Lithium und Schilddrüse zurück
Schilddrüsen bremsende Wirkung des Lithiums
In den meisten Fällen gilt:
Lithium führt zu einer Bremsung der SD-Funktion , so daß sich bei einer sonst normalen SD ein Trend zur SD Unterfunktion einstellen kann.
Durch die abfallenden T3 und T4 Werte kommt es wie üblich als Gegenregulation der Hypophyse zu einem TSH Anstieg .
Der erhöhte TSH Spiegel regt an der SD wiederum eine gewiße Vergrößerung des Organes im Sinne einer leichten Kropfbildung an.
So reagieren die meisten Patienten auf Lithium und man kann den SD bremsenden Effekt bei einer SD Überfunktion ganz gut nutzen.
Bildet sich unter der Therapie mit Lithium eine SD Unterfunktion aus , so muß man diese durch die Gabe von SD Hormon T4 = Thyroxin in angepasster Dosis behandeln.
Autoimmunstimulierende Wirkung des Lithiums
In einigen wenigen Fällen liegen die Dinge anders:
Lithium hat auch einen immunstimulierenden Effekt: Leider führt dies nicht zu einer besseren Abwehrlage sondern zu einem vermehrten Auftreten von Autoimmunerkrankungen.
Es gibt wenige Fallberichte die zeigen , daß Lithium an der SD sowohl einen Basedow als auch eine Autoimmunthyreoiditis auslösen kann.
Will man herauszufinden , wie denn nun das Lithium im Einzelfall an der SD reagiert , so muß man dies austesten.
Auf den Fall einer Hyperthyreose bezogen:
Läßt man das Lithium weg und es kommt zu einem Anstieg des T3 und T4 Spiegels , trotz gleichbleibender Carbimazol und T4 Therapie, reagiert das Lithium wie in der Mehrzall der Fälle bremsend auf die SD und wirkt sich günstig auf die Hyperthyreose aus.
Läßt man das Lithium weg und es kommt nicht zu einem Anstieg des T3 und T4 Spiegels , sondern eher zu einer Normalisierung der SD Funktion , so daß man Carbimazol weglassen kann, dann muß man davon ausgehen , daß das Lithium über seinen autoimmunen Effekt , die Hyperthyreose erst erzeugt hat und sich ungünstig auf die SD auswirkt.
==> Man muß sich gut überlegen , ob man so eine Testprozedur machen soll, die über mehrere Wochen und mit mehreren Messung durchgeführt werden muß.
Man riskiert ein Rezidiv der Depression .
Wenn man also meint , daß man auf das Lithium nicht verzichten kann, dann muß man bei einer Hyperthyreose :
Regelmäßig die SD Funktion testen und danach angepasst die Carbimazol und T4 Therapie einstellen. Außerdem sollte man die SD Größe sonografisch kontrollieren und die körperlichen Zeichen der SD Überfunktion immer wieder abfragen .
Insbesondere die Herzfrequenz in Ruhe und der Blutdruck sind da ganz brauchbare Kontrollwerte
Nervenarzt 1998 Mar;69(3):189-95
Thyroid gland function in lithium treatment.
[Article in German]
Bschor T, Bauer M
Psychiatrische Klinik und Poliklinik, Freien Universitat Berlin.
Lithium is widely used in the acute and prophylactic treatment of affective disorders. Lithium affects thyroid hormone metabolism via different mechanisms. In patients this leads to a compensatory increase in pituitary thyroid stimulating hormone (TSH) which usually maintains the euthyroid status. This is probably the reason for the relatively high prevalence of goitre in lithium-treated patients; however, the enlargement of the gland is only moderate in most cases. Due to its immunostimulating effects lithium may support the appearance of thyroid autoantibodies and the development of thyroiditis, which may be the reason for a higher prevalence of hypothyroidism in patients receiving lithium. However, also cases of hyperthyroidism in such patients have been reported repeatedly. Therapeutic recommendations for the treatment of disturbances of thyroid function during lithium treatment are given.
PMID: 9565972, UI: 98227094
Bogazzi F, Bartalena L, Brogioni S, Scarcello G, Burelli A, Campomori A, Manetti L, Rossi G, Pinchera A, Martino E.
Comparison of radioiodine with radioiodine plus lithium in the treatment of Graves' hyperthyroidism.
J Clin Endocrinol Metab. 1999 Feb;84(2):499-503.
PMID: 10022407; UI: 99145005
Hoogenberg K, Beentjes JA, Piers DA.
Lithium as an adjunct to radioactive iodine in treatment-resistant Graves
thyrotoxicosis.
Ann Intern Med. 1998 Oct 15;129(8):670. No abstract available.
PMID: 9786822; UI: 98442944
Sadoul JL, Kezachian B, Freychet P.
Lithium therapy and hyperthyroidism: disease caused or facilitated by lithium?
Review of the literature apropos of a case of hyperthyroidism preceded by transient hypothyroidism.
Ann Endocrinol (Paris). 1994;54(5):353-8. Review. French.
PMID: 8085784; UI: 94368055
Service de Medecine Interne et d'Endocrinologie (I4), Hopital Pasteur, CHU de Nice.
A case of hyperthyroidism occurring in a 68 year old man receiving lithium carbonate (1 g/day) for 5 years is reported. The clinical history of the patient, treated for bipolar affective disorder, was remarkable for transient hypothyroidism followed several months later by tremor, increased free thyroxine and triiodothyronine, and decreased TSH levels which led to lithium withdrawal. Two months later, clinical and biological signs were unchanged, Tc99m-scan displayed a homogeneous and increased isotope uptake. In this setting, high levels of autoantibodies against TSH-receptor, and grade I exophthalmos and slightly ocular muscle enlargement at CT-scan favored the diagnosis of Graves' disease (perhaps facilitated by lithium therapy). Carbimazole treatment was effective in controlling hyperthyroidism. Review of the literature disclosed 44 cases of hyperthyroidism occurring in lithium-treated patients. Most of these cases concerned specific thyroid diseases, particularly with an autoimmune mechanism. There is also evidence for an actual role of lithium in increasing intrathyroid iodide pool and for an impact of lithium on the immune system. Thus, the hypothesis that lithium may trigger the development of an autoimmune thyroid disease in predisposed patients deserves further investigation.
Takami H.
Lithium in the preoperative preparation of Graves' disease.
Int Surg. 1994 Jan-Mar;79(1):89-90.
PMID: 8063564; UI: 94342062
Mochinaga N, Eto T, Maekawa Y, Tsunoda T, Kanematsu T, Izumi M.
Successful preoperative preparation for thyroidectomy in Graves' disease using lithium alone: report of two cases.
Surg Today. 1994;24(5):464-7.
PMID: 8054820; UI: 94331941
Byrne AP, Delaney WJ.
Regression of thyrotoxic ophthalmopathy following lithium withdrawal.
Can J Psychiatry. 1993 Dec;38(10):635-7.
PMID: 8313300; UI: 94147316
Persad E, Forbath N, Merskey H.
Hyperthyroidism after treatment with lithium.
Can J Psychiatry. 1993 Nov;38(9):599-602.
PMID: 8306232; UI: 94138820
Hiromatsu Y, Sato M, Tanaka K, Nonaka K, Kojima K, Sato K, Kurose S, Hoshino T, Nakashima A.
Anti-eye muscle antibodies and hypothyroid Graves' disease: a case report.
Endocrinol Jpn. 1992 Dec;39(6):593-600.
PMID: 1363467; UI: 93193650
Takami H, Shikata J.
Graves' disease with severe iodine allergy: successful surgery after lithium carbonate treatment. Case report.
Eur J Surg. 1991 Aug;157(8):489-90.
PMID: 1681939; UI: 92032010
Tsunoda T, Mochinaga N, Eto T, Yamaguchi M, Tsuchiya R, Izumi M.
Lithium carbonate in the preoperative preparation of Graves' disease.
Jpn J Surg. 1991 May;21(3):292-6.
PMID: 1713279; UI: 91311902
Bhansali A, Nalini K, Dash RJ.
Lithium carbonate therapy for induction of euthyroid state in thyrotoxicosis. A preliminary study.
J Assoc Physicians India. 1990 Dec;38(12):911-3.
PMID: 2128939; UI: 91258279
Schaaf L, Greschner M, Paschke R, Kusterer K, Teuber J, Huck K, Schmidt R, Sager HD, Usadel KH.
Thyrotoxic crisis in Graves' disease: indication for immediate surgery.
Klin Wochenschr. 1990 Nov 9;68(21):1037-41.
PMID: 1707465; UI: 91194200
Balabolkin MI, Petunina NA, Tsaguriia KG.
The use of lithium carbonate in treating patients with diffuse toxic goiter
Klin Med (Mosk). 1990 Oct;68(10):68-9. Russian. No abstract available.
PMID: 1706446; UI: 91171615
Arabin B, Endrikat J, Bogner U, Weitzel H.
Diagnosis and therapy of hyperthyroidism in pregnancy.
Geburtshilfe Frauenheilkd. 1990 Jan;50(1):64-8. German.
PMID: 2311908; UI: 90185081
Chang TC.
Influence of lithium carbonate on the thyrotropin receptor in vitro.
Taiwan I Hsueh Hui Tsa Chih. 1989 Jan;88(1):13-7.
PMID: 2547015; UI: 89328376
Slobozhanin MI, Chudnova VS, Kuznetsov IS.
Use of combined complexes and lithium carbonate in the preoperative care of patients with toxic goiter].
Klin Khir. 1989;(12):32-3. Russian.
PMID: 2517312; UI: 90219646
Angel M.
Treatment of Graves-Basedow disease
Med Clin (Barc). 1988 May 7;90(18):748-54. Review. Spanish. No abstract available.
PMID: 2902259; UI: 89013281
MacGregor GA.
Asymptomatic Graves' disease during lithium therapy.
Postgrad Med J. 1986 Dec;62(734):1159-60. No abstract available.
PMID: 3658858; UI: 88015881
McDermott MT, Burman KD, Hofeldt FD, Kidd GS.
Lithium-associated thyrotoxicosis.
Am J Med. 1986 Jun;80(6):1245-8.
PMID: 3755288; UI: 86265694
Primary hypothyroidism developed in a 57-year-old woman treated for eight years with lithium carbonate for manic-depressive illness, and nine months later she became thyrotoxic. Although autoimmune disease appeared to be responsible, lithium was suspected to play a contributory role in both phases of her illness. This is the first reported case of hyperthyroidism following hypothyroidism in a lithium-treated patient. The 24 reported cases of lithium-associated thyrotoxicosis and the possible mechanisms that may explain this poorly understood phenomenon are also reviewed.
PMID: 3755288, UI: 86265694
Petrov NM.
Lithium carbonate in the treatment of patients with diffuse toxic goiter.
Vrach Delo. 1986 Jun;(6):64-6. Russian. No abstract available.
PMID: 3092467; UI: 86317878
Balabolkin MI.
Treatment of diffuse toxic goiter
Probl Endokrinol (Mosk). 1986 May-Jun;32(3):45-8. Russian. No abstract available.
PMID: 3755532; UI: 86287216
Bistriceanu M, Rosca TR, Mocanu I, Bistriceanu I, Voinea F.
Effect of short-term lithium carbonate administration in hyperthyroidism, with or without associated ophthalmopathy.
Endocrinologie. 1986 Apr-Jun;24(2):109-13.
PMID: 3090679; UI: 86289180
Thompson CJ, Baylis PH.
Asymptomatic Graves' disease during lithium therapy.
Postgrad Med J. 1986 Apr;62(726):295-6.
PMID: 3086856; UI: 86233017
Lithium salts are widely recognized to cause biochemical hypothyroidism and have been used to treat thyrotoxicosis. We present a case of Graves' disease which developed during lithium therapy. The patient was asymptomatic until the lithium was discontinued; she subsequently developed florid symptoms of thyrotoxicosis.
PMID: 3086856, UI: 86233017
Petrov IM.
Changes in the hormone profile, central hemodynamics and tissue blood flow in patients with thyrotoxic goiter during treatment with lithium carbonate.
Med Radiol (Mosk). 1986 Apr;31(4):13-5. Russian.
PMID: 3083189; UI: 86174054
Petrov NM, Semenov VV.
Lithium in the treatment of thyrotoxicosis (clinico-biological aspects).
Probl Endokrinol (Mosk). 1986 Mar-Apr;32(2):83-6. Review. Russian. No abstract available.
PMID: 2424005; UI: 86233191
Reed J, Bradley EL 3d.
Postoperative thyroid storm after lithium preparation.
Surgery. 1985 Nov;98(5):983-6.
PMID: 3933136; UI: 86044906
Balazs C, Leovey A, Szerze P, Bako G, Vertes T.
Lithium treatment of Basedow's disease.
Ther Hung. 1984;32(2):69-73. No abstract available.
PMID: 6443752; UI: 86316574
Petrov NM, Petrova NS.
Dynamics of the hormone profile and cardiovascular changes in toxic goiter as affected by lithium carbonate.
Probl Endokrinol (Mosk). 1983 Nov-Dec;29(6):23-7. Russian.
PMID: 6318217; UI: 84095575
Spesivtseva VG.
Treatment of patients with toxic diffuse goiter.
Klin Med (Mosk). 1983 Oct;61(10):118-23. Russian. No abstract available.
PMID: 6417398; UI: 84065872
Sato K.
Treatment of Basedow's disease with 131-I combined with lithium.
Kaku Igaku. 1983 Mar;20(2):171-7. Japanese. No abstract available.
PMID: 6688446; UI: 83295165
Schweiz Med Wochenschr 1978 Nov 25;108(47):1850-3 , Books,
LinkOut
Lithium acetate, a useful and well tolerated thyrostatic for selected cases of hyperthyroidism].
[Article in German]
Eigenmann F, Burgi H
Lithium acetate treatment of 6 patients with hyperthyroid Graves' disease and 6 patients with toxic nodular goiter is reported. Lithium acetate was administered either as monotherapy (group A) or combined with 45 mg carbimazole or methimazole (group B). A control group of 8 patients received methimazole or carbimazole only (group C). Lithium either alone or combined with thionamide drugs consistently lowered serum thyroxine and triiodothyronine with marked clinical improvement. After 7 days of treatment thyroxine was reduced by 28% (group A), 43% (group B) and 36% (group C). The respective decrease in triiodothyronine was 42%, 50% and 46%. The differences between three groups were not statistically significant. We conclude that lithium is a useful antithyroid agent for selected patients, since it is safe and effective even in severe cases, does not interfere with radioiodine uptake for diagnostic or therapeutic purposes and provides an alternative for patients allergic to thionamides.
PMID: 581407, UI: 79056043
Lancet 1974 Nov 16;2(7890):1160-3 , Books, LinkOut
Treatment of thyrotoxicosis with lithium carbonate.
Lazarus JH, Richards AR, Addison GM, Owen GM
PMID: 4139588, UI: 75044498
Thyroid 1998 Oct;8(10):909-13 , Books, LinkOut
The effects of lithium therapy on thyroid and thyrotropin-releasing hormone.
Lazarus JH
Department of Medicine, University of Wales College of Medicine, Cardiff, UK.
Lithium is used in the prophylaxis of bipolar depressive disorder in augmentation treatment of depression and in the therapy of some cases of unipolar depression.
Lithium affects cell function via its inhibitory action on adenosine triphosphatase (ATPase) activity, cyclic adenosine monophosphate (cAMP), and intracellular enzymes. The inhibitory effect of lithium on inositol phospholipid metabolism affects signal transduction and may account for part of the action of the cation in manic depression.
Lithium also alters the in vitro response of cultured cells to thyrotropin-releasing hormone (TRH) and can stimulate DNA synthesis. Lithium is concentrated by the thyroid and inhibits thyroidal iodine uptake. It also inhibits iodotyrosine coupling, alters thyroglobulin structure, and inhibits thyroid hormone secretion. The latter effect is critical to the development of hypothyroidism and goiter. Effects on brain deiodinase enzymes and alterations in thyroid hormone receptor concentration in the hypothalamus are under investigation in relation to the therapeutic effect of lithium.
The ion affects many aspects of cellular and humoral immunity in vitro and in vivo. This accounts for a rise in antithyroid antibody titer in patients having these antibodies before lithium administration whereas there is no induction of thyroid antibody synthesis de novo. Goiter, due to increased thyrotropin (TSH) after inhibition of thyroid hormone release, occurs at various reported incidence rates from 0%-60% and is smooth and nontender. Subclinical and clinical hypothyroidism due to lithium is usually associated with circulating anti-thyroid peroxidase (TPO) antibodies but may occur in their absence. Iodine exposure, dietary goitrogens, and immunogenetic background may all contribute to the occurrence of goiter and hypothyroidism during long-term lithium therapy. It is currently unclear whether the reported association of lithium therapy and hyperthyroidism are causal, although there is suggestive epidemiological evidence. Finally, lithium therapy is associated with exaggerated response of both TSH and prolactin to TRH in 50%-100% of patients, although basal levels are not usually high. It is probable that the hypothalamic pituitary axis adjusts to a new setting in patients receiving lithium.
PMID: 9827658, UI: 99043360
Encephale 1979;5(2):171-88 , Books, LinkOut
Lithium and thyroid function. Significance of the TRH test in the diagnosis of lithium- induced thyroid dysfunction.
[Article in French]
Singer L, Schlienger JL, Kammerer F, Stephan F
The treatment by lithium is known to involve certain endocrine complications. Those concerning the thyroid function, with risk of a frank hypothyroidy, are the most important. Aiming to appreciate the frequence and the intensivity of the endocrine effects of lithium, the thyroid parameters and the steady state of the hypothalamo pituitary-thyroid axis were tested using the TRH test in 52 patients with maniacodepressive psychosis with special attention to TSH, prolactin and growth hormone: 24 out of them were treated for 1 month to 6 years by lithium; the 28 others were considered as controls. The lithium treatment involves a decrease in the free thyroxine index (1.78 +/- 0.09 vs 2.16 +/- 0.09; p less than 0.01), an increase in the mean baseline TSH level (5.80 +/- 1.49 vs 2.70 +/- 0.24 microU/ml; p less than 0.05) and a noteworthy increase in the TSH responsiveness to TRH (22.7 +/- 2.14 vs 9.75 +/- 1.63 microU/ml; p less than 0.005). The TSH supranormal responses were neither correlated with the length of the treatment nor with the age of the patients. They appear as the consequence of a decrease in the thyroidal hormone secretion. The basal and stimulated prolactinemias remain comparable in the two groups of patients and no response of growth hormone occured after TRH. The TRH test must be considered as a useful complement for the surveillance of the patients treated with lithium because it permits to diagnose early the lithio-induced thyroid dysfunction.
PMID: 113202, UI: 80003479
J Endocrinol Invest 1993 Apr;16(4):259-63 , Books
Effects of lithium treatment on hypothalamic-pituitary-thyroid axis: a longitudinal study.
Lombardi G, Panza N, Biondi B, Di Lorenzo L, Lupoli G, Muscettola G, Carella C, Bellastella A
Dipartimento di Endocrinologia, Universita di Napoli, Italy.
Lithium carbonate, widely used in the treatment of bipolar patients, is well known to induce thyroid alterations. In this longitudinal study the thyroid function was investigated during lithium treatment over a period of 12 months in 12 euthymic bipolar patients with a normal thyroid function and absence of thyroid antibodies. Nine of the 12 patients were further studied on the 15th month, 5 of these 9 on the 18th month and 4 of the last-mentioned 5 on the 24th month. The mean basal and TRH-stimulated TSH values during lithium therapy were significantly higher as compared to those at the beginning of the treatment. More particularly, during lithium therapy, a significant increase of basal TSH over the normal range was found in 10 out of the 12 patients. A rise of TRH-stimulated TSH was found in 11 out of the 12 patients. The impairment of the hypothalamic-pituitary-thyroid (HPT) axis was transitory in the majority of cases. Two patients developed a nodular goiter during the treatment. Plasma T3, T4, FT3 and FT4 levels did not change during the treatment. Thyroid antibodies remained undetectable. The conclusions of the study are twofold: 1) Subclinical hypothyroidism during lithium therapy is much more frequent than previous cross-sectional studies suggest; 2) Thyroxine replacement in lithium-treated patients is advisable in order to prevent subclinical hypothyroidism and the risk of a subsequent goiter.
PMID: 8514981, UI: 93294145
Arzneimittelforschung 1978;28(8):1297-8 , Books
Thyroid function in prophylactic therapy with lithium.
[Article in German]
Wasilewski B, Steinbock H, Kohl R, Greil W, Bottermann P
In 62 out-patients under maintenance treatment with lithium, thyroid function was evaluated. 21% of the patients exhibited goiter II0; 34% showed elevated thyrotrophin (TSH) serum levels; in 42% exaggerated TSH response to intravenous thyrotrophin releasing hormone (TRH) was found.
PMID: 111680, UI: 79231643
Am J Psychiatry 1990 Nov;147(11):1518-21 , Books, LinkOut
Thyroid function and ultrasonically determined thyroid size in patients receiving long-term lithium treatment.
Perrild H, Hegedus L, Baastrup PC, Kayser L, Kastberg S
Department of Internal Medicine C, Bispebjerg Hospital, Copenhagen NV, Denmark.
Thyroid function was investigated in 100 manic-depressive patients. Goiter was more common in patients treated with lithium for 1-5 years (44%) or more than 10 years (50%) than in patients who never received lithium (16%). Smoking contributed significantly to thyroid size and goiter. In nonsmoking patients, ultrasonically determined thyroid volume was significantly related to treatment duration. The mechanism behind this increased thyroid volume is unclear, as most patients had normal serum thyrotropin levels and no thyroid autoimmunity. Subclinical or overt hypothyroidism was found in 4% and 21% of patients treated for 1-5 and more than 10 years, respectively. Since few hypothyroid patients had autoimmunity or goiter, lithium may affect the thyroid gland directly.
PMID: 2221166, UI: 91023204