MyMedR

Slow carbamazepine clearance in a nonadherent Malay woman with epilepsy and thyrotoxicosis

Yeap LL, Lim KS, Ng CC, Hui-Ping Khor A, Lo YL

Ther Drug Monit, 2014 Feb;36(1):3-9.

PMID: 24342894 DOI: 10.1097/FTD.0000000000000024

The authors describe a case of a 37-year-old Malay lady with an unusually slow carbamazepine clearance, which may be related to genetic polymorphisms of drug metabolizing enzymes and transporters. When given a small daily dose of 200 mg immediate-release carbamazepine, this patient experienced drowsiness. Subsequently, she reduced her carbamazepine dose to 200 mg twice a week (on Mondays and Fridays), resulting in poor seizure control. At the same time, the patient was diagnosed with hyperthyroidism and was given carbimazole and propranolol. Hyperthyroidism and the concurrent use of these antihyperthyroid agents may have further slowed down the metabolism of carbamazepine. Therapeutic drug monitoring of carbamazepine was carried out, and a slow carbamazepine clearance of 1.45 L·h⁻¹ per 70 kg was observed. Genotyping of selected genetic variants in CYP3A4, CYP3A5, EPHX1, ABCB1, and ABCC2 revealed that she has CYP3A5*3/*3 and ABCB1 3435-CC genotypes. Both genotypes have been shown to be associated with higher adjusted mean serum carbamazepine concentration in Chinese and Korean patients with epilepsy. Physicians should be vigilant about the risk of adverse effects among patients with a slow carbamazepine clearance, especially in Malays. Simulations of carbamazepine dosing regimen based on the pharmacokinetic parameters of this patient were performed to allow individualization of drug therapy.

Matched MeSH terms: Thyrotoxicosis/drug therapy; Thyrotoxicosis/physiopathology*

Fulltext Thyrotoxic neuropathy- an under diagnosed condition

Sahni V, Gupta N, Anuradha S, Tatke M, Kar P

Med J Malaysia, 2007 Mar;62(1):76-7.

PMID: 17682580

Many neurological diseases like myopathy, periodic paralysis, ophthalmoplegia, and myasthenia gravis are known associations of thyrotoxicosis. However the association of neuropathy with thyrotoxicosis is not frequently recognized. First described by Charcot in 1889, thyrotoxic neuropathy or 'Basedow's Paraplegia' is a rarely reported entity. We describe here a case of a young woman with subacute distal neuropathy as the presenting manifestation of thyrotoxicosis. The neuropathy improved on antithyroid treatment. A careful literature search leads us to believe that peripheral neuropathy in thyrotoxicosis is under recognised. Thyroid function tests can be helpful in the diagnosis of this treatable neuropathy and should be included in the routine work up.

Matched MeSH terms: Thyrotoxicosis/complications*; Thyrotoxicosis/physiopathology

Fulltext Comparison of the efficacy of single and multiple regimens of carbimazole in the treatment of thyrotoxicosis

Mafauzy M, Wan Mohamad WB, Zahary MK, Mustafa BE

Med J Malaysia, 1993 Mar;48(1):71-5.

PMID: 8341175

Carbimazole, in 3 divided daily doses, is commonly prescribed for the treatment of thyrotoxicosis. However, based on its long intra-thyroid half-life, the drug may be effective when used as a single or twice daily dose. This study was undertaken to determine the effect of once, twice or thrice daily doses of carbimazole on thyroid function in patients with thyrotoxicosis. Seventy previously untreated thyrotoxic patients were randomly allocated to receive carbimazole 30 mg once (group 1), 15 mg twice (group 2) and 10 mg thrice (group 3) daily. All patients were also prescribed propranolol 20 mg thrice daily for the first 4 weeks. Blood was taken for total T3, T4, TSH, blood counts and liver enzymes determinations at the beginning and at 6 weeks of treatment. Only 48 (68.6%) patients were included in the analysis, as the rest defaulted follow-up (20.0%) or blood samples were not available at review (11.4%). Of the 48 patients, 17 were in group 1, 16 in group 2 and 15 in group 3. Following 6 weeks of treatment, there was no significant difference in the mean serum levels of total T3 and T4 between the 3 groups. However, there was a significant decrease in the mean serum levels of total T3 and T4 as compared to the start of the treatment. Four patients (23.5%) in group 1, 4 patients (25%) in group 2 and 3 patients (20%) in group 3 were still thyrotoxic at 6 weeks of treatment, whilst 10 patients (58.8%) in group 1, 6 patients (37.5%) in group 2 and 3 (20%) in group 3 were biochemically hypothyroid.(ABSTRACT TRUNCATED AT 250 WORDS)

Matched MeSH terms: Thyrotoxicosis/drug therapy*

Fulltext The prevalence of skin manifestations in thyrotoxicosis--a retrospective study

Ramanathan M, Abidin MN, Muthukumarappan M

Med J Malaysia, 1989 Dec;44(4):324-8.

PMID: 2520042

The presenting features of 236 thyrotoxic patients seen in the thyroid clinic were reviewed. 18.65% of these patterns had one or more dermatological complaints at presentation. There was no specific difference in this group of patients when compared with the general hyperthyroid population with regard to age, race, sex, duration of hyperthyroidism or biochemical indices of thyrotoxicosis. The two major complaints were itching and alopecia. The prevalence of pruritus at 6.4% in our series was identical to that of other workers, but we had a much lower occurrence of alopecia at 2.6%. The diagnosis of thyrotoxicosis was delayed in two patients in whom the only major complaint was pruritus. These symptoms cleared quickly when these patients became euthyroid. However there were other patients who noted hair loss with anti-thyroid medications. The incidence of vitiligo, eczema, onycholysis in our series was much lower those quoted in the Western literature The occurrence of pretibial myoxoedema in our series is similar to that of other workers from this region. The other miscellaneous manifestations include urticaria, xanthelasma and systemic lupus erythematosis. In conclusion we feel the cutaneous manifestations of hyperthyroidism are common in our patients.

Matched MeSH terms: Thyrotoxicosis/complications*; Thyrotoxicosis/diagnosis

Fulltext Thyrotoxicosis simulating lymphoma. A case report

Ramanathan M

Med J Malaysia, 1988 Mar;43(1):59-61.

PMID: 3244322

We report a patient with unusual manifestations of hyperthyroidism which initially suggested lymphoma. The pathophysiology of these features in thyrotoxicosis is discussed. The need to consider thyrotoxicosis in an otherwise unexplained case of lymphoid hyperplasia will be stressed.

Matched MeSH terms: Thyrotoxicosis/diagnosis*

Fulltext Euthyroid hyperthyroxinemia: a case report

Ramanathan M

Med J Malaysia, 1987 Mar;42(1):65-7.

PMID: 3431505

This report deals with the problems of a young man who was clinically euthyroid but biochemically hyperthyroid. The possibility of peripheral resistance to thyroid hormones to explain this paradoxical state is discussed. The importance of recognising this condition to avoid the erroneous diagnosis of thyrotoxicosis and inappropriate therapy is stressed.

Matched MeSH terms: Thyrotoxicosis/blood*

Fulltext Psychoses associated with thyrotoxicosis: a retrospective study of twenty cases

Tan CK

Med J Malaysia, 1985 Sep;40(3):247-51.

PMID: 3842721

A total of 23 patients with psychoses associated with thyrotoxicosis were admitted to the psychiatric unit of a University Hospital over a 13-year period, of which 20 patients were included in this retrospective study. It was found that a parallel relationship between thyrotoxicosis and psychosis appears to exist in six patients, while in the remaining 14 patients, the course of the two disease processes were largely independent of each other. Paranoid delusions and auditory hallucinations were the most prominent psychiatric symptoms. Depression was commonly seen even in patients who were not having an affective illness. In four patients, a mixed schizo-affective psychosis was seen, suggesting that the diagnostic distinction between the affective and schizophrenic reactions are often blurred in psychosis associated with thyrotoxicosis.

Matched MeSH terms: Thyrotoxicosis/complications*

Fulltext Dysphagia as a primary manifestation of thyrotoxicosis: a case report

Ramanathan M

Med J Malaysia, 1989 Mar;44(1):83-6.

PMID: 2626117

This report deals with a middle aged man in whom the presenting symptom of the disorder was dysphagia. The clinical approach to the final diagnosis of thyrotoxic myopathy causing dysphagia is outlined and the pathophysiology of dysphagia then discussed. The need to include thyrotoxicosis in the differential diagnosis of an otherwise unexplained case of dysphagia is stressed.

Matched MeSH terms: Thyrotoxicosis/complications; Thyrotoxicosis/diagnosis*

Fulltext Transient hypothyroidism following I131 treatment for thyrotoxicosis

Zaini A, Ngan A, Paramsothy M, Khoo BH, Ch'ng SL

Med J Malaysia, 1983 Dec;38(4):331-3.

PMID: 6599994

Matched MeSH terms: Thyrotoxicosis/radiotherapy*

Thyrotoxicosis with special reference to treatment with neomercazole; a study of 120 cases

ONG WH

Med J Malaya, 1959 Mar;13(3):201-14.

PMID: 13666188

Matched MeSH terms: Thyrotoxicosis*

Fulltext Thyrotoxic periodic paralysis: a report of 3 Malaysian cases and a review of its pathology

Sthaneshwar P, Prathibha R, Yap SF

Malays J Pathol, 2005 Jun;27(1):29-32.

PMID: 16676690

Thyrotoxic periodic paralysis (TPP) is a medical emergency characterised by sudden onset of muscle weakness with hypokalemia that resolves with the treatment of hyperthyroidism. We report three cases of thyrotoxic periodic paralysis seen at the Accident and Emergency Care Department, University of Malaya Medical Centre in a period of four months. We also review the clinical presentation, pathophysiology, biochemical features and management of TPP. All three patients were young Asian males, presenting with muscle weakness of sudden onset. The first patient presented with lower limb weakness and had symptoms of thyrotoxicosis and goitre. He had a previous similar episode which resolved spontaneously. The second patient presented with quadriplegia, respiratory acidosis and had no signs and symptoms of thyrotoxicosis. The electrocardiogram of this patient showed normal sinus rhythm with U wave in V3 and a flat T wave, which are characteristic of hypokalaemia. The third patient, who was a known case of thyrotoxicosis, was admitted thrice for hypokalemic paralysis during the study period. All cases had low serum potassium, suppressed TSH and elevated T4 confirming thyrotoxic periodic paralysis. Potassium therapy was useful during the crisis; however prophylactic potassium has not been shown to prevent attacks as seen in one of our cases.

Matched MeSH terms: Thyrotoxicosis/diagnosis; Thyrotoxicosis/pathology*; Thyrotoxicosis/physiopathology

Fulltext Results of long-term follow-up after compensated fixed-dose therapy for thyrotoxicosis

Zaini A, Khir A, Doi SA, Chan SP, Paramsothy M, Khoo BH

J Int Med Res, 1992 Jun;20(3):279-88.

PMID: 1397673

To evaluate the effects of simple compensated fixed-dose iodine-131 therapy for thyrotoxicosis, the long-term results for 74 patients treated with a fixed dose of iodine-131 ranging from 5 to 12 mCi (185 to 444 MBq) were evaluated in the first 2 years of a trial. The dose selected was loosely based on the gross size of the thyroid gland. Routine antithyroid drug therapy was given for a minimum of 3 months after iodine-131 therapy. The mean (+/- SD) duration of follow-up was 74.5 +/- 42 months. The results indicated that roughly 25% of patients treated in this way will become hypothyroid after 5 years and that 85% are cured (need no further therapy during the follow-up period) using a single dose of iodine-131. Of those cured using a single iodine-131 dose, 81% were no longer receiving drugs after 6 months and 85% after 1 year. Such a regimen seems currently to be among the best available where prolonged periods of medication-free euthyroidism after therapy are sought.

Matched MeSH terms: Thyrotoxicosis/radiotherapy*

Thyrotoxic periodic paralysis and intravenous propranolol in the emergency setting

Birkhahn RH, Gaeta TJ, Melniker L

J Emerg Med, 2000 Feb;18(2):199-202.

PMID: 10699522

A 27-year-old male of Malaysian descent presented to the Emergency Department (ED) with rapidly progressive flaccid paralysis that quickly compromised his respiratory effort. The patient was found to have a serum potassium of 1.9 meq/L, and was diagnosed as having an acute paralytic episode secondary to thyrotoxic periodic paralysis. The paralytic attack was aborted with a combination of potassium replacement and parenteral propranolol in large doses. We report the use of a rarely described, yet possibly more effective, therapy for an acute attack of thyrotoxic periodic paralysis.

Matched MeSH terms: Thyrotoxicosis/complications; Thyrotoxicosis/diagnosis*

Fulltext Primary thyroid lymphoma with elevated free thyroxine level

Yahaya N, Din SW, Ghazali MZ, Mustafa S

Singapore Med J, 2011 Sep;52(9):e173-6.

PMID: 21947158

Primary thyroid lymphoma (PTL) is a rare form of thyroid cancer that is known to be associated with Hashimoto thyroiditis. This association is supported by the presence of elevated titres of both antithyroglobulin and antimicrosomal antibodies in up to 95 percent of patients with PTL. Most patients with PTL present with a rapidly enlarging neck mass and compressive symptoms. The majority of thyroid cancer patients have normal levels of thyroid hormones; they are rarely hyperthyroid, with no obvious clinical features of thyrotoxicosis. We describe a patient who presented with minimal clinical features of thyrotoxicosis despite having markedly elevated serum free thyroxine and suppressed serum thyroid-stimulating hormone levels.

Matched MeSH terms: Thyrotoxicosis/blood; Thyrotoxicosis/diagnosis

Fulltext Thyrotoxicosis in pregnancy--a six year review

Lim BH, Raman S, Sivanesaratnam V, Ngan A

Singapore Med J, 1989 Dec;30(6):539-41.

PMID: 2635396

Twenty eight patients with hyperthyroidism complicating their pregnancies were seen at the Obstetrics and Gynaecology Department, University Hospital, Kuala Lumpur, Malaysia in a six-year period. All patients were treated with antithyroid drugs, carbimazole being the mainstay of treatment. The incidence of the disease was 0.9 per 1000 births and was similar with other series. No cases of fetal goitre were noted. The mean birth weight was 2952 g; there was no significant difference in the birth weight of term live births in patients treated with carbimazole alone or carbimazole combined with propranolol.

Matched MeSH terms: Thyrotoxicosis/drug therapy*; Thyrotoxicosis/epidemiology

Fulltext Weathering the Crisis: A Case of Thyroid Crisis with Propranolol-Induced Circulatory Collapse Successfully Treated with Therapeutic Plasma Exchange

Cheah JM, Ng D, Low MY, Foo SH

J ASEAN Fed Endocr Soc, 2019;34(2):206-209.

PMID: 33442157 DOI: 10.15605/jafes.034.02.12

Thyroid crisis is a life-threatening form of thyrotoxicosis characterized by multi-system dysfunction. Therapeutic plasma exchange has been reported to be effective in removing excessive circulating thyroid hormones. We present a 46-year-old female with recently diagnosed Graves' disease associated with thyrotoxic cardiomyopathy admitted for thyroid crisis complicated by propranolol-induced circulatory collapse, acute kidney injury and ischemic hepatitis. The tachyarrhythmia was refractory to conventional therapy. Initiation of TPE resulted in rapid clinical and biochemical stabilization.

Matched MeSH terms: Thyrotoxicosis

Prolonged Exercise Test in Patients With History of Thyrotoxicosis

Tan HT, Tan CY, Teong CS, Ratnasingam J, Goh KJ

J Clin Neurophysiol, 2020 Aug 05.

PMID: 32773648 DOI: 10.1097/WNP.0000000000000766

PURPOSE: Thyrotoxic periodic paralysis is characterized by recurrent episodes of reversible, severe proximal muscle weakness associated with hypokalemia and hyperthyroidism. Prolonged exercise test is an easy, noninvasive method of demonstrating abnormal muscle membrane excitability in periodic paralyses. Although abnormal in thyrotoxic periodic paralysis patients, the effects thyroid hormone levels in non-thyrotoxic periodic paralysis thyrotoxicosis patients have not been well studied. The study aims to evaluate thyrotoxicosis patients (regardless of thyrotoxic periodic paralysis history) with prolonged exercise test and correlate it with their thyroid status.

METHODS: This is a prospective, cross-sectional study of consecutive thyrotoxicosis patients seen at the endocrine clinic of a tertiary medical center. Thyroid status was determined biochemically before prolonged exercise test. Compound muscle action potential (CMAP) amplitudes postexercise were compared against pre-exercise amplitudes and recorded as percentage of mean baseline CMAP amplitude. Comparisons of time-dependent postexercise CMAP amplitudes and mean CMAP amplitude decrement were made between hyperthyroid and nonhyperthyroid groups.

RESULTS: Seventy-four patients were recruited, 23 (31%) men, 30 (41%) Chinese, and the mean age was 48.5 ± 16.8 years. Of 74 patients, 32 (43%) were hyperthyroid and 42 (57%) were nonhyperthyroid viz. euthyroid and hypothyroid. Time-dependent CMAP amplitudes from 10 to 45 minutes after exercise were significantly lower in hyperthyroid patients compared with nonhyperthyroid patients (P < 0.01). Mean CMAP amplitude decrement postexercise was significantly greater in hyperthyroid than nonhyperthyroid patients (23.4% ± 11.4% vs. 17.3% ± 10.5%; P = 0.02).

CONCLUSIONS: Compound muscle action potential amplitude declines on prolonged exercise test were significantly greater in hyperthyroid patients compared with nonhyperthyroid patients. Muscle membrane excitability is highly influenced by thyroid hormone level. Thyrotoxic periodic paralysis occurs from increased levels of thyroid hormone activity in susceptible patients.

Matched MeSH terms: Thyrotoxicosis

A reversible dilated cardiomyopathy due to thyrotoxicosis

Jeyamalar R, Chan SP

Int J Cardiol, 1995 Nov 10;52(1):83-4.

PMID: 8707441

Thyrotoxicosis gives rise to a high output cardiac failure. Rarely, it can cause a dilated cardiomyopathy with severe impairment of myocardial function which improves significantly following treatment.

Matched MeSH terms: Thyrotoxicosis/complications*; Thyrotoxicosis/therapy

Plasma renin and aldosterone in thyroid diseases

Asmah BJ, Wan Nazaimoon WM, Norazmi K, Tan TT, Khalid BA

Horm. Metab. Res., 1997 Nov;29(11):580-3.

PMID: 9479560 DOI: 10.1055/s-2007-979105

The effect of thyroid hormones on the renin-angiotensin-aldosterone system has not been fully resolved. Highly specific immunoassays for measurement of renin, aldosterone, free T4 (fT4), free T3 (fT3) and ultrasensitive TSH enables a direct and more accurate measurement of these hormones. We investigated the relationship between plasma renin, aldosterone and thyroid hormones in the basal state and after intravenous frusemide. This is a cross-sectional study involving 37 patients with thyrotoxicosis, 42 rendered euthyroid with normal fT4, fT3 and TSH levels, 17 with euthyroid levels of fT4 and fT3 but suppressed TSH, and 11 with hypothyroidism. Basal plasma renin was significantly higher in thyrotoxicosis (63.4 +/- 9.8 microU/ml, mean +/- SEM) compared to euthyroid (32.7 +/- 4.4 microU/ml) and hypothyroid (26.7 +/- 9.8 microU/ml). Basal plasma renin for euthyroid with suppressed TSH (41.0 +/- 7.4 microU/ml) was significantly higher than hypothyroid (p = 0.02). Basal plasma aldosterones were not significantly different except for suppressed TSH (157.7 +/- 13 pg/ml), which was higher than normal (109.9 +/- 10.4 pg/ml; p = 0.04). Following frusemide, plasma renin and aldosterone were significantly increased in all groups. Plasma renin was highly correlated to fT3 (r = 0.405, p < 0.001), total T3 (r = 0.359, p < 0.001), fT4 (r = 0.331, p < 0.001) and TSH (r = 0.300, p < 0.001) in the basal state, but less to total T4 (r = 0.248, p < 0.01). Plasma renin correlated poorly to serum aldosterone (r = 0.212, p < 0.03). This study clearly showed that regulation of renin was mainly influenced by fT3, and that aldosterone response to frusemide was blunted in thyrotoxicosis despite normal electrolytes.

Matched MeSH terms: Thyrotoxicosis/blood

Thyrotoxicosis in pregnancy

Ong HC

Family Practitioner, 1977;2:25-28.

Matched MeSH terms: Thyrotoxicosis

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