appropriate therapy for DKA and thyrotoxicosis (hydrocortisone, methimazole, Lugol's solution) and was discharged a few days later.

Hyperthyroidism.

Hyperthyroidism is characterised by increased thyroid hormone synthesis and secretion from the thyroid gland, whereas thyrotoxicosis refers to the clinical syndrome of excess circulating thyroid hormones, irrespective of the source. The most common cause of hyperthyroidism is Graves' disease, followed by toxic nodular goitre. Other important causes of thyrotoxicosis include thyroiditis, iodine-induced and drug-induced thyroid dysfunction, and factitious ingestion of excess thyroid hormones. Treatment options for Graves' disease include antithyroid drugs, radioactive iodine therapy, and surgery, whereas antithyroid drugs are not generally used long term in toxic nodular goitre, because of the high relapse rate of thyrotoxicosis after discontinuation. ß blockers are used in symptomatic thyrotoxicosis, and might be the only treatment needed for thyrotoxicosis not caused by excessive production and release of the thyroid hormones. Thyroid storm and hyperthyroidism in pregnancy and during the post-partum period are special circumstances that need careful assessment and treatment.

RELATIONSHIP BETWEEN THE EFFECTIVENESS OF INORGANIC IODINE AND THE SEVERITY OF GRAVES THYROTOXICOSIS: A RETROSPECTIVE STUDY.

OBJECTIVE: Inorganic iodine is often used to treat patients with Graves thyrotoxicosis who do not tolerate thionamides due to adverse effects. However, predictors of continued inorganic iodine efficacy have not been fully elucidated. This study aimed to investigate the factors affecting the continued efficacy of potassium iodide (KI) in patients with Graves thyrotoxicosis. METHODS: In this study, among 1,197 patients with Graves disease who were initially treated with thionamides, we retrospectively studied 24 consecutive Japanese patients whose treatment was changed to KI alone due to the adverse effects of thionamides. We divided these patients into 2 groups: patients who had maintained euthyroid function for at least 180 days (nonrecurrence group, n = 11), and patients who had not maintained euthyroid function for 180 days (recurrence group, n = 13). RESULTS: Free triiodothyronine (FT3) and free thyroxine (FT4) levels on the day of changing from thionamides to KI were statistically higher in the recurrence group than in the nonrecurrence group (FT3, 9.3 [range, 5.2-11.6] vs. 3.7 [3.3-4.8] pg/mL, P = .02 and FT4, 3.6 [1.8-4.5] vs. 1.4 [1.2-1.9] ng/dL, P = .02). FT4 levels on the day of drug change were significantly higher in the recurrence group, even after adjusting for thionamide or KI dose. In the recurrence group, the duration of KI effect was inversed correlated with FT3 and FT4 levels on the day of drug change. CONCLUSION: Continued efficacy of KI after thionamides might be inversely correlated with thyrotoxicosis severity on the day of drug change. ABBREVIATIONS: ANOVA = analysis of variance eTV = estimated thyroid volume FT3 = free triiodothyronine FT4 = free thyroxine IQR = interquartile range KI = potassium iodide MMI = thiamazole PTU = propylthiouracil RAIT = radioactive iodine therapy TRAb = TSH receptor antibody TSH = thyroid stimulating hormone.

Convexity Subarachnoid Hemorrhage Due to Cardioembolic Stroke in a Woman with Thyrotoxicosis: Α Case Report.

BACKGROUND: Non-traumatic convexity subarachnoid hemorrhage (cSAH) is a rarely reported condition with a wide spectrum of etiologies. Cerebral ischemia secondary to extracranial or intracranial atherosclerotic disease has been identified as a relatively uncommon cause of cSAH. CASE REPORT: We report a case of cSAH caused by cardioembolic stroke. A 69-year old female patient developed suddenly left-sided face and body weakness and numbness and visual neglect on the left. She was newly detected with paroxysmal atrial fibrillation on the ground of thyrotoxicosis. Brain magnetic resonance imaging revealed ischemia of embolic pattern with cSAH. Further evaluation excluded other cause of hemorrhage. Dilation of leptomeningeal collateral vessels and rupture of pial vessels in distal cortical arteries may caused cSAH. Full anticoagulation was initiated. After one month, her condition improved significantly (NIHSS from 6 to 2). CONCLUSIONS: cSAH may be a rare complication of cardioembolic stroke.

Thyrotoxic Channelopathies.

Thyrotoxic periodic paralysis (TPP), a disorder most commonly seen in Asian men, is characterized by abrupt onset of hypokalemia and paralysis. The condition primarily affects the lower extremities and is secondary to thyrotoxicosis. Early recognition of TPP is vital to initiating appropriate treatment and to avoiding the risk of rebound hyperkalemia that may occur if high-dose potassium replacement is given. Here we present a case of 31 year old male with thyrotoxic periodic paralysis with diagnostic and therapeutic approach.

Role of a gitogenin-type steroidal saponin (3-O-ß-d-glucopyranosyl (1→2)-ß-d-glucopyranosyl (1→4)-ß-d-galactopyranoside-25R,5α-spirostane-2α,3ß-diol), isolated from the leaves of Malvastrum coromandelianum in regulating thyrotoxicosis in rats.

The hitherto unknown role of saponin in the regulation of thyrotoxicosis has been revealed in chemically-induced thyrotoxic rats. l-T4 (l-thyroxine) administration at pre-standardized dose of 500-µg/kg body weight for 12days increased the levels of thyroid hormones, enhanced the activity of hepatic 5'-monodeiodinase I (5'DI) and glucose-6-phosphatase (G-6Pase) as well as lipid peroxidation (LPO) with a parallel decrease in the levels of antioxidative enzymes. However, administration of the isolated saponin for 15days ameliorated the T4-induced alterations in serum thyroid hormones, hepatic LPO, G-6-Pase and 5'DI activity, and improved the cellular antioxidant status, indicating its antithyroidal and antioxidative potential. These effects of the test compound were comparable to a reference antithyroid drug, Propylthiouracil (PTU), suggesting that the test saponin may act as a potent anti-thyroid agent.