- Email: [email protected]
Lithium
Mogens Schou
3 L I T H I U M (SED-12, 79; SEDA-12, 26; SEDA-13, 17, SEDA-14, 18; SEDA-15, 20)
N e w interactions Lithium has been used in clinical practice now f o r more than 40years, and unexpected adverse effects are unlikely to appear. However, the emergence o f new drugs may involve the risk o f new interactions with lithium. The concurrent administration o f A C E inhlbitors with lithium may lead to impaired glomerular filtration, with increased serum creatinine and serum lithium concentrations. Drugs involved have included enalapril (1C-8C), eaptopril (9C - 12c), and lisinopril (13 c _ 15c). The 1990 edition o f "The Physicians" Desk Reference" contains a warning against the combination (16). The mechanism involved is not known, but A CE inhibitors may cause renal insufficiency in patients with low renal blood flow, and it has been suggested (11 C) that in patients who do not respond to lithium-induced diabetes insipidus with adequate water intake, volume depletion and a low renal blood f l o w might result. It has yet to be demonstrated that polyuric patients are particularly vulnerable to this interaction. The new specific serotonin (5-HT) uptake inhibitors fluoxetine and fluvoxamine are felt to combine f e w adverse effects with a high degree o f efficacy, e.g. in combination with lithium in treatment-refractory depression (17 C - 20c). However, when given concurrently with lithium, they may induce mania (21 C) or give rise to a toxic encephalopathy, with somnolence, confusion, dizziness, ataxia, tremor and impaired co-ordination (22 C - 27c). The U.K. Committee on Safety o f Medicines has issued a warning against the combination (28).
9 1993 Elsevier Science Publishers. All rights reserved
Side Effects of Drugs Annual 16 M.N.G. Dukes and J.K. Aronson, eds.
Lithium The mechanism may be an increase in the concentration o f 5-HT in the brain. Since there is no information about how often fluoxetine and fluvoxamine are used together with lithium, it is not clear whether such interactions are rare or common
GENERAL An extensive review of lithium-induced adverse effects has been published in Italian (29R). A comparative study of carbamazepine and lithium showed that 60~ of the patients taking carbamazepine and 43 070of those taking lithium had adverse effects (30c).
EFFECTS ON ORGANS A N D SYSTEMS
Cardiovascular system Although adverse effects of lithium on the heart are rare, effects on the myocardium have occasionally been signalled by increases in serum creatine kinase and creatine kinase-MB during lithium poisoning and in old people with therapeutic serum lithium concentrations (3 l c); except in one patient with pre-existing cardiac disease, the enzyme changes were not accompanied or followed by clinical signs or symptoms. A patient with toxic serum lithium concentrations showed a repolarization delay, which was proportional to the serum lithium concentration and inversely proportional to the serum potassium concentration (32c); the abnormality was reversed and lithium well tolerated when additional potassium was given. A patient with pre-existing conduction tissue disease developed sinus arrest and asystole during lithium intoxication (33c), and the same happened to another patient with serum lithium concentrations within the recommended range (34c). A patient with multiple myeloma developed atrial fibrillation and A V block, which required temporary pacing (35c). Four out of 40 patients treated with lithium 13
Chapter 3
14 alone or lithium in combination with amitriptyline had increases in blood pressure up to 200/145 mmHg (36c). This finding is in contrast with the outcome of a systematic study of a large patient group (n --- 377) examined before and repeatedly during lithium treatment (37c); lithium had no effect on the average blood pressure, and the frequency of arterial hypertension was not higher during lithium treatment than it had been before.
Neuromuscular system Non-traumatic rhabdomyolysis is a rare complication of lithium treatment; only 3 cases have been reported (38 c - 40c). It has been suggested (40 c) that it may develop as a result of hyperosmolality secondary to a lithium-induced reduction in renal concentrating ability. Two further reports have appeared of a Creutzfeldt-Jakob-like syndrome during treatment with lithium or with lithium plus other drugs (41 c, 42c). During lithium treatment a patient developed a polyneuropathy, which disappeared after withdrawal (43c). Some cases of pseudotumor cerebri during lithium treatment may have been caused by undetected hypothyroidism (44c). A patient taking well-tolerated lithium therapy developed a left hemiplegia; thereafter lithium treatment, with serum concentrations around 0.8 mmol/1, led to an increase in thepatient's left-sided spasticity, while his right side remained unaffected (45r In patients treated with lithium for 9 - 1 6 years the frequency of abnormal involuntary movements (tardive dyskinesia) correlated with advanced age, low body weight, early onset of affective illness, a family history of dementia, and high serum lithium concentrations (46c). Multiple regression analyses were not carried out. In rats lithium causes changes in the retina and enhancement o f acute light effects, and ophthalmological examination of lithiumtreated patients has shown increased visualfieM defects and raised dark adaptation and color recognition thresholds ( 4 7 c - 5 1 c ) . It seems possible that lithium-treated patients are at increased risk of acquiring retinal lesions if they are exposed to bright light, e.g. during light therapy for seasonal affective disorder. Mind
Attempts to assess the car-driving skills
M. Schou
of patients taking prophylactic lithium have given variable results. Healthy volunteers given lithium for 2 weeks showed some impairment of choice reaction performance in a car simulator (52c). Patients with Meni6re's disease who had participated in a controlled prophylactic trial for 6 months were also exposed to a car simulator (53c); there was no difference in driving skills between those given lithium and those given placebo. In a recent study 16 manicdepressive patients in remission on prophylactic lithium, given for at least 3 months, were compared with 22 healthy controls (54c). The patients had a median reaction time of 0.72 seconds, significantly longer than that of the controls, 0.58 seconds. The authors suggested that patients should be warned that lithium may affect their ability to drive or operate machinery. Presumably most of the many thousands of manic-depressive patients taking lithium drive a car or operate machinery, but I have never heard of any car or machine accident in which lithium treatment was implicated. However, I make it a habit to give the following warning: 'It may be wise for patients starting lithium treatment to abstain from car driving until they have found out how much the treatment affects their driving ability' (55). A hypothesis that dementia might have been caused by long-term lithium treatment has not been supported by literature studies, which revealed other causes of the dementia (56c). An increase in depression scores in patients who had taken lithium for many years turned out to be the result of worsening disease rather than of the treatment, because the same changes were seen in patients who had stopped taking lithium (57c).
Thyroid and parathyroid Lithium treatment may cause the formation of thyroid antibodies in susceptible individuals (58 c, 59c). In a recent review (60 R) the similarities between the actions of lithium and the cardiac drug, amiodarone, on the thyroid have been discussed. With both drugs the nature of the thyroid abnormality (hypothyroidism or hyperthyroidism) is influenced by the patient's iodine status and by the presence of pre-existing, often subclinical, thyroid pathology. Lithium-induced goiter is significantly correlated with treatment duration and with smoking (61 c). Reports continue to appear about the
Lithium Chapter3 frequencies of lithium-induced goiter and hypothyroidism (62c, 63c), but they convey little useful information when control frequencies are lacking, either from control subjects or from the patients themselves before lithium treatment started. Three cases of thyroid carcinoma have appeared in a surgical department's account of 'lithiumogenic' disorders of the thyroid and parathyroid glands (64c). Although hyperparathyroidism usually disappears when lithium treatment is discontinued, continuation of treatment may be necessary for the patient's mental health, and surgical intervention may be indicated (65 C - 67c).
Liver
Lithium generally neither causes nor aggravates liver disease (68R), but in a patient with pre-existing Gilbert's disease (partial deficiency of bilirubin glucuronyl transferase) lithium treatment was associated with a temporary increase in his indirect bilirubin concentration without concomitant changes in his other liver function tests (69r
Urinary system
The effects of lithium on kidney function have been the subject of recent reviews (SEDA-14, 18; 70R, 71R). On the basis o f studies both longitudinal (over 1000 patients) and cross-sectional (over 3000 patients) it was concluded that although lithium treatment may reduce renal concentrating ability and cause polyuria, it does not, even when given for many years, lead to changes in glomerular filtration rate, let alone renal failure. At the time those reviews were written not a single case of renal failure had occurred which could be ascribed with reasonable certainty to lithium. Since then 1 case of uremia during lithium treatment has been reported (72c). In a 71year-old woman the serum creatinine concentration started to rise gradually after 10 years of lithium treatment and over another 10 years of treatment rose to 571 /zmol/1; her chromium EDTA clearance had at that time fallen to 15 ml/min per 1.73 m 2 body surface, and she was started on hemodialysis. The patient had not suffered from lithium intoxication and no signs of independent kidney disease could be found. This may be the first established case of uremia caused by long-term lithium treatment with non-toxic doses. However, failure to find
15 other causes of the uremia does not prove their absence. At any rate, the publication of a single case does not alter the main conclusion of the large systematic studies of long-term lithium treatment, namely that the risk of lithiuminduced impairment of glomerular function is extremely small. This is supported by a prospective follow-up study carried out on 46 patients after an average time of 20 years on lithium (73c). There was a significant fall in glomerular filtration rate, but it was related to increasing age. Two patients developed renal insufficiency but after withdrawal of lithium. Arguments continue to be presented for administering lithium in one rather than in 2 or 3 daily doses, a procedure which may lead to less polyuria (74 C, 75c). However, the hypothesis has been tested in only one study with random allocation of treatment regimens, and that study did not support it (76c). A peculiar side effect was seen in a pregnant woman who developed polyhydramnios as a result of fetal polyuria (77c).
Skin and appendages Alopecia related to lithium treatment has been reviewed (78R). A case of Darier's disease, well controlled with etretinate, worsened markedly on two separate occasions after lithium ingestion and improved after its discontinuation (79c). In another patient keratodermia appeared twice after institution of lithium therapy and resolved both times after discontinuation (80c). After 10 years of lithium treatment a patient developed erythema multiforme, which disappeared after discontinuation of lithium and reappeared on readministration (81c). Second-generation effects Problems relating to lithium treatment during pregnancy, delivery, and lactation have recently been reviewed (82R). From a strictly scientific point of view, the numbers involved are too small to provide definitive proof of a teratogenic action of lithium. Teratogenesis, with a risk of perhaps 5 - 10o70, nevertheless does seem a possibility, which it appears imprudent to disregard. The counsel given at present is the following (82R): as a general rule, women of fertile age should use contraception while on lithium, treatment should be stopped before a planned pregnancy, and it should be stopped as soon as an unplan-
16 ned pregnancy is discovered; on the other hand, it is important that the individual patient's situation is considered, and lithium treatment may have to be continued uninterrupted throughout pregnancy in women who know from past experience that they are apt to develop severe mania or depression soon after having stopped lithium. It should be remembered that prophylactic alternatives to lithium, such as carbamazepine and valproate, may also have teratogenic effects (83 c, 84c). A baby born to a mother taking lithium had hypothyroidism (in addition to an atrial septal defect) (85c). An 18-year-old patient with Ebstein "s anomaly was found to have been exposed to lithium in utero (86c).
Intoxication Neurotoxic effects of lithium, mostly resulting from lithium intoxication, have been reviewed (87 R - 89R). An irreversible cerebellar syndrome developed in an alcoholic patient who started lithium immediately after having suffered a neuroleptic malignant syndrome with fever (90c). Occasionally neurological and mental sequelae after lithium intoxication can resolve after having lasted as long as 3 - 4 months (91 r 92c). Other instances of lithium intoxication have occurred, precipitated by such circumstances as large neuroleptic dosages (93c), operation with anesthesia (94c), pulmonary infection with fever (95c), co-administration of digoxin (96 c) or of the loop diuretic, bumetanide (97c), and insufficient fluid intake by a mentally retarded patient during lithium-induced polyuria (98r Fatal intoxication developed on the fifth day of a religious fast, during which the patient consumed only a glass of milk and a teacup o f porridge daily but continued to take lithium in unaltered dosage (99c). Gradually developing lithium intoxication may be characterized by T-wave abnormalities and is more dangerous than acute lithium intoxication (100c). Occasionally lithium intoxication can present as worsening mental state (101c), and intoxication masquerading as a manic episode has been seen (102c). Hemodialysis, repeated when the serum lithium concentration rebounds, remains the preferred treatment (103 c, 104c); continuous arteriovenous hemofiltration can also be used (105c).
Chapter 3
M. Schou
Whole-bowel irrigation (106 c) and gastric lavage (107 c) have been suggested as treatments for acute ingestion of overdoses of sustained-release lithium tablets.
Interactions A n acute extrapyramidal reaction followed the concurrent administration of lithium and sulpiride (108c). The interaction with neuroleptics in general has been the subject of two reviews (109 R, 110 R) and a special symposium (111R-II7R). Permanent brain damage is not a characteristic feature of lithium-neuroleptic interaction, which seems to occur only when drug dosages are high. With the use of moderate dosages there seems to be no reason to abandon a combination which is useful in the treatment of acute mania and in the maintenance therapy of schizoaffective illness. It has been suggested that hyperthermia is involved in determining the extent of brain damage which may be caused by the combination of lithium and neuroleptics (118C). Adverse interactions with benzodiazepines remain rare and doubtful (119 c, 120c), Interactions of lithium with antidepressants are infrequent and mild, but fluoxetine and fluvoxamine may be exceptions (see the'Special Review' above). A 71-year-old patient developed malignant hyperthermia 1 month after lithium was added to amitriptyline (121c); it resolved within 10 days during treatment with dantrolene and hypothalamic phospholipid liposomes. The combination of lithium and doxepin led to a condition resembling neuroleptic malignant syndrome with fever (122c). Interactions of lithium with non-steroidal anti-inflammatory agents have been reported (123c), reviewed (124R), and debated (125, 126). Indomethacin seems to increase serum lithium concentrations most, while sulindac and aspirin do not do so to a clinically significant degree. If one follows a recommendation to treat lithium-induced nephrogenic diabetes insipidus with a combination of indomethacin and the vasopressin analog DDAVP (127c), one should therefore pay particular heed to the warning that 'indomethacin must be used with care because it may impair renal function'. Only two reports have appeared this year about interactions of lithium with diuretics (97 c, 128c). Perhaps warnings are working.
Lithium
Chapter3
Studies on human volunteers suggest that furosemide may be safer than thiazides if diuretic treatment is indicated during lithium treatment (129, 130). The much-debated question of an interaction of lithium with electroconvulsive therapy (ECT) has again been reviewed (131R); the authors advise that lithium should be discontinued ahead of time in patients referred for E C T . In emergencies, when this cannot be accomplished, close observation is called for. Lithium in relation to anesthesia has been dealt with in a broader review (132R). A patient on long-term lithium developed an acute psychosis when the calcium antagonist diltiazem was added for the treatment o f hypertension (133 c). The author s suggested an interaction between the two drugs, but could not exclude an effect of diltiazem alone. C o m bined treatment with lithium and another calcium antagonist, verapamil, led to dysarthria and ataxia, which was relieved on substitution of nifedipine for verapamil; upon
17 reinstitution o f verapamil the patient once again displayed neurotoxicity (134r A study o f 9 healthy volunteers suggested that alcohol may accelerate the excretion o f lithium in w o m e n (135). Absorption o f lithium from the gastrointestinal tract may be inhibited by psyllium (136c). Miscellaneous A 36-year-old w o m a n took lithium for 20 days and developed polyarthritis with swelling, pain and stiffness o f joints, associated with erythema, tenderness and limitation o f movements; there was no fever (137c). The same authors had seen 4 patients who had reported significant worsening o f rheumatoid arthritis during lithium treatment. A b o u t one-fifth of patients on lithium had increased serum amylase values (138); none of them had clinical signs or symptoms of parotid gland or pancreatic ailments. Obstructive sleep apnea may be secondary to marked weight gain, which again may be secondary to lithium treatment (139c).
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241, 1 - 7. 47. Kropf D, Miiller-Oerlinghausen B (1986) Effects of lithium on visual perception in manicdepressive patients without acute symptomatology. Neuropsychobiology, 15, 34-42. 48. Seggie J, Carney PA, Parker J, Grof E, Grof P (1989) Effect of chronic lithium on sensitivity to light in male and female bipolar patients. Prog.
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Lithium
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Depressive Illness: A practical Guide, 4th rev. ed., p. 36, Karger, Basel. 56. Renier L (1990) Langdurige lithiuminname en dementie. Tijdschr. Psychiatr., 32, 6 4 0 - 646. 57. Nilsson A, Axelsson R (1990) Lithium discontinuers. I. Clinical characteristics and outcome. Acta Psychiatr. Scand., 82, 433- 438. 58. Wilson R, McKillop JH, Crocket GT, Pearson C, Jenkins C, Burns F, Burnett AK, Thomsen JA (1991) The effect of lithium therapy on parameters thought to be involved in the development of autoimmune thyroid disease. Clin. Endocrinol., 34, 357-361. 59. Bolo-Deoku J, Wilcox H (1991) Thyroid dysfunction and affective illness. Br. Med. J., 302, 1403. 60. Chow CC, Cockram CS (1990) Thyroid disorders induced by lithium and amiodarone: an overview. Adverse Drug React. Acute Poison. Rev., 9, 207 - 222. 61. Perrild H, Hegediis L, Baastrup PC, Kayser L, Kastberg S (1990) Thyroid function and ultrasonically determined thyroid size in patients receiving long-term lithium treatment. Am. J. Psychiatry, 147, 1518-1521. 62. Aiello A, Barone G, Cristofaro M, Vendittelli N, Carrozza F, Buongusto G, Carile L (1990) Alterazioni della funzionalit~ tiroidea durante il trattamento di disturbi psichiatrici con sale di litio. Clin. Ter., 133, 173- 175. 63. Bocchetta A, Bernardi F, Pedditzi M, Loviselli A, Velluzzi F, Martino E, del Zompo M (1991) Thyroid abnormalities during lithium treatment. Acta Psychiatr. Scand., 83, 193 - 198. 64. McHenry CR, Rosen IB, Rotstein LE, Forbath N, Walfish PG (1990) Lithiumogenic disorders of the thyroid and parathyroid glands as surgical disease. Surgery, 108, 1001 - 1005. 65. Feldman MG, Pachman JS (1990) Surgical management of lithium-induced hypercalcemia.
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Conn. Med., 54, 614-615. 66. Ananth J, Wohl M, Zegers C, Remmel R (1991) Hyperparathyroid adenoma with lithium therapy. Lithium, 2, 5 4 - 57. 67. Ouvry O, Artru L, Allilaire JF (1991) A l'occasion d'un cas clinique, mise au point de l'association: hyperparathyroidie et traitement par lithium. Ann. Psychiatr., 5 9 - 62. 68. Viegut V, Jefferson JW (1990) Lithium and the liver. Lithium, 1, 9 - 13. 69. Cohen LS, Cohen DE (1991) Lithium-induced hyperbilirubinemia in an adolescent. J. Clin. Psychopharmacol., 11, 274-275. 70. Schou M (1988) Effects of long-term lithium treatment on kidney function: an overview. J. Psychiatr. Res., 22, 287- 296. 71. Schou M (1990) Lithiumbehandling og nyrefunktion. Ugeskr. Laeger, 152, 2343- 2345. 72. von Knorring L, Wahlin A, Nystr6m K, Bohman SO (1990) Uraemia induced by long-term lithium treatment. Lithium, 1, 251 - 253. 73. Hetmar O, Povlsen UJ, Ladefoged J, Bolwig TG (1990) Lithium: long-term effects on the kidney. A prospective follow-up study ten years after kidney biopsy. Br. J. Psychiatry, 158, 5 3 - 58. 74. Mellerup ET, Plenge P (1990) The side effects of lithium. Biol. Psychiatry, 28, 4 6 4 - 466. 75. Bowen RC, Grof P, GrofE (1991) Less frequent lithium administration and lower urine volume. Am. J. Psychiatry, 148, 189- 192. 76. Muir A, Davidson R, Silverstone T, Dawnay A, Forsling ML (1989) Two regimens of lithium prophylaxis and renal function. Acta Psychiatr. Scand., 80, 579-583. 77. Ang MS, Thorp JA, Parisi VM (1990) Maternal lithium therapy and polyhydramnios. Obstet. Gynecol., 76, Suppl. II, 517-519. 78. Warnock JK (1991) Psychotropic medication and drug-related alopecia. Psychosomatics, 32, 149- 151. 79. Milton GP, Peck GL, Fu JJL, Digiovanni J J, Nordlund J J, Thomas JH, Sanders SF (1990) Exacerbation of Darier's disease by lithium carbonate. J. Am. Acad. Dermatol., 23, 926-928. 80. Labelle A, Lapierre YD (1991) Keratodermia: side effects of lithium. J. Clin Psychopharmacol., 11, 149- 150. 81. Balldin J, Berggren U, Heijer A, Mobacken H (1991) Erythema multiforme caused by lithium. J. Am. Acad. Dermatol., 16, 1015 - 1016. 82. Schou M (1990) Lithium treatment during pregnancy, delivery, and lactation: an update. J. Clin. Psychiatry, 51, 410-413. 83. Jones KL, Lacro RV, Johnson KA, Adams J (1989) Pattern of malformations in the children of women treated with carbamazepine during pregnancy. N. Engl. J. Med., 320, 1661 - 1666. 84. Markovitz P J, Calabrese JR (1990) Use of anticonvulsants for manic depression during pregnan-
Chapter 3
20 cy. Psychosomatics, 31, 118-119. 85. Robert E, Francannet C (1990) Comments on 'Teratogen update on lithium' by J. Warnaky. Teratology, 42, 205. 86. Steffelaar JW, van Wesemael JWJ (1991) Anomalie van Ebstein van de tricuspidalisklep na expositie aan lithium voor de geboorte. Ned. Tijdschr. Geneeskd., 135, 996- 998. 87. Kemperman CJF, Tulner DM (1990) Neurotoxicity of lithium. Lithium, 1, 195 -202. 88. Jefferson JW (1991) Lithium poisoning. Emerg. Care, 7, 18- 28. 89. Verdoux H, Bourgeois M (1991) S6quelles neurologiques irr~versibles induites par le lithium. Encdphale, 17, 221 - 224. 90. Verdoux H, Bourgeois ML (1990) A case of lithium neurotoxicity with irreversible cerebellar syndrome. J. Nerv. Ment. Dis., 178, 761-762. 91. Van Scheyen JD (1990) Herstel na neurotoxische symptomen door lithium: een casus. Acta Neuropsychiatr., 2, 2 6 - 29. 92. Nambudiri DE, Meyers BS, Young RC (1991) Delayed recovery from lithium neurotoxicity.
J. Geriatr. Psychiatry Neurol., 4, 40-43. 93. Benitez MH, de las Cuevas Castresana C, Gonz~ilez de Rivera JL, Perdomo AF (1990) Intoxicaci6n por litio, afectaci6n renal y diabetes insipida nefrog6nica. Psiquis, 11, 41 - 4 4 . 94. Biron R, Diraison Y, Ladagnous JF, Brinquin L, Bonsignou RJP (1990) A propos d'une enc6phalopathie postop6ratoire: le lithium et ses pi~ges. Cah. Anesth~siol., 38, 3 9 - 40. 95. Codine P, Kotzki N, Enjalbert M, Pelissier J, Simon L (1991) Complications de l'intoxication au lithium: aspects en m6dicine de r66ducation. A propos de 2 cas. Ann. Rdadapt. Mdd. Phys., 34, 211-216. 96. Del Real MA, Iniguez C, Marco J, Corral I, Gimeno Alva A (1990) Deterioro cognitivo y parkinsonismo secundarios a intoxicaci6n por litio. Rev. Esp. Neurol., 5, 430-432. 97. Huang LG (1990) Lithium intoxication with coadministration of a loop-diuretic. J. Clin. Psychopharmacol., It), 228. 98. Neithercut WD, Spooner RJ, Hendry A, Dagg JH (1990) Persistent nephrogenic diabetes insipidus, tubular proteinuria, aminoaciduria, and parathyroid hormone resistance following longterm lithium administration. Postgrad. Med. J., 66, 479 482. 99. Daisley H, Barton EN, Williams CT (1990) Fatal lithium toxicity during a religious fast. South. Med. J., 83, 364. 100. Shannon MW, Eisen T, Linakis J, Woolf A (1990) Clinical features of acute versus chronic lithium intoxication. Ann. Emerg. Med., 19, 630. 101. Goddard J, Bloom SR, Krackowiak RSJ, Pusey CD, MacDermot J, Liddle PF (1991) Lithium intoxication can present as worsening mental state. -
M. Schou
Br. Med. J., 302, 1267- 1269. 102. Bassingthwaighte ME (1991) Lithium toxicity in an elderly woman. J. Clin. Psychiatry, 52, 181. 103. Scoble JE, McLean A, Munn S, Varghese Z, Sweny P, Moorhead JF (1990) Lithium nephrotoxicity and red cell lithium. Nephrol. Dialysis Transplant., 5, 904. 104. Martin TG, Mallinger AG, Michelson EA, Schneider SM (1991) RBC lithium kinetics during an acute intoxication treated with hemodialysis. Vet. Hum. ToxicoL, 33, 363. 105. Bellomo R, Kearly Y, Parkin G, Love J, Boyce N (1991) Treatment of life-threatening lithium toxicity with continuous arterio-venous hemofiltration. Crit. Care Med., 19, 836-837. 106. Smith SW, Ling LJ, Halstenson CE (1991) Whole-bowel irrigation as a treatment for acute lithium overdose. Ann. Emerg. Med., 20,536 - 539. 107. Friedberg RC, Spyker DA, Herold DA (1991) Massive overdoses with sustained-release lithium carbonate preparations: pharmacokinetic model based on two case studies. Clin. Chem., 37, 1205 - 1209. 108. Dinan TG, O'Keane V (1991) Acute extrapyramidal reactions following lithium and sulpiride co-administration: two case reports. Hum. Psychopharmacol., 6, 6 7 - 69. 109. Karki SD, Holden JMC (1990) Combined use of haloperidol and lithium. Psychiatr. Ann., 20, 154- 158. 110. Schou M (1990) Adverse lithium - neuroleptic interaction: frequency, permanency, dosage dependence. Psychiatriki, 1, 136- 139. 111. Lowe MR, Batchelor DH (1990) Preface. Hum. Psychopharmacol., 5, 262. 112. Lowe MR, Batchelor DH (1990) Lithium and neuroleptics in the management of manic depressive psychosis. Hum. Psychopharmacol., 5, 2 6 7 - 274. 113. Batchelor DH, Lowe MR (1990) Reported neurotoxicity with the lithium/haloperidol combination and other neuroleptics: a literature review. Hum. Psychopharmacol., 5, 2 7 5 - 280. 114. Schou M (1990) Adverse lithium - neuroleptic interactions: are there permanent effects? Hum. Psychopharmacol., 5, 2 6 3 - 265. 115. Amdisen A (1990) Lithium neurotoxicity: the reliability of serum lithium measurements. Hum. Psychopharmacol., 5, 281 - 285. 116. Waddington JL (1990) Some pharmacological aspects relating to the issue of possible neurotoxic interactions during combined lithium - neuroleptic therapy. Hum. Psychopharmacol., 5, 293- 297. 117. von Knorring L (1990) Possible mechanisms for the presumed interaction between lithium and neuroleptics. Hum. Psychopharmacok, 5, 287 - 292. 118. Pelletier J, Habib M, Pellissier JF, Crevat A, Khalil R (1991) S6quelles neurologiques de l'association neuroleptiques- lithium: r61e de l'hyperther-
Lithium
Chapter 3
21
mie. Rev. M~d. Interne, 12, 187 - 191. 119. McGinness J, Kishimoto A, Hollister LE (1990) Avoiding neurotoxicity with lithium - carbamazepine combinations. Psychopharmacol. Bull., 26, 181 - 184. 120. Evans RL, Nelson MV, Melethil S, Townsend R, Hornstra R, Smith RB (1990) Evaluation of the interaction of lithium and alprazolam. J. Clin. Psychopharmacol., 10, 355- 359. 121. de Maio D, Laviani M (1991) L i t h i u m - T C A induced malignant syndrome: case report. Progr.
Neuro-Psychopharmacol.
Biol. Psychiatry,
15,
427 - 431. 122. Rosenberg PB, Pearlman CA (1991) NMS-like syndrome with a lithium/doxepin combination. J. Clin. Psychopharmacol., 11, 7 5 - 76. 123. Khan IH (1991) Lithium and non-steroidal anti-inflammatory drugs. Br. Med. J., 302, 1537 - 1538. 124. Ragheb M (1990) The clinical significance of lithium-nonsteroidal anti-inflammatory drug interactions. J. Clin. Psychopharmacol., 10, 350354. 125. Vierhapper H (1990) Indomethacin in the treatment of lithium-induced nephrogenic diabetes insipidus. Arch. Intern. Med., 150, 2420. 126. Allon M (1990) Indomethacin in the treatment of lithium-induced nephrogenic diabetes insipidus. Arch. Intern. Med., 150, 2420. 127. Weinstock RS, Moses AM (1990) Desmopressin and indomethacin therapy for nephrogenic diabetes insipidus in patients receiving lithium carbonate. South. Med. J., 83, 1475 - 1477. 128. Hanna ME, Lobao CB, Stewart JT (1990) Severe lithium toxicity associated with indapamide therapy. J. Clin. PsychopharmacoL, 10, 379 - 380. 129. Crabtree BL, Mack JE, Johnson CD, Amyx
BC (1991) Comparison of the effects of hydrochlorothiazide and furosemide on lithium disposition. Am. J. Psychiatry, 148, 1060- 1063. 130. Shalmi M, Thomsen K (1991) Renal elimination of lithium. In: Birch NJ (Ed.), Lithium and the Cell: Pharmacology and Biochemistry, pp. 249271. Academic Press, London. 131. Small JG, Milstein V (1990) Lithium interactions: lithium and electroconvulsive therapy. J. Clin. Psychopharmacol., 10, 346-350. 132. Sedgwick JV, Lewis IH, Linter SPK (1990) Anesthesia and mental illness. Int. J. Psychiatry Med., 20, 2 0 9 - 225. 133. Binder EF, Cayabyab L, Ritchie D J, Birge SJ (1991) Diltiazem-induced psychosis and a possible diltiazem - lithium interaction. Arch. Intern. Med., 151, 373 - 374. 134. Wright BA, Jarrett DB (1991) Lithium and calcium channel blockers: possible neurotoxicity. Biol. Psychiatry, 30, 6 3 5 - 636. 135. Tyrer SP, Peat MA, Minty PSB (1990) The effect of alcohol on lithium kinetics. Lithium, 1, 163- 168. 136. Toutoungi M, Schulz P, Widmer J, Tissot R (1990) Probable interaction entre le psyllium et le lithium. Th&apie, 45, 358- 360. 137. Khanna R, Chatterjee S (1991) Polyarthritis: an unusual side effect of lithium. J. Clin. Psychiatry, 52, 4 3 - 44. 138. Thamm A, Johnson L, Math6 AA (1990) Serum amylase in patients treated with lithium. Psychopharmacology, 102, 417 - 418. 139. Strakowski SM, Hudson JI, Keck PE, Wilson DR, Frankenburg FR, Alpert JE, Teschke GC, Tohen M (1991) Four cases of obstructive sleep apnea associated with treatment-resistant mania. J. Clln. Psychiatry, 52, 156- 158.
3 L I T H I U M (SED-12, 79; SEDA-12, 26; SEDA-13, 17, SEDA-14, 18; SEDA-15, 20)
N e w interactions Lithium has been used in clinical practice now f o r more than 40years, and unexpected adverse effects are unlikely to appear. However, the emergence o f new drugs may involve the risk o f new interactions with lithium. The concurrent administration o f A C E inhlbitors with lithium may lead to impaired glomerular filtration, with increased serum creatinine and serum lithium concentrations. Drugs involved have included enalapril (1C-8C), eaptopril (9C - 12c), and lisinopril (13 c _ 15c). The 1990 edition o f "The Physicians" Desk Reference" contains a warning against the combination (16). The mechanism involved is not known, but A CE inhibitors may cause renal insufficiency in patients with low renal blood flow, and it has been suggested (11 C) that in patients who do not respond to lithium-induced diabetes insipidus with adequate water intake, volume depletion and a low renal blood f l o w might result. It has yet to be demonstrated that polyuric patients are particularly vulnerable to this interaction. The new specific serotonin (5-HT) uptake inhibitors fluoxetine and fluvoxamine are felt to combine f e w adverse effects with a high degree o f efficacy, e.g. in combination with lithium in treatment-refractory depression (17 C - 20c). However, when given concurrently with lithium, they may induce mania (21 C) or give rise to a toxic encephalopathy, with somnolence, confusion, dizziness, ataxia, tremor and impaired co-ordination (22 C - 27c). The U.K. Committee on Safety o f Medicines has issued a warning against the combination (28).
9 1993 Elsevier Science Publishers. All rights reserved
Side Effects of Drugs Annual 16 M.N.G. Dukes and J.K. Aronson, eds.
Lithium The mechanism may be an increase in the concentration o f 5-HT in the brain. Since there is no information about how often fluoxetine and fluvoxamine are used together with lithium, it is not clear whether such interactions are rare or common
GENERAL An extensive review of lithium-induced adverse effects has been published in Italian (29R). A comparative study of carbamazepine and lithium showed that 60~ of the patients taking carbamazepine and 43 070of those taking lithium had adverse effects (30c).
EFFECTS ON ORGANS A N D SYSTEMS
Cardiovascular system Although adverse effects of lithium on the heart are rare, effects on the myocardium have occasionally been signalled by increases in serum creatine kinase and creatine kinase-MB during lithium poisoning and in old people with therapeutic serum lithium concentrations (3 l c); except in one patient with pre-existing cardiac disease, the enzyme changes were not accompanied or followed by clinical signs or symptoms. A patient with toxic serum lithium concentrations showed a repolarization delay, which was proportional to the serum lithium concentration and inversely proportional to the serum potassium concentration (32c); the abnormality was reversed and lithium well tolerated when additional potassium was given. A patient with pre-existing conduction tissue disease developed sinus arrest and asystole during lithium intoxication (33c), and the same happened to another patient with serum lithium concentrations within the recommended range (34c). A patient with multiple myeloma developed atrial fibrillation and A V block, which required temporary pacing (35c). Four out of 40 patients treated with lithium 13
Chapter 3
14 alone or lithium in combination with amitriptyline had increases in blood pressure up to 200/145 mmHg (36c). This finding is in contrast with the outcome of a systematic study of a large patient group (n --- 377) examined before and repeatedly during lithium treatment (37c); lithium had no effect on the average blood pressure, and the frequency of arterial hypertension was not higher during lithium treatment than it had been before.
Neuromuscular system Non-traumatic rhabdomyolysis is a rare complication of lithium treatment; only 3 cases have been reported (38 c - 40c). It has been suggested (40 c) that it may develop as a result of hyperosmolality secondary to a lithium-induced reduction in renal concentrating ability. Two further reports have appeared of a Creutzfeldt-Jakob-like syndrome during treatment with lithium or with lithium plus other drugs (41 c, 42c). During lithium treatment a patient developed a polyneuropathy, which disappeared after withdrawal (43c). Some cases of pseudotumor cerebri during lithium treatment may have been caused by undetected hypothyroidism (44c). A patient taking well-tolerated lithium therapy developed a left hemiplegia; thereafter lithium treatment, with serum concentrations around 0.8 mmol/1, led to an increase in thepatient's left-sided spasticity, while his right side remained unaffected (45r In patients treated with lithium for 9 - 1 6 years the frequency of abnormal involuntary movements (tardive dyskinesia) correlated with advanced age, low body weight, early onset of affective illness, a family history of dementia, and high serum lithium concentrations (46c). Multiple regression analyses were not carried out. In rats lithium causes changes in the retina and enhancement o f acute light effects, and ophthalmological examination of lithiumtreated patients has shown increased visualfieM defects and raised dark adaptation and color recognition thresholds ( 4 7 c - 5 1 c ) . It seems possible that lithium-treated patients are at increased risk of acquiring retinal lesions if they are exposed to bright light, e.g. during light therapy for seasonal affective disorder. Mind
Attempts to assess the car-driving skills
M. Schou
of patients taking prophylactic lithium have given variable results. Healthy volunteers given lithium for 2 weeks showed some impairment of choice reaction performance in a car simulator (52c). Patients with Meni6re's disease who had participated in a controlled prophylactic trial for 6 months were also exposed to a car simulator (53c); there was no difference in driving skills between those given lithium and those given placebo. In a recent study 16 manicdepressive patients in remission on prophylactic lithium, given for at least 3 months, were compared with 22 healthy controls (54c). The patients had a median reaction time of 0.72 seconds, significantly longer than that of the controls, 0.58 seconds. The authors suggested that patients should be warned that lithium may affect their ability to drive or operate machinery. Presumably most of the many thousands of manic-depressive patients taking lithium drive a car or operate machinery, but I have never heard of any car or machine accident in which lithium treatment was implicated. However, I make it a habit to give the following warning: 'It may be wise for patients starting lithium treatment to abstain from car driving until they have found out how much the treatment affects their driving ability' (55). A hypothesis that dementia might have been caused by long-term lithium treatment has not been supported by literature studies, which revealed other causes of the dementia (56c). An increase in depression scores in patients who had taken lithium for many years turned out to be the result of worsening disease rather than of the treatment, because the same changes were seen in patients who had stopped taking lithium (57c).
Thyroid and parathyroid Lithium treatment may cause the formation of thyroid antibodies in susceptible individuals (58 c, 59c). In a recent review (60 R) the similarities between the actions of lithium and the cardiac drug, amiodarone, on the thyroid have been discussed. With both drugs the nature of the thyroid abnormality (hypothyroidism or hyperthyroidism) is influenced by the patient's iodine status and by the presence of pre-existing, often subclinical, thyroid pathology. Lithium-induced goiter is significantly correlated with treatment duration and with smoking (61 c). Reports continue to appear about the
Lithium Chapter3 frequencies of lithium-induced goiter and hypothyroidism (62c, 63c), but they convey little useful information when control frequencies are lacking, either from control subjects or from the patients themselves before lithium treatment started. Three cases of thyroid carcinoma have appeared in a surgical department's account of 'lithiumogenic' disorders of the thyroid and parathyroid glands (64c). Although hyperparathyroidism usually disappears when lithium treatment is discontinued, continuation of treatment may be necessary for the patient's mental health, and surgical intervention may be indicated (65 C - 67c).
Liver
Lithium generally neither causes nor aggravates liver disease (68R), but in a patient with pre-existing Gilbert's disease (partial deficiency of bilirubin glucuronyl transferase) lithium treatment was associated with a temporary increase in his indirect bilirubin concentration without concomitant changes in his other liver function tests (69r
Urinary system
The effects of lithium on kidney function have been the subject of recent reviews (SEDA-14, 18; 70R, 71R). On the basis o f studies both longitudinal (over 1000 patients) and cross-sectional (over 3000 patients) it was concluded that although lithium treatment may reduce renal concentrating ability and cause polyuria, it does not, even when given for many years, lead to changes in glomerular filtration rate, let alone renal failure. At the time those reviews were written not a single case of renal failure had occurred which could be ascribed with reasonable certainty to lithium. Since then 1 case of uremia during lithium treatment has been reported (72c). In a 71year-old woman the serum creatinine concentration started to rise gradually after 10 years of lithium treatment and over another 10 years of treatment rose to 571 /zmol/1; her chromium EDTA clearance had at that time fallen to 15 ml/min per 1.73 m 2 body surface, and she was started on hemodialysis. The patient had not suffered from lithium intoxication and no signs of independent kidney disease could be found. This may be the first established case of uremia caused by long-term lithium treatment with non-toxic doses. However, failure to find
15 other causes of the uremia does not prove their absence. At any rate, the publication of a single case does not alter the main conclusion of the large systematic studies of long-term lithium treatment, namely that the risk of lithiuminduced impairment of glomerular function is extremely small. This is supported by a prospective follow-up study carried out on 46 patients after an average time of 20 years on lithium (73c). There was a significant fall in glomerular filtration rate, but it was related to increasing age. Two patients developed renal insufficiency but after withdrawal of lithium. Arguments continue to be presented for administering lithium in one rather than in 2 or 3 daily doses, a procedure which may lead to less polyuria (74 C, 75c). However, the hypothesis has been tested in only one study with random allocation of treatment regimens, and that study did not support it (76c). A peculiar side effect was seen in a pregnant woman who developed polyhydramnios as a result of fetal polyuria (77c).
Skin and appendages Alopecia related to lithium treatment has been reviewed (78R). A case of Darier's disease, well controlled with etretinate, worsened markedly on two separate occasions after lithium ingestion and improved after its discontinuation (79c). In another patient keratodermia appeared twice after institution of lithium therapy and resolved both times after discontinuation (80c). After 10 years of lithium treatment a patient developed erythema multiforme, which disappeared after discontinuation of lithium and reappeared on readministration (81c). Second-generation effects Problems relating to lithium treatment during pregnancy, delivery, and lactation have recently been reviewed (82R). From a strictly scientific point of view, the numbers involved are too small to provide definitive proof of a teratogenic action of lithium. Teratogenesis, with a risk of perhaps 5 - 10o70, nevertheless does seem a possibility, which it appears imprudent to disregard. The counsel given at present is the following (82R): as a general rule, women of fertile age should use contraception while on lithium, treatment should be stopped before a planned pregnancy, and it should be stopped as soon as an unplan-
16 ned pregnancy is discovered; on the other hand, it is important that the individual patient's situation is considered, and lithium treatment may have to be continued uninterrupted throughout pregnancy in women who know from past experience that they are apt to develop severe mania or depression soon after having stopped lithium. It should be remembered that prophylactic alternatives to lithium, such as carbamazepine and valproate, may also have teratogenic effects (83 c, 84c). A baby born to a mother taking lithium had hypothyroidism (in addition to an atrial septal defect) (85c). An 18-year-old patient with Ebstein "s anomaly was found to have been exposed to lithium in utero (86c).
Intoxication Neurotoxic effects of lithium, mostly resulting from lithium intoxication, have been reviewed (87 R - 89R). An irreversible cerebellar syndrome developed in an alcoholic patient who started lithium immediately after having suffered a neuroleptic malignant syndrome with fever (90c). Occasionally neurological and mental sequelae after lithium intoxication can resolve after having lasted as long as 3 - 4 months (91 r 92c). Other instances of lithium intoxication have occurred, precipitated by such circumstances as large neuroleptic dosages (93c), operation with anesthesia (94c), pulmonary infection with fever (95c), co-administration of digoxin (96 c) or of the loop diuretic, bumetanide (97c), and insufficient fluid intake by a mentally retarded patient during lithium-induced polyuria (98r Fatal intoxication developed on the fifth day of a religious fast, during which the patient consumed only a glass of milk and a teacup o f porridge daily but continued to take lithium in unaltered dosage (99c). Gradually developing lithium intoxication may be characterized by T-wave abnormalities and is more dangerous than acute lithium intoxication (100c). Occasionally lithium intoxication can present as worsening mental state (101c), and intoxication masquerading as a manic episode has been seen (102c). Hemodialysis, repeated when the serum lithium concentration rebounds, remains the preferred treatment (103 c, 104c); continuous arteriovenous hemofiltration can also be used (105c).
Chapter 3
M. Schou
Whole-bowel irrigation (106 c) and gastric lavage (107 c) have been suggested as treatments for acute ingestion of overdoses of sustained-release lithium tablets.
Interactions A n acute extrapyramidal reaction followed the concurrent administration of lithium and sulpiride (108c). The interaction with neuroleptics in general has been the subject of two reviews (109 R, 110 R) and a special symposium (111R-II7R). Permanent brain damage is not a characteristic feature of lithium-neuroleptic interaction, which seems to occur only when drug dosages are high. With the use of moderate dosages there seems to be no reason to abandon a combination which is useful in the treatment of acute mania and in the maintenance therapy of schizoaffective illness. It has been suggested that hyperthermia is involved in determining the extent of brain damage which may be caused by the combination of lithium and neuroleptics (118C). Adverse interactions with benzodiazepines remain rare and doubtful (119 c, 120c), Interactions of lithium with antidepressants are infrequent and mild, but fluoxetine and fluvoxamine may be exceptions (see the'Special Review' above). A 71-year-old patient developed malignant hyperthermia 1 month after lithium was added to amitriptyline (121c); it resolved within 10 days during treatment with dantrolene and hypothalamic phospholipid liposomes. The combination of lithium and doxepin led to a condition resembling neuroleptic malignant syndrome with fever (122c). Interactions of lithium with non-steroidal anti-inflammatory agents have been reported (123c), reviewed (124R), and debated (125, 126). Indomethacin seems to increase serum lithium concentrations most, while sulindac and aspirin do not do so to a clinically significant degree. If one follows a recommendation to treat lithium-induced nephrogenic diabetes insipidus with a combination of indomethacin and the vasopressin analog DDAVP (127c), one should therefore pay particular heed to the warning that 'indomethacin must be used with care because it may impair renal function'. Only two reports have appeared this year about interactions of lithium with diuretics (97 c, 128c). Perhaps warnings are working.
Lithium
Chapter3
Studies on human volunteers suggest that furosemide may be safer than thiazides if diuretic treatment is indicated during lithium treatment (129, 130). The much-debated question of an interaction of lithium with electroconvulsive therapy (ECT) has again been reviewed (131R); the authors advise that lithium should be discontinued ahead of time in patients referred for E C T . In emergencies, when this cannot be accomplished, close observation is called for. Lithium in relation to anesthesia has been dealt with in a broader review (132R). A patient on long-term lithium developed an acute psychosis when the calcium antagonist diltiazem was added for the treatment o f hypertension (133 c). The author s suggested an interaction between the two drugs, but could not exclude an effect of diltiazem alone. C o m bined treatment with lithium and another calcium antagonist, verapamil, led to dysarthria and ataxia, which was relieved on substitution of nifedipine for verapamil; upon
17 reinstitution o f verapamil the patient once again displayed neurotoxicity (134r A study o f 9 healthy volunteers suggested that alcohol may accelerate the excretion o f lithium in w o m e n (135). Absorption o f lithium from the gastrointestinal tract may be inhibited by psyllium (136c). Miscellaneous A 36-year-old w o m a n took lithium for 20 days and developed polyarthritis with swelling, pain and stiffness o f joints, associated with erythema, tenderness and limitation o f movements; there was no fever (137c). The same authors had seen 4 patients who had reported significant worsening o f rheumatoid arthritis during lithium treatment. A b o u t one-fifth of patients on lithium had increased serum amylase values (138); none of them had clinical signs or symptoms of parotid gland or pancreatic ailments. Obstructive sleep apnea may be secondary to marked weight gain, which again may be secondary to lithium treatment (139c).
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Concours M~d., 15, 1363. 10. Pulik M, Lida H (1988) Interaction lithium-inhibiteurs de l'enzyme de conversion. Presse Mdd., 17, 755. 11. Rimmer JM, Santella RN (1988) Combination angiotensin converting enzyme inhibitor/lithium therapy contraindicated in renal disease. Am. J. Med., 85, 894. 12. Santella RN, Rimmer JM, MacPherson BR (1988) Focal segmental glomerulosclerosis in patients receiving lithium carbonate. Am. J. Med., 84, 951 - 954. 13. Baldwin CM, Safferman AZ (1990) A case of lisinopril-induced lithium toxicity. Drug Intell. Clin. Pharm. Ann. Pharmacother., 24, 946- 947. 14. Zagermann P (1990) Lisinopril: ein neuer ACEHemmer. Pharm. Zng., 135, 21 - 22. 15. Griffin JS, Hahn SM (1991) Lisinopril-induced lithium toxicity. Drug lntell. Clin. Pharm. Ann. Pharmacother., 25, 101. 16. Amadio P (1990) ACE inhibitors and lithium Postgrad. Med., 87, 31. 17. Delgado PL, Price LH, Charney DS, Heninger GR (1988) Efficacy of fluvoxamine in treatmentrefractory depression. J. Affect. Disord., 15, 55 - 60. 18. Pope HG, McElroy SL, Nixon RA (1988) Possible synergism between fluoxetine and lithium in refractory depression. Am. J. Psychiatry, 145,
Chapter 3
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19
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Chapter 3
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Lithium
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21
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