Use of Lithium/ Iodine Combination for Grave’s Disease
by Jeffrey Dach MD
In this article, we will present the case for combined use of Lithium and Potassium Iodid (KI) for treatment of Graves’ Autoimmune hyperthyroidism. Header Image Thyroid Gland Microscopic View of Graves Disease Courtesy of WIkimedia Commons.
Lithium for Manic Depression
Lithium Carbonate has been used as a psychiatric drug to treat manic depression for well over a century. Similar to KI, Lithium is actively concentrated within the thyroid cells to achieve a concentration three to four times higher than that of plasma. The Sodium/Iodide Symporter is the active transport for both Lithium and Iodide.(1-2)
Lithium Blocks Thyroid Hormone Synthesis and Release
Lithium improves retention of iodine in the thyroid while blocking hormone synthesis and release. These properties make Lithium ideal as an adjunct to radioactive iodine therapy with I-131. Lithium increases radio-iodine uptake even after iodine administration. In 2020, Dr. Czarnywojtek writes:
the thyroid shows an increased ability to accumulate iodine during lithium carbonate treatment regardless of the degree of prolonged iodine retention in the thyroid gland…[Lithium salts] inhibit the formation of colloid in thyrocytes, change the structure of thyroglobulin, weaken the iodination of tyrosines, and disrupt their coupling… An additional benefit is the use of adjuvant lithium therapy to increase the iodine uptake of the thyroid gland, which allows to obtain satisfactory results in treatment with radioactive iodine and potentially facilitates the treatment of thyrotoxicosis. In addition, because of the numerous side effects of lithium and its narrow therapeutic index, its concentration in the blood must be constantly monitored. Emphasis Mine (2)
As mentioned above, Lithium increases the retention of iodine in the thyroid, a useful feature when combined with KI in treatment of Graves’ thyrotoxicosis, thus preventing the escape from the inhibitory effects of KI.
Jonathan Wright MD – Success with Lithium Iodine Combination
Jonathan Wright MD, a legendary pioneer in natural medicine, found success with the combination of Lithium and Lugol’s Iodine for the long-term treatment of Graves’. Dr. Wright writes:
I have my patients use five drops of Lugol’s iodine three times a day for two or three days. (90-100 mg/day) Then I have them add 300 milligrams of lithium carbonate three times a day in addition to the Lugol’s Solution …In 1972, Dr. R Temple at the Mayo Clinic published the first clinical investigation of lithium treatment for Graves’ disease. Using high-dose lithium for 10 individuals, they reported that thyroid hormone levels fell by 20-30 percent within five days. Twenty-six years later, in a review of more than 10 successful trials of lithium therapy for Graves’ disease, the authors wrote:
a small number of studies have documented [Lithium’s] use in the treatment of patients with Graves’ disease… it’s efficacy and utility as an alternative anti-thyroid [treatment] are not widely recognized…Lithium normalizes [thyroid hormone] levels in one to two weeks…toxicity precludes its use as a first-line or long-term therapeutic agent…(Temple,R, 1972)…
But if they had just added flaxseed oil and vitamin E to their treatment, they would have basically eliminated the risk of toxicity. In fact, every individual (except one) whom I’ve (Dr. Wright) treated with iodine-iodide (in the form of Lugol’s Solution) and high dose lithium has had blood tests for thyroid hormone return to normal within two weeks. Their tests then stay normal as long as they use the Lugol’s solution and high dose lithium. (3-4) end quote Dr. Jonathan Wright.
Comparing Iodine and Lithium for Thyrotoxicosis
In 1980, Dr. T. M. Boehm and Wartofsky at Walter Reed Army Hospital compared the relative efficacy of iodine and lithium in 17 patients with thyrotoxicosis. Half the patients also received methimazole (MMI). Further studies using radiolabeled Iodine-125 provided an index of thyroid hormone release from the thyroid gland. I-131 Radiolabeled T4 was used as a marker of the T4 disposal, or degradation by the liver. The slope of the ratio of I-125/I-131 in the serum indicated the per cent inhibition of T4 release from the thyroid gland.(5)
The Iodine and Lithium treatments induced a similar reduction in T4 thyroidal release. The combination of KI and Lithium showed an additive inhibition on T4 release only if KI was started first, and then Lithium added a few days later. This explains why Dr Wright’s protocol starts the KI first. Treatment with Lithium caused a similar reduction in T4 thyroidal release with or without MMI. The MMI had no additive effect when combined with Lithium. However, when MMI was combined with KI, there was a more profound reduction indicating an additive effect of KI with MMI. This additive effect of combining KI with Methimazole was used to advantage by Dr. Okamura in his 2022 study treating 504 Graves disease patients with Potassium Iodide alone. The problem of KI resistant or “escaped” patients was solved by adding methimazole 5-15 mg per day in combination with the potassium iodide 100 mg per day, resulting in good control of the hyperthyroidism.(5-6)
Methimazole Mechanism of Action
When compared to KI or Lithium, Methimazole has a different mechanism of action, irreversibly blocking the TPO enzyme responsible for iodination of thyroglobulin, thus blocking hormone synthesis. In 2005, Dr. Cooper writes:
MMI [Methimazole] inhibits thyroid hormone synthesis by preventing the iodination of tyrosine residues in thyroglobulin by thyroid peroxidase. (7)
Kinetic Studies of Lithium in Graves Disease
In 1972, Dr. R.M. Temple studied the use of Lithium to treat thyrotoxicosis, performing I-131 kinetic studies in seven thyrotoxic women with Lithium levels of 1 mEq/L. Dr Temple found Lithium treatment “inhibited hormonal and nonhormonal thyroid iodine release,” while MMI did not inhibit release. Dr. Temple felt that Lithium and Iodine have a similar mechanism of action, and for prolonged therapy, Lithium must be combined with a second drug, MMI. Dr. Temple writes:
Neither inhibition of release nor hormone disappearance seemed affected by methimazole [MMI]…For prolonged therapy, therefore, a thiocarbamide drug [methimazole or propylthiouracil] must be used in conjunction with Lithium. The similarity of inhibition of iodine release from the thyroid produced by Lithium and iodides is discussed. (4)
Lithium Alone for Long Term Control of Graves’ Thyrotoxicosis
In 1974, Dr. J. Lazarus used Lithium as sole therapy for six months in eleven thyrotoxic Graves’ Disease patients. All had long-standing severe disease (mean duration five and a half years) with characteristic relapsing, remitting course. Eight of the eleven were clinically euthyroid (normal hormone levels) after 2 weeks of Lithium treatment and remained so for the 6 months of the study. Dr. J. Lazarus comments that there was “no iodide type escape phenomenon even after 6 months.” This is an obvious advantage over KI alone, limited to short term use because of the iodine escape phenomenon in 10-12 per cent of patients treated. Dr. J. Lazarus writes:
This study has shown that an adequate dosage of lithium is effective in rapidly producing a euthyroid state in a thyrotoxic patient. Lithium administration maintained the euthyroid state for the duration of therapy but clearly had no significant effect on Graves’ disease [The auto-immune component] itself in this group of patients. However, all these patients had long-standing severe disease (mean duration five and a half years) characterized by several relapses and remissions. In the present study there was no iodide type escape phenomenon even after 6 months… It [Lithium] seems to be as effective as iodide in blocking hormone release … Its use is therefore indicated in cases of hyperthyroidism in which it is necessary to reduce hormone levels very rapidly, especially if the patient is sensitive to iodides…Also, lithium could be administered for longer than 2 weeks with no danger of an escape phenomenon as seen with iodides…This study has shown that the therapeutic effect depends on the serum level, which is readily and easily measured. In general, side effects are few and rapidly disappear once the patient is stabilized on therapy. Nevertheless, lithium does have toxic effects and should not be administered when renal function is impaired or serum-electrolytes are abnormal. (8)
Comparing Lithium to Methimazole – No Significant Difference
In 1976, Dr. Kristensen compared the use of Lithium to the use of Methimazole in 24 patients with newly diagnosed Graves’ thyrotoxicosis. 13 were treated with Methimazole(MMI) alone 40 mg/d and 11 with Lithium Carbonate alone rendering a serum level of 0.5 to 1.3 mEq/L. Dr. Kristensen found a similar reduction in Free T4 levels for both treatment modalities. However, the Lithium treated patients had more side effect. He writes:
The lithium treatment brought about a fall in serum-thyroxine iodine (T4I) of 27.0%, and in the free-thyroxine index (F.T.I.) of 38.1% after 10 days. A comparison of the two patient groups with regard to the fall in F.T.I. after 3 and 10 days showed no statistically significant difference… 8 of the 11 patients subjected to lithium treatment had side-effects, so that the general condition, which was already affected by the hyperthyroidism, was worsened. It is concluded that lithium cannot be considered superior to thiocarbamides [Methimazole] for the rapid control of thyrotoxicosis.(9) Emphasis Mine
How to Avoid Lithium Side Effects
Most of the Lithium side effects can be prevented with Vitamin E, Flax Seed Oil and Vitamin B6 (pyridoxine, P-5-P version), and zinc. In 2004, Dr. Jonathan Wright recommended the use of these supplements to prevent and alleviate Lithium Toxicity, writing:
An initial dosage of flaxseed oil, one tablespoon (15ccs) three times daily, along with 800 IU of vitamin E (mixed tocopherols). Later dosage is reduced to flaxseed oil to one tablespoon daily along with 400 IU of vitamin E. (10-19)
Lithium Induced Hand Tremor
A common adverse effect of Lithium is hand tremor, alleviated with addition of Vitamin B6. Make sure to use the P-5-P version of B6. Lithium toxicity may be avoided with the use of Flax Seed Oil Essential Fatty Acids, and Vitamin E as mentioned above. (10-19)
Auto-Immune Thyroid Disease – Greater Sensitivity to Inhibitory Effect of Lithium and Iodine
In 1976, Dr. Kenneth Burman studied six euthyroid Graves’ Disease patients, all euthyroid for 11 months following treatment with radioactive iodine, and one patient euthyroid following medical treatment with methimazole. The 7 euthyroid Graves Disease patients were given lithium carbonate 300 mg three times daily which maintained the serum lithium level between 0.5 and 1.0 mEq/L. Dr. Berman comments that in normal healthy controls, lithium does not usually induce hypothyroidism. However, in the 7 euthyroid Graves patients, Lithium did cause hypothyroidism with reduction in Free T3 and Free T4 in all seven.
Dr. Berman writes people with auto-immune thyroid disease are more sensitive to the inhibitory effects of either agent, lithium, or iodide, as their mechanism of action appears similar, producing hypothyroidism. Healthy normal controls are resistant to this effect and can compensate using autoregulatory properties of the normal thyroid. In Dr. Berman’s opinion, the beneficial effect of Lithium may be due its ability to increase the intrathyroidal iodine content, and this increased iodine then inhibits both thyroid hormone synthesis and release. If this is true, then this would explain why the Lithium/KI combination is so effective to control thyrotoxicosis. Dr Berman writes:
Recently it has become apparent that subjects with a history of thyroid abnormalities such as diffuse toxic goiter [Graves’ Disease] or Hashimoto’s thyroiditis may be extremely sensitive to the antithyroid effects of iodine even though they may be euthyroid prior to the administration of this drug…Lithium decreases hormonal synthesis and thyroidal secretion, but does not appear to affect iodine uptake. [i.e. allows iodine uptake] Consequently, intrathyroidal iodine content may actually increase during lithium administration, and excessive quantities of intrathyroidal iodine may inhibit both thyroid hormone synthesis and release. The normal thyroid gland, however, will gradually overcome the inhibitory effects of iodine upon thyroid hormone synthesis and restore normal synthetic ability despite intrathyroidal iodine concentrations that remain elevated. Patients with diffuse toxic goiter [Graves’ Disease] may be unable to re-establish normal autoregulation of thyroidal iodine economy, possibly due to a defect in organic binding. As a result, there may be enhanced sensitivity for the development of hypothyroidism during treatment with either lithium or iodine… these observations support the thesis that the inhibitory effects of lithium and iodine upon thyroid hormone synthesis or secretion may involve a similar mechanism of action since increased thyroidal iodine content may be a consequence of therapy with either agent.(20)
Note the above comment, Lithium increases intrathyroidal iodine content. This is advantageous for radioablation in the Graves’ Disease patient in which accumulation of radioactive iodine within the thyroid is desired for more effective treatment. This also explains the advantage of combined Lithium and Iodine treatment of Graves’ disease, as the Lithium makes the Iodide accumulate and remain within the thyroid gland, providing more effective inhibition of both organification and thyroid hormone release. In addition, this combination of Lithium and KI prevents the Iodine escape phenomenon with relapse of thyrotoxicosis, also named the Jod-Basedow Phenomenon. (20-21)
Lithium for Radiographic Contrast and Amiodorone Thyrotoxicosis
In 1984, Dr. C. Wunsch studied the short-term combination of lithium and methimazole in hyperthyroidism induced by iodine containing radiographic contrast material finding Lithium effective without severe side effects. (22-25)
Lithium for Methimazole Failures
In 1998, Dr. Benbassat used Lithium effectively to treat four patients in whom Methimazole had failed to control hyperthyroidism. Dr. Benbassat writes:
We describe four patients treated with lithium for the control of hyperthyroidism. Conventional therapy with propylthiouracil and/or methimazole was tried initially, but the patients were either unresponsive or developed side effects during the drug administration. Within several days of reaching therapeutic levels of lithium, a euthyroid state was achieved in three of the four cases. Our observations support the use of lithium as an alternative antithyroid drug in the treatment of hyperthyroidism in certain defined indications, a clinical use that is not widely known. (26) Emphasis Mine.
Methimazole Resistance Treated with Lithium, Iodine and Dexamethasone Pre-Thyroidectomy for Graves’
In 2021, Dr. Yusaki Mori reported a very rare case of Methimazole Resistance in a 21 year old female with Graves’ disease. This patient had been started on Methimazole at the age of 14, and did well until seven years later, at age 21, she became MMI resistant. On thyroid ultrasound, she had a very large hypervascular thyroid gland without nodules. Although the MMI dosage was increased to 120 mg per day, her thyroid hormone levels were above measurable levels. In order to prepare the patient for thyroidectomy, her doctors increased the MMI to 150 mg per day, and added Lithium Carbonate 800 mg per day, dexamethasone 6mg/day and inorganic iodine 306 mg/day. This combined regimen normalized thyroid hormone levels within 14 days allowing thyroidectomy to be performed one week after hospitalization. The authors speculated the reason for MMI resistance was inability to concentrated the MMI within the thyroid gland, writing:
After its absorption, MMI accumulates at high concentrations in the thyroid gland, to levels approximately two-to-five times higher than those in the plasma…Therefore, it is probable that the concentration of MMI in the thyroid gland, rather than in the circulation, has the largest impact on its anti-thyroid effect. Indeed, in a patient who needed a high dose (150 mg/day) of MMI to control their hyperthyroidism, the concentration of MMI in their thyroid tissue was lower than that in the thyroid of MMI-sensitive patients…The present patient responded to treatment with lithium carbonate, inorganic iodine and corticosteroid, in addition to MMI. Lithium carbonate and inorganic iodine ameliorate hyperthyroidism by inhibiting the release of thyroid hormone from the thyroid gland and corticosteroids principally work by suppressing the conversion of T4 to T3 in peripheral tissues, whereas MMI blocks thyroid hormone synthesis within the thyroid gland…We found that the addition of lithium carbonate (200 mg/day) to basal MMI treatment reduced the thyroid hormone concentration of the present patient. Because anti-thyroid effects of lithium carbonate have been reported at doses of 600 to 900 mg/day,11,33,34 we increased her lithium carbonate dose to 800 mg/day… We found that the combination of inorganic iodine, which was initiated at 153 mg/day and increased to 306 mg/day, and dexamethasone, which was initiated at 4mg/day and increased to 6mg/day, normalized the very high thyroid hormone concentration of the patient within 14 days. (37)
Lithium in Preparation for Radioablation or Thyroidectomy
In 2006, Dr Shek used Lithium in 13 thyrotoxic patients in preparation for radioablation or thyroidectomy for Grave’s Disease. Contrary to Dr. J. Lazarus in 1974, Dr. Shek reports one of the 13 patients “escaped” from the effects of Lithium, writing:
A satisfactory response, defined as a fall by 40% or more in free thyroxine levels and clinical improvement, was achieved in eight patients within 1 to 2 weeks of lithium therapy. In four others, response occurred in 3 to 5 weeks. Response was slow and inadequate in one patient due to ‘escape’. The median dosage of lithium was 750 mg daily, with a range of 500 to 1500 mg daily. The median serum lithium level was 0.63 mmol/L. Lithium toxicity was observed in one patient…A relatively low dose of lithium offers a safe and effective alternative means of controlling thyrotoxicosis in patients who cannot tolerate or do not respond to thionamides [methimazole]. (27)(8)
Lithium in Preparation for Radio-Ablation
In 2008, Dr. Fulya Akin used Lithium to prepare 5 patients with Graves’ disease and one patient with toxic nodular goiter for radioablation with I-131. Lithium was used as second line because of adverse reactions or ineffectiveness of Thionamides (Methimazole). Dr. Fulya Akin writes:
This report shows that lithium carbonate can be safely used preoperatively or prior to radioiodide therapy in circumstances where antithyroid medications are contraindicated and are ineffective in obtaining an euthyroid status. When administered (800–1,200 mg daily) to patients suffering from Graves’ thyrotoxicosis, the serum T4 and T3 levels have been shown to decrease by as much as 35% and most patients become clinically euthyroid within 2 weeks of treatment. (28-35)
Lithium in Preparation for Thyroidectomy
In 2018, Dr. G. Nair preferred thionamide drugs rather than SSKI (Super Saturated Potassium Iodide) to prepare 162 thyrotoxic patients for thyroidectomy. However, in six patients who could not tolerate thionamides, Dr. Nair switched to Lithium in preparation for thyroidectomy. Lithium was combined with dexamethasone and propranolol (Beta Blocker). Dr. Nair writes:
Lithium is concentrated by the follicular cells…and inhibits iodotyrosine coupling, alters thyroglobulin structure, and thereby inhibits thyroid hormone secretion. We had used combination of lithium carbonate and dexamethasone in refractory HT [hyperthyroidism] as preoperative regimen…. Lithium carbonate was used in combination with dexamethasone and propranolol in six patients. Indications for lithium salts were drug reactions (n = 3) and failure to control toxicity with 60 mg of carbimazole for 2 months (n = 3)…The entire cohort underwent total thyroidectomy… We used a combination of lithium carbonate and dexamethasone in selected patients of the series and found effective biochemical and clinical control of toxicity. None of the patients experienced drug-related side effects…The rate of complications did not differ in six patients who received lithium salts from the other subgroups. (8)(29)
Case Report, Graves’ Disease Treated with Lithium and Iodine (SSKI) Combination
In 2022, Dr. Pranjali P. Sharma reported a case of Graves’ Disease managed with combinaton of Lithium and Super Saturated Potassium Iodide (SSKI) in a 26 year old male in blast phase of CML (chronic myeloid leukemia). Methimazole was contraindicated because of low white blood cell count. Dr. Pranjali P. Sharma writes:
A 26-year-old man, admitted with acute blast crisis secondary to chronic myeloid leukemia (CML), reported palpitations, 40-lb weight loss, heat intolerance, and fatigue. An examination revealed sinus tachycardia, elevated body temperature, and thyromegaly. Laboratory evaluation confirmed hyperthyroidism (TSH <0.005 mU/L, FT4 5.57 ng/dl, TT3 629 ng/dl) secondary to GD (TRAb >40 IU/l, TSIg 178%). Thionamides and surgery were contraindicated due to pancytopenia from a blast crisis… after 2 weeks of inpatient hospital stay, oral Li carbonate 300 mg 3 times a day, with SSKI 50 mg/drop 1 drop 3 times a day, was introduced. Li levels were monitored every 2–3 days. Two weeks into treatment, FT4 and TT3 dropped to 4.51 ng/dl and 359 ng/dl, respectively…At hospital discharge 1 month later, thyroid tests showed improvement (TSH 0.007 mcIU/l, FT4 0.82 ng/dl, TT3 122 ng/dl) with stable Li level (within 0.5–0.8 mmol/l)…So far, he [the patient] remains on oral Li carbonate 300 mg 3 times a day and SSKI 50 mg/drop 1 drop 3 times a day, without adverse effects. Most recent laboratory test results continue to show an undetectable TSH, but FT4 and TT3 are within normal range (1.42 ng/dl and 98 ng/dl, respectively). The ultimate plan for this patient is a total thyroidectomy when his cell counts improve…Conclusions: Li [Lithium] inhibits…tyrosine iodination, thyroglobulin structure changes, peripheral deiodinase blockage, and preventing TSH and TSIg stimulation. Our case shows that a low therapeutic level of Li, in combination with oral iodine, can suppress thyroid overactivity without adverse effects. We suggest that low-dose Li carbonate is a safe and effective adjunctive antithyroid medication to be considered if primary therapies for hyperthyroidism are unavailable…Methimazole and propylthiouracil (PTU) are the most common ATDs [anti-thyroid drugs] used in the United States. Relatively mild adverse effects from ATDs include pruritus, rash, urticaria, arthralgias, arthritis, nausea, vomiting, or abnormal taste, occurring in up to 13% patients. Serious adverse effects include agranulocytosis, hepatotoxicity, and vasculitis. Agranulocytosis is more likely to occur with any dose of PTU than with low-dose methimazole and can be life-threatening, while it is dose-dependent with methimazole. It usually occurs within the first 2–3 months of therapy; however, the overall incidence is relatively low, at 0.1–0.5%.(36)
Lithium and Iodine Combination Treatment
Because of “Iodine escape” in 10-12 per cent of cases, KI alone was deemed inadequate for long term control of the Graves’ disease. Perhaps a combination of KI with a second drug could be effective? In 2022, Dr. Okamura succesfully used methimazole (MMI) combined with KI.(6)
Another effective combination is KI with Lithium. The combination of KI with Lithium Carbonate is effective for long term treatment of Graves’ Disease, and a subset of patients go into remission. Lithium carbonate dosage for Grave’s Disease is usually 300 mg three times a day. Blood levels are checked periodically to avoid toxicity.
Conclusion: Another error in modern endocrinology is ignoring the use of Lithium for treatment of Graves’ thyrotoxicosis, or as preparation for either radioactive I-131 ablation or thyroidectomy. The Lithium/KI combination is a promising treatment, yet ignored by conventional mainstream endocrinology.
Articles with Related Content
Iodine for Treatment of Graves Disease Part One
Iodine for Treatment of Graves Disease Part Two
Jeffrey Dach MD
7450 Griffin Road, Suite 190
Davie, Fl 33314
954-792-4663
www.jeffreydachmd.com
References
1) Amdisen, A. “Lithium treatment of mania and depression over one hundred years.” Current trends in lithium and rubidium therapy. Springer, Dordrecht, 1984. 11-26.
2) Czarnywojtek, A., et al. “Effect of lithium carbonate on the function of the thyroid gland: Mechanism of action and clinical implications.” J Physiol Pharmacol 71.2 (2020): 191-199.
3) Wright, Jonathan,”Reversing hyperthyroidism by Jonathan Wright MD”, Nutrition & Healing Newsletter Sept 8, 2011.
4) Temple, R. M. J. J., et al. “The use of lithium in the treatment of thyrotoxicosis.” The Journal of Clinical Investigation 51.10 (1972): 2746-2756.
5) Boehm, Timothy M., et al. “Lithium and iodine combination therapy for thyrotoxicosis.” European Journal of Endocrinology 94.2 (1980): 174-183.
6) Okamura, Ken, et al. “Iodide-sensitive Graves’ hyperthyroidism and the strategy for resistant or escaped patients during potassium iodide treatment.” Endocrine Journal (2022): EJ21-0436.
7) Cooper, David S. “Antithyroid drugs.” New England Journal of Medicine 352.9 (2005): 905-917.
8) Lazarus, J. H., et al. “Treatment of thyrotoxicosis with lithium carbonate.” The Lancet 304.7890 (1974): 1160-1163.
9) Kristensen, O., H. Harrestrup Andersen, and G. Pallisgaard. “Lithium carbonate in the treatment of thyrotoxicosis: a controlled trial.” The Lancet 307.7960 (1976): 603-605.
10) Wright, Jonathan V. “Lithium, part 1: protect and renew your brain.” Townsend Letter for Doctors and Patients 247-248 (2004): 78-82.
11) Wright, Jonathan V. “Lithium, part 2: other effects.” Townsend Letter for Doctors and Patients 249 (2004): 59-62.
12) Miodownik, Chanoch, Eliezer Witztum, and Vladimir Lerner. “Lithium-induced tremor treated with vitamin B6: a preliminary case series.” The International Journal of Psychiatry in Medicine 32.1 (2002): 103-108.
13) Umar, Musa U., Aliyu A. Isa, and Asmaul H. Abba. “High dose pyridoxine for the treatment of tardive dyskinesia: clinical case and review of literature.” Therapeutic Advances in Psychopharmacology 6.2 (2016): 152-156.
14) Reda FA, Escobar JJ, Scanlan JM. Lithium Carbonate in the Treatment of tardive dyskinesia. Am J Psych 1975;132(5):560-562.
15) Ibrahim, Ahmed Th, et al. “The protective effects of vitamin E and zinc supplementation against lithium-induced brain toxicity of male albino rats.” Environment and Pollution 4.1 (2015): 9.
16) Omar, H. E., et al. “The protective effects of zinc and vitamin E supplementation against kidney toxicity by lithium in rats.” European Journal of Biological Research 6.1 (2016): 21-27.
17) Bondok, Adel A., et al. “Lithium Carbonate-Induced Nephrotoxicity in Albino Rats and the Possible Protective Effect of Vitamin E: Histological and Immunohistochemical Study.” The Egyptian Journal of Anatomy 41.1 (2018): 105-118.
18) Gupta, Neena, Meghan Gibson, and Ellen C. Wallace. “Lithium-induced chronic kidney disease in a pediatric patient.” Case Reports in Pediatrics 2019 (2019).
19) GA, Modawe, and N. M. ElBagir. “Lithium Carbonate Therapy Causes Nephrotoxicity and its Alleviation with Ascorbic Acid in Wistar Albino Rats.”
20) Burman, Kenneth D., et al. “Sensitivity to lithium in treated Graves’ disease: effects on serum T4, T3 and reverse T3.” The Journal of Clinical Endocrinology & Metabolism 43.3 (1976): 606-613.
21) Rose, Hannah R., and Hassam Zulfiqar. “Jod Basedow Syndrome.” StatPearls [Internet]. StatPearls Publishing, 2022.
22) Wünsch, C., and H. J. Heberling. “Results of lithium treatment in severe hyperthyroidism.” Deutsche Zeitschrift fur Verdauungs-und Stoffwechselkrankheiten 44.1 (1984): 26-31.
23) Dickstein, G., et al. “Lithium treatment in amiodarone-induced thyrotoxicosis.” The American journal of medicine 102.5 (1997): 454-458.
24) Boeving, Anke, et al. “Use of lithium carbonate for the treatment of amiodarone-induced thyrotoxicosis.” Arquivos Brasileiros de Endocrinologia & Metabologia 49 (2005): 991-995.
25) Claxton, Scott, et al. “Refractory amiodarone‐associated thyrotoxicosis: An indication for thyroidectomy.” Australian and New Zealand Journal of Surgery 70.3 (2000): 174-178.
26) Benbassat, Carlos A., and Mark E. Molitch. “The Use of Lithium in the Treatment of Hyperthyroidism.” The Endocrinologist 8.5 (1998): 383-388.
27) Shek, C. C., et al.”Use of lithium in the treatment of thyrotoxicosis.” Hong Kong Med J 12.4 (2006): 254-9.
28) Akin, Fulya, Guzin Fidan Yaylali, and Mehmet Bastemir. “The use of lithium carbonate in the preparation for definitive therapy in hyperthyroid patients.” Medical Principles and Practice 17.2 (2008): 167-170.
29) Nair, Gopalakrishnan C., et al. “Preoperative preparation of hyperthyroidism for thyroidectomy–Role of supersaturated iodine and lithium carbonate.” Indian Journal of Endocrinology and Metabolism 22.3 (2018): 392.
30) Abd-ElGawad, Mohamed, et al. “Lithium carbonate as add-on therapy to radioiodine in the treatment on hyperthyroidism: a systematic review and meta-analysis.” BMC endocrine disorders 21.1 (2021): 1-11.
31) Thakkar, Aditi, and Constance Lee Chen. “A Case for Lithium Pretreatment Prior to Radioactive Iodine Ablation in Grave’s Disease.” Journal of the Endocrine Society 5.Suppl 1 (2021): A906.
32) Kumar, Sanny B., et al. “Dose optimization of lithium to increase the uptake and retention of I-131 in rat thyroid.” Radiation and Environmental Biophysics 58.2 (2019): 257-262.
33) Dharan, Shalini Sree, et al. “A prospective clinical trial on the efficacy of lithium as adjuvant therapy to radioiodine in the treatment of hyperthyroidism (RAILIT study).” Endocrine Abstracts. Vol. 65. Bioscientifica, 2019.
34) Martin, Niamh M., et al. “Adjuvant lithium improves the efficacy of radioactive iodine treatment in Graves’ and toxic nodular disease.” Clinical endocrinology 77.4 (2012): 621-627.
35) Bogazzi, Fausto, et al. “Impact of lithium on efficacy of radioactive iodine therapy for Graves’ disease: a cohort study on cure rate, time to cure, and frequency of increased serum thyroxine after antithyroid drug withdrawal.” The Journal of Clinical Endocrinology & Metabolism 95.1 (2010): 201-208.
36) Sharma, Pranjali P. “Use of Lithium in Hyperthyroidism Secondary to Graves’ Disease: A Case Report.” The American Journal of Case Reports 23 (2022): e935789-1.
37) Mori, Yusaku, et al. “Very rare case of Graves’ disease with resistance to methimazole: a case report and literature review.” The Journal of International Medical Research 49.3 (2021).
After its absorption, MMI accumulates at high concentrations
in the thyroid gland, to levels approximately two-to-five times higher than those in the plasma.26
The present patient responded to treatment with lithium carbonate, inorganic iodine and corticosteroid, in addition to MMI. Lithium carbonate and inorganic iodine ameliorate hyperthyroidism by inhibiting the release of thyroid hormone from the thyroid gland,30,31 and corticosteroids
principally work by suppressing the conversion of T4 to T3 in peripheral tissues, 32 whereas MMI blocks thyroid hormone synthesis within the thyroid gland.
We found that the addition o flithium carbonate (200 mg/day) to basal
MMI treatment reduced the thyroid hormone concentration of the present patient. Because anti-thyroid effects of lithium carbonate
have been reported at doses of 600 to 900 mg/day,11,33,34 we increased her lithium carbonate dose to 800 mg/day
We found that the combination of inorganic iodine, which was initiated
at 153 mg/day and increased to 306 mg/day, and dexamethasone, which
was initiated at 4mg/day and increased to 6mg/day, normalized the very high thyroid hormone concentration of the patient within 14 days.
38) Thakkar, Aditi, and Constance Lee Chen. “A Case for Lithium Pretreatment Prior to Radioactive Iodine Ablation in Grave’s Disease.” Journal of the Endocrine Society 5.Suppl 1 (2021): A906.
39) Fantin, Esther H., and Iuri Martin Goemann. “Successful Management of Hyperthyroidism With Lithium and Radioiodine in a Patient With Previous Methimazole-Induced Agranulocytosis.” Journal of the Endocrine Society 5.Supplement_1 (2021): A958-A958.
40) Tay, Wei Lin, et al. “High thyroid stimulating receptor antibody titre and large goitre size at first-time radioactive iodine treatment are associated with treatment failure in Graves’ disease.” Ann Acad Med Singap 48.6 (2019): 181-187.
41) Ahmed, Fahad Wali, et al. “Meta-analysis of randomized controlled trials comparing the efficacy of radioactive iodine monotherapy versus radioactive iodine therapy and adjunctive lithium for the treatment of hyperthyroidism.” Endocrine Research 46.4 (2021): 160-169.
42) Bogazzi, Fausto, et al. “Impact of lithium on efficacy of radioactive iodine therapy for Graves’ disease: a cohort study on cure rate, time to cure, and frequency of increased serum thyroxine after antithyroid drug withdrawal.” The Journal of Clinical Endocrinology & Metabolism 95.1 (2010): 201-208.
43) Dickstein, G., et al. “Lithium treatment in amiodarone-induced thyrotoxicosis.” The American journal of medicine 102.5 (1997): 454-458.
44) Eigenmann, F., and H. Bürgi. “Lithium acetate, a useful and well tolerated thyrostatic for selected cases of hyperthyroidism.” Schweizerische Medizinische Wochenschrift 108.47 (1978): 1850-1853.
45) Turner, J. G., et al. “An evaluation of lithium as an adjunct to carbimazole treatment in acute thyrotoxicosis.” European Journal of Endocrinology 83.1 (1976): 86-92.
46) Eulry, F., J. Orgiazzi, and R. Mornex. “Do lithium salts have a place in the treatment of severe hyperthyroidism?(author’s transl).” La Nouvelle Presse Medicale 6.33 (1977): 2955-2958.
47) Jonderko, G., and C. Marcisz. “Short-term use of lithium carbonate in the treatment of thyrotoxicosis.” Zeitschrift fur die Gesamte Innere Medizin und Ihre Grenzgebiete 34.15 (1979): 408-411.
48) Hedley, J. M., et al. “Low dose lithium-carbimazole in the treatment of thyrotoxicosis.” Australian and New Zealand journal of medicine 8.6 (1978): 628-630.
49) Kauschansky, A., and M. Genel. “Preoperative treatment of intractable hyperthyroidism with acute lithium administration.” European journal of pediatric surgery 6.05 (1996): 301-302.
Jeffrey Dach MD
7450 Griffin Road, Suite 190
Davie, Fl 33314
954-792-4663
www.jeffreydachmd.com
www.drdach.com
Heart Book by Jeffrey Dach
www.naturalmedicine101.com
www.bioidenticalhormones101.com
www.truemedmd.com
Click Here for: Dr Dach’s Online Store for Pure Encapsulations Supplements
Click Here for: Dr Dach’s Online Store for Nature’s Sunshine Supplements
Web Site and Discussion Board Links:
jdach1.typepad.com/blog/
disc.yourwebapps.com/Indices/244066.html
disc.yourwebapps.com/Indices/244067.html
http://sci.med.narkive.com/covV2Qo2/jeffrey-dach-book-announcment-natural-medicine-101
The reader is advised to discuss the comments on these pages with his/her personal physicians and to only act upon the advice of his/her personal physician. Also note that concerning an answer which appears as an electronically posted question, I am NOT creating a physician — patient relationship. Although identities will remain confidential as much as possible, as I can not control the media, I can not take responsibility for any breaches of confidentiality that may occur.
Copyright (c) 2023 Jeffrey Dach MD All Rights Reserved. This article may be reproduced on the internet without permission, provided there is a link to this page and proper credit is given. See Repost Guidelines.
FAIR USE NOTICE: This site contains copyrighted material the use of which has not always been specifically authorized by the copyright owner. We are making such material available in our efforts to advance understanding of issues of significance. We believe this constitutes a ‘fair use’ of any such copyrighted material as provided for in section 107 of the US Copyright Law. In accordance with Title 17 U.S.C. Section 107, the material on this site is distributed without profit to those who have expressed a prior interest in receiving the included information for research and educational purposes.
Serving Areas of: Hollywood, Aventura, Miami, Fort Lauderdale, Pembroke Pines, Miramar, Davie, Coral Springs, Cooper City, Sunshine Ranches, Hallandale, Surfside, Miami Beach, Sunny Isles, Normandy Isles, Coral Gables, Hialeah, Golden Beach ,Kendall,sunrise, coral springs, parkland,pompano, boca raton, palm beach, weston, dania beach, tamarac, oakland park, boynton beach, delray,lake worth,wellington,plantation
Leave a Reply
You must be logged in to post a comment.