Hyperthyroidism treatment by alternative therapies based on cupping and dietary-herbal supplementation: a case report.

OBJECTIVES: Hyperthyroidism is characterized by increasing production of thyroid hormone (TH) and decreasing of thyroid stimulation hormone (TSH) secretion. The treatment of hyperthyroidism includes such as anti-thyroid drugs, radioiodine, and thyroidectomy have many side effects without complete curing results. We described a successful treatment of hyperthyroidism patient with dietary-herbal supplementation with wet cupping without any medicine. CASE PRESENTATION: A 29-years female, blood analysis showed that she had low TSH (0.012 mlU/mL), and normal levels of T3 and T4. After completing 16 weeks on Carbimazole, TSH value still low (0.024 mlU/mL) and urticaria was appeared. She decided to stop Carbimazole and try alternative therapy choices. She received wet cupping and dietary-herbal supplementations (including royal jelly, green barley grass and Taraxaf®) for two months. Notably, TSH values was increased during-after intervention and urticaria was disappeared. CONCLUSIONS: Alternative therapy could be a beneficial choice for hyperthyroidism treatment without any side effects or complications under physician supervision.

Thyrotoxic Periodic Paralysis with Hypokalemia in an Adult Male from Nepal: A Case Report.

Thyrotoxic periodic paralysis is rare complication of hyperthyroidism characterized by the sudden onset of hypokalemia and muscle paralysis. It is typically present in young Asian males. There are very few literatures regarding the occurrence of thyrotoxic hypokalemic periodic paralysis in Nepal. We reported a case of a 35-year-old male presented with the chief complaints of weakness of all four limbs of 1 day duration. He was diagnosed as a case of hyperthyroidism in the past, received treatment for 6 months and left medications on his own 6 months ago. Evaluation during admission revealed severe hypokalemia with serum potassium level 1.3mEq/l and high serum Triiodothyronine (>20.00µg/L) and low serum Thyroid Stimulating Hormone (<0.01µg/L). Potassium supplements resolved muscle weakness and the patient was restarted with anti-thyroid drugs. Hence, hypokalemic paralysis is a reversible cause of paralysis and high index of suspicion as well as timely interventions are required to prevent potential harm. Keywords: hyperthyroidism; hypokalemia; muscle paralysis; thyrotoxic periodic paralysis.

Graves' disease in a 3 year-old patient with agranulocytosis due to anti-thyroid drugs: Radioiodine ablation therapy as an effective alternative. / Enfermedad de Graves en un paciente de 3 años con agranulocitosis asociada a fármacos antitiroideos: terapia ablativa con radioyodo como una alternativa eficaz.

The case is presented of a 3 year-old girl with mitochondrial disease (subacute necrotizing encephalomyelopathy of Leigh syndrome), v-stage chronic kidney disease of a diffuse mesangial sclerosis, as well as developmental disorders, and diagnosed with hyperthyroidism Graves-Basedow disease. Six weeks after starting the treatment with neo-carbimazole, the patient reported a serious case of agranulocytosis. This led to stopping the anti-thyroid drugs, and was treated successfully with 131I ablation therapy. The relevance of the article is that Graves' disease is uncommon in the paediatric age range (especially in children younger than 6 years old), and developing complications due to a possible late diagnosis. Agranulocytosis as a potentially serious adverse effect following the use of anti-thyroid drugs, and the few reported cases of ablation therapy with 131I at this age, makes this case unique.

Post-radioiodine De Novo Onset Graves' Ophthalmopathy: Case Reports and a Review of the Literature.

New-onset Graves' ophthalmopathy (GO) following radioiodine treatment (RAI) and worsening of existing GO are well-described in the endocrinology literature. These phenomena are recognized by ophthalmologists, yet poorly documented in the ophthalmology literature. Two male patients, aged 43 and 62 years, respectively, with Graves' disease without GO, received RAI. Four months later, one patient developed acute GO with unilateral reduction in visual acuity, conjunctival chemosis, lagophthalmos, bilateral severely restricted ocular motility, and lid retraction. High-dose intravenous steroids, followed by oral steroids, led to a dramatic clinical improvement. The second patient received a second dose of RAI for persistent hyperthyroidism and subsequently developed acute GO-comprising restricted ocular motility, peri-orbital swelling, and conjunctival chemosis. Symptoms gradually resolved on continued carbimazole treatment. Neither patient received pre-RAI prophylactic glucocorticoids, as currently they are only recommended for patients with pre-existing GO or multiple risk factors. We discuss the limitations of using this risk-based approach in preventing new-onset GO following RAI therapy.

Hypokalaemia in a hyperthyroid domestic shorthair cat with adrenal hyperplasia.

A 13-year-old female domestic shorthair cat presented with polyphagia and weight loss. Marked systolic hypertension was found on examination. Elevated total thyroxine levels confirmed hyperthyroidism, and hypokalaemia was also documented. A euthyroid state and normotension were achieved following 4 weeks of treatment with carbimazole and amlodipine. Despite potassium supplementation, the hypokalaemia worsened. Abdominal ultrasonography revealed left adrenomegaly. Plasma aldosterone concentrations were initially in the lower half of the reference interval and, when repeated 2 months later, were undetectable. Urea and creatinine remained in the lower half of the reference interval throughout treatment, and urine specific gravity suggested good urine concentrating ability. The fractional excretion of potassium confirmed a renal source of potassium loss. Blood gas analysis was unremarkable. It was theorised that an aldosterone precursor was causing signs of mineralocorticoid excess and undetectable plasma aldosterone levels. Treatment with an aldosterone receptor antagonist successfully increased the serum potassium concentration. Owing to difficulties administering medication and associated effects on life quality the cat was euthanased. Adrenal hyperplasia was apparent on post-mortem histopathology.

Elevated free thyroxine and non-suppressed thyrotropin.

A young man was diagnosed with hyperthyroidism 10 years prior to current presentation after a random health screening revealed an elevated free thyroxine (fT4) of 36.9 pmol/L. During that time, he saw multiple physicians and was treated with carbimazole intermittently. His repeat thyroid function tests showed persistently elevated fT4 ranging 25-35.7 pmol/L and non-suppressed thyroid-stimulating hormone (TSH) concentrations of 6.78-22.1 mIU/L. He had a smooth, firm and non-tender goitre. At our institution, laboratory interference was first excluded by serial dilution study (TSH) and retesting of TSH and fT4 on alternate assay, which gave reproducible results. His normal α-subunit and sex hormone binding globulin, partially suppressed TSH by high dose triiodothyronine (T3), and positive TSH response to thyrotropin-releasing hormone stimulation were consistent with resistance to thyroid hormone syndrome. The diagnosis was confirmed by direct sequencing of thyroid hormone receptor-ß gene, revealing a heterozygous R320 L mutation that causes reduced T3 affinity and reduced corepressor dissociation.

An unusual cause of muscle weakness: a diagnostic challenge for clinicians.

The authors describe a 27-year-old male who presented with acute flaccid quadriparesis. The patient denied any history of similar episodes in the past. At presentation, the patient was tachycardiac with normal systolic blood pressure. He had marked flaccid weakness of both upper and lower limbs and furthermore, he was hypotonic and without tendon reflexes. Biochemical analyses revealed severe hypokalaemia (1.9 meq/l). The patient was given potassium supplementation. He showed complete recovery after the medical intervention. Successive investigations documented an undiagnosed case of Graves' disease. Hypokalaemia secondary to thyrotoxicosis was diagnosed as the cause of the paralysis. Thyrotoxic periodic paralysis is a rare neurologic manifestation of thyrotoxicosis. Absence of obvious signs of thyrotoxicosis poses a diagnostic challenge for the clinicians.

[Graves' disease and papillary thyroid cancer--coincidence or association?]. / Basedow-Struma mit papillärem Schilddrüsenkarzinom--Zufall oder Zusammenhang?

HISTORY AND ADMISSION FINDINGS: A 41-year-old woman presented with hyperhydrosis, tremor, restlessness, sleeplessness and diarrhea. She had a tachycardia and later she developed soreness of her conjunctives. A tender goitre could be palpated. INVESTIGATIONS: Laboratory results showed thryeotoxicosis and later elevated TRAK. Ultrasound revealed a thyroid nodule. Scintigraphic uptake was generally elevated. Graves disease was diagnosed. TREATMENT AND COURSE: After 12 months of thyreostatic medication recurrence occurred and a thyroidectomy was performed. Histologically a papillary cancer was found and postoperative radioiodinetherapy was added. CONCLUSION: Due to leading symptoms of thyreotoxicosis the thyroid nodule has preoperatively not been paid enough attention to. A pathophysiologic association of Graves disease and differentiated thyroid cancer is controversely discussed but seems possible considering present literature data. Scintigraphically "cold" nodules in graves disease, as in simple nodular goitre, have a higher probability of malignancy.

Effect of iopanoic acid on radioiodine therapy of hyperthyroidism: long-term outcome of a randomized controlled trial.

CONTEXT: Telepaque [iopanoic acid (IA)] is believed to rapidly ameliorate hyperthyroidism; however, it may preclude subsequent 131I therapy, possibly delaying it for several months. OBJECTIVE: Our objective was to see how early patients, made euthyroid with Telepaque, can be treated with 131I and to compare their short- and long-term outcome with patients treated with 131I, after making them euthyroid with carbimazole and beta-blockers. DESIGN: We conducted a randomized controlled trial. SETTING AND PATIENTS: We studied 200 hyperthyroid patients at a tertiary care teaching institute. INTERVENTIONS: The IA group received Telepaque, 500 mg/d orally, for 7 d and then no medication for 1 wk followed by 131I therapy if radioiodine neck uptake had recovered. The control group received 30-40 mg oral carbimazole daily until patients became euthyroid followed by 131I. MAIN OUTCOME: After 1 wk of Telepaque therapy and 6 wk of carbimazole, almost all patients became clinically and biochemically euthyroid, and 86 and 94% of patients were ready for 131I therapy after 1 and 2 wk off Telepaque, respectively. The cure rate, defined as euthyroid plus hypothyroid, after the first dose of 131I in controls and the IA group was 80 and 76.2%, respectively (P = 0.54). Thirty-two percent among controls and 25% in the IA group became hypothyroid within 1 yr (P = 0.33); thereafter, the annual rate of hypothyroidism was about 2% in both groups. After a mean follow-up duration of 11 yr, 58% of patients in the control group and 51% in the IA group were hypothyroid. CONCLUSIONS: Telepaque rapidly ameliorates hyperthyroidism without jeopardizing the subsequent radioiodine therapy, and the outcome of radioiodine therapy in this subset of patients is in no way different compared with those prepared by carbimazole.

[Thyrotoxic hypokalaemic periodic paralysis in a Caucasian male]. / Paralysie périodique hypokaliémique thyréotoxique chez un Caucasien.

We report the case of a caucasian patient with a presentation of a periodic paralysis associated with hypokalaemia disclosing Graves' disease. Major pathophysiologics hypothesis are discused in order to explain relationships between hyperthyroidism and paralysis through a disturbance of the excitability of the muscle fibres. A genetic predisposition explain the high incidence of this affection in asiatic population while it is uncommon in caucasian race. Potassium supplementation is not needed in order to correct hypokalaemia except in case of cardiac disturbances. Treatment by beta-blockers is advisable with the specific treatment of hyperthyroidism.

A randomized trial of short-term treatment of Graves' disease with high-dose carbimazole plus thyroxine versus low-dose carbimazole.

OBJECTIVE: The optimal treatment regimen with thionamide drugs remains a matter for debate. We have investigated whether high doses of carbimazole, when compared with low doses, reduce relapse rates of Graves' disease. DESIGN: In an open label, randomized, prospective trial of treatment of Graves' disease we compared high doses of carbimazole (6 months of 100 mg carbimazole per day plus thyroxine) to low-dose carbimazole treatment (starting at 25 mg and titrating the carbimazole dose with the aim to maintain serum thyroid function test results within the normal reference range). PATIENTS: Thirty-seven patients with a first episode of Graves' disease were enrolled. MEASUREMENTS: During the 6 months of treatment we evaluated the rate of normalization of serum thyroid function tests, changes in serum thyroid auto-antibody levels and the rate of side-effects during treatment. After completion of the 6-month treatment course patients were observed for 2 years for evidence of relapse of Graves' disease. RESULTS: There were no differences between the two groups either in the rate of normalization of serum thyroid function tests or in serum thyroid auto-antibody levels during treatment. Of the 17 patients randomized to high-dose treatment seven suffered treatment side-effects, compared to only one of the 20 patients receiving low-dose treatment (P < 0.006). There was no significant difference in 2-year post-treatment remission rates on an intention-to-treat basis between the two treatment groups (18.7% vs. 5.9%, P = NS). However, for those patients who completed 6 months of treatment (high-dose group = 9, low-dose group = 16), multivariate survival analysis demonstrated a significantly longer median relapse-free interval (P < 0.04) in the high-dose group (27 weeks; 25th percentile: 9.6 weeks, 75th percentile: 75 weeks) versus the low-dose group (6 weeks; 25th percentile: 4.8 weeks, 75th percentile: 13.1 weeks). CONCLUSIONS: High-dose carbimazole treatment delays, but does not prevent, relapse from Graves' disease in those patients able to tolerate the treatment. However, it leads to more frequent side-effects than conventional dose treatment.

Evidence for carbimazole as an antioxidant?

There is evidence in the literature to support the view that antioxidants are involved in the pathogenesis of Graves disease and that antioxidants may act as free radical scavengers. This study has compared the effects of a 12 month course of conventional Carbimazole therapy on peripheral blood antioxidant levels with those of a 12 month course of a higher dose treatment regime. Fifty seven patients were enrolled into the study. Those in Group 1 (n = 23) received a 12 month course of 60 mg/day Carbimazole. Those in Group 2 (n = 34) received 45 mg/day for the first month, 30 mg/day for the second and 20 mg/day for the remaining 10 months of treatment. T3 was added in both groups after 2-4 months to maintain patients euthyroid. Baseline samples were also obtained from 30 control subjects. Blood samples were taken for the measurement of plasma thiol (PSH), lysate thiol (LSH), superoxide dismutase (SOD) and caeruloplasmin (CP) and for routine thyroid function tests (TT4, TT3 and TSH). In untreated Graves' patients, serum levels of PSH and SOD were reduced and levels of LSH increased compared to controls. Following 2 months high dose Carbimazole therapy there was a significant increase in PSH levels and a significant reduction in CP levels compared to presentation levels. In the more conventional dose Group 2 patients PSH levels also rose significantly during the first 2 months of treatment. Levels for both groups were still significantly lower than the control group. After 12 months high dose Carbimazole therapy PSH levels had decreased so that they no longer differed from untreated levels. LSH and SOD levels still remained abnormal. CP levels continued to fall. Similar findings were obtained in those patients receiving the more conventional course of treatment. At no point was their any significant difference in antioxidant levels between the two treatment groups. The abnormal levels of antioxidants in the serum of untreated Graves' patients confirm their involvement in the pathogenesis of Graves' disease. Carbimazole therapy appeared to have only short term effects on the peripheral blood levels of the antioxidants measured. Carbimazole appeared to act only on the extra cellular markers of antioxidant activity (PSH, CP) although the disease itself had marked intracellular effects (LSH, SOD). These findings suggest that Carbimazole does not act as a free radical scavenger.

Antiresorptive therapy in hyperthyroid patients: longitudinal changes in bone and mineral metabolism.

The effect of antiresorptive therapy with nasal calcitonin (CT) in recently diagnosed hyperthyroid patients on conventional medical therapy as well as the evolution of bone metabolism were assessed. Forty-five patients with recent-onset hyperthyroidism (<12 weeks) were sex and menopause stratified and randomly allocated to treatment with carbimazole (Neotomizol), carbimazole plus low dose CT (Calsynar; 100 IU/day, 2 days/week), or carbimazole plus high dose CT (Calsynar; 100 IU/day, 14 days/month). Bone mineral density was measured by dual x-ray absorptiometry in lumbar spine, femoral neck, and Ward's triangle at 0, 9, and 18 months of treatment. We also determined free T4, free T3, TSH, osteocalcin, total and bone alkaline phosphatases, tartrate-resistant acid phosphatase, type I collagen C telopeptide, and urinary hydroxyproline every 3 months of follow-up. No significant difference was observed among treatments. A euthyroid state was attained at 3 months. Bone mass increased significantly at the 9 month evaluation (P < 0.05), with a 5-10% net gain during follow-up. Nevertheless, final bone mass was 4-8% smaller than expected. Bone formation markers were increased at 0 and 3 months, with reductions at 6-9 months; resorption bone markers showed a significant reduction at the 3 month evaluation. These results indicate that the euthyroid state partially reduces hyperthyroidism-associated osteopenia, with a bone mass recovery period during the 6-9 early months of effective treatment. This recovery phase is characterized by raised bone formation markers and reduced bone resorption markers. The treatment with nasal CT at the doses assayed has no additional effect over that of attainment of the euthyroid state.

Late and transient increases in free T4 after radioiodine treatment for Graves' disease.

The objective of this retrospective study was to evaluate the fall in free T4 (FT4) in patients with Graves' disease after treatment with radioiodine in a fixed dose of 600 MBq. The study was performed at our outpatient clinic with patients referred from primary care during the time period January 1989 to January 1995. Only patients not given anti thyroid drugs after radioiodine were included. FT4 and TSH were measured every second week for the first three months, and thyroxine substitution started when the FT4 was at or below 15 pmol/l. Of the 60 patients thus available for evaluation, 7 required retreatment, giving a "success rate" of 88%. Of the 53 patients successfully treated with one dose of radioiodine, 36 had not been pretreated with anti thyroid drugs. Among these patients 13 (36%) had a transient increase in FT4 after radioiodine therapy, which mostly occurred after 4 to 6 weeks. The remaining 17 patients had been given carbimazole prior to radioiodine. In this group 8 (53%) had a transient increase in FT4, generally after 2 weeks. In conclusion, giving a fixed large dose of radioiodine and starting thyroxine substitution before hypothyroidism has developed is a workable clinical routine. Although a gradual fall in FT4 was the rule, a transient increase in FT4 was noticed in 30-50% of the patients 2 to 6 weeks after treatment.

Radioprotective action of carbimazole in radioiodine therapy for thyrotoxicosis--influence of the drug on iodine kinetics.

Pretreatment with carbimazole of patients given radioiodine (131I) therapy for thyrotoxicosis reduces the incidence of early hypothyroidism. The possibility that this radioprotective effect might be a consequence of drug induced alteration in thyroidal iodide turnover, leading to a reduction in thyroid irradiation, was investigated in a prospective study of 24 thyrotoxic patients. Subjects were randomly assigned to receive 131I alone or to be treated with carbimazole for a minimum of three months before 131I. Thyroxine supplements were given in the latter group to prevent iatrogenic hypothyroidism. The effective half-life of therapeutic 131I in the thyroid was measured using a gamma camera/computer system after oral administration of the dose, allowing the biological half life of the anion and estimated radiation dose to the thyroid to be derived. Effective half life of 131I, biological half life of 131I and estimated radiation dose to the thyroid were similar in the two groups of subjects. It is concluded that the radioprotective action of carbimazole is not a consequence of altered thyroidal iodide kinetics.

[Surgical treatment of Basedow's disease. I--Traditions and new methods in preparation for thyroidectomy: use of dexamethasone]. / Traitement chirurgical de la maladie de Basedow. I--Traditions et nouveautés dans la préparation à la thyroïdectomie: utilisation de la dexaméthasone.

The combination of dexamethasone (2 mg every 6 hours) carbimazole (15 mg every 8 hours) and potassium iodide (XV drops every 8 hours) has been proposed in the preparation of 21 patients with hyperthyroid Graves' disease for surgery. The combination was administered for 6 days and the subtotal thyroidectomy was performed on day 7. All patients had normal serum Triiodothyronine levels after 4 days of such treatment. This combined drug therapy appears to be a rapid, sage and effective preparation for thyroid surgery in patients with Graves' disease and should replace conventional preparation with carbimazole and potassium iodide and beta-blocker preparation in all cases where there are no contra-indications to the use of corticosteroids.

Total body potassium in relation to thyroid hormones and hyperthyroidism.

1. Body weight and total body potassium were measured in 23 hyperthyroid patients before and at various stages during treatment and in 19 athyreotic patients who were being treated with high-dose L-thyroxine. 2. In the hyperthyroid patients the total body potassium rose by 23 +/- 2.8% (SEM) within a few weeks of restoring the blood thyroid hormone levels to normal. The body potassium values after treatment were close to that expected in these individuals if they were healthy indicating that a considerable loss of body potassium is usual in hyperthyroidism. 3. The gain of total body potassium in hyperthyroidism averaged 71 +/- 8 mmol for each kg of body weight gained (compared with muscle potassium concentration of about 92 mmol/kg). In contrast, weight loss produced by dietary treatment of obesity caused very little change of body potassium (maximum averaged was 14 +/- 4 mmol/kg wt. loss). 4. Among the patients with hyperthyroidism, the greatest muscular weakness was present in those with the greatest body potassium loss and these patients regained a large amount of potassium relative to weight on recovery. 5. Total body potassium changes were closely related to total plasma tri-iodothyronine concentrations but unrelated to the thyroxine levels.

Osteoporosis in hyperthyroidism estimated by photon absorptiometry.

The degree of osteoporosis in hyperthyroidism before and during treatment with carbimazole was studied by photon absorption technique of the right forearm and calcaneus. In addition serum total calcium, serum ionized calcium, serum phosphorus and serum alkaline phosphatase were determined. A group of 96 patients suffering from untreated hyperthyroidism (85 women and 11 men) was studied (79 of these patients were also followed during treatment) and compared to a control group of 157 persons (107 women and 50 men). The women were divided into two groups: less than or equal to 45 years old and more than 45 years old. In all groups untreated hyperthyroid patients showed lower bone densities compared to the control group, but this was only significant in women. During treatment all groups showed a significant increase in density. After 3-6 months of treatment bone density in the calcaneus increased 12% and in the forearm 1.5%; after 6 months - 3 years 33% and 31%, respectively. At that time bone density was normalized. There was no correlation between bone density in hyperthyroid patients and duration and severity of the disease. The biochemical changes were characterised by increases in serum alkaline phosphatase (26%), serum total calcium (16%) and serum ionized calcium concentration (17%) in cases of untreated hyperthyroidism. Serum phosphorus concentration did not change. A correlation was found between elevation of the alkaline phosphatase and decreased bone density.