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PubMed1979

Chronic interstitial nephropathy in patients on long-term lithium treatment.

One-hundred and ten patients treated with lithium for more than six months were studied in order to determine the prevalence of lithium induced nephropathy. Eighteen of 69 patients (26 per cent) who had been treated for more than two years presented a chronic interstitial nephropathy characterized by a marked decrease in renal concentrating ability with a disproportionate preservation of glomerular filtration rate. Histologically, increased amounts of fibrotic tissue in the medulla and the cortex were found together with tubular atrophy. In 40 per cent of the patients who underwent renal biopsy, cystic formations in the cortex were found. The impairment of renal concentrating ability could be related to the duration of lithium treatment and the degree of tubular damage correlated with the degree of impairment of renal concentrating ability. Lithium induced, chronic nephropathy is a rather common complication of long-term lithium treatment and reduces the patients capacity to regulate water and electrolyte metabolism. As water and electrolyte loss appears to precede the slowly progressing lithium intoxication, the main hazard of lithium induced nephropathy is lithium intoxication.

Adult↗
PubMed1981

Action of lithium on the adrenergic nerve ending.

The effect of lithium on adrenergic neurotransmission was investigated using the lateral saphenous vein of the dog as a model of the neuroeffector process. Helically cut vein strips were mounted in either an organ bath where tension was recorded or in a superfusion system where both tension and the overflow of [3H]norepinephrine and its metabolites were determined. Lithium was used at both therapeutic (0.5-1.5 mEq/l) and toxic (2.5-14.4 mEq/l) concentrations. Lithium had no effect on basal tension or overflow [3H]norepinephrine. At therapeutic concentrations, the neuronal amine uptake mechanism was augmented, whereas at toxic concentrations monoamine oxidase was inhibited. In therapeutic concentrations, lithium attenuated the response of the adrenergic nerve ending to electrical stimulation (0.5-10 Hz). This response was due in part to the augmentation of the neuronal amine uptake mechanism. At toxic concentrations, responses to low frequency (0.2-1.0 Hz) electrical stimulation were augmented, whereas those at higher frequencies (5-10 Hz) were attenuated. Inhibition of monoamine oxidase by lithium accounted for only a part of the augmented overflow of transmitter and subsequent contractile response since inhibition of monoamine oxidase did not prevent the augmentation by lithium of [3H]norepinephrine overflow. The mechanism by which lithium in both therapeutic and toxic concentrations reduces transmitter overflow and subsequently contractile responses remains to be elucidated. Thus, lithium alters the disposition and release of norepinephrine and, as a result, affects adrenergic neurotransmission.

Animals↗
PubMed1981

Lithium inhibits adenylate cyclase of human platelets.

The ADP-induced aggregation of human platelets is markedly increased after preincubation with lithium chloride, whereas lithium has the opposite effect on rabbit platelets. Since this phenomenon might be related to cAMP metabolism, the influence of lithium on total cAMP content and adenylate cyclase activity was investigated. Lithium does not significantly change the total cAMP content of human platelets neither during incubation nor during ADP-induced aggregation. Basal adenylate cyclase activity, however, was slightly inhibited by lithium in human platelets. The inhibition of adenylate cyclase by ADP appeared to be enhanced by lithium. Prostacyclin induced stimulation of adenylate cyclase is counteracted by this ion. In rabbit platelets the prostacyclin stimulated adenylate cyclase activity is not affected by lithium. These data suggest that a correlation exists between the influence of lithium on the aggregation of human and rabbit platelets and the sensitivity of their adenylate cyclase for this ion.

Adenylyl Cyclase Inhibitors↗
PubMed1981

[Pharmacokinetics and toxicology of lithium].

The pharmacokinetics of lithium is reviewed in regard to the pattern of lithium concentration in plasma, red blood cells, saliva and urine and to a four-compartmental model of lithium distribution. An overview of lithium toxicology is given summarizing the gastrointestinal, cardiovascular, endocrine, hematological, dermatologic, teratogenic and neurological side effects of lithium. The results of two controlled studies are described in detail. The investigation of thyroid function in 88 patients under lithium treatment revealed abnormally high values of TSH and/or of TSH response to TRH in 50% of the subjects. By use of daily protocols of eating and drinking over a period of 14 days, a distinctly higher caloric intake (from solid food, not fluids) was found in 10 patients who gained weight during lithium therapy as compared to 10 lithium-treated patients without weight gain.

Animals↗
PubMed1982

Lithium does not prevent agonist-induced subsensitivity of human adenylate cyclase.

In a previous study 11 depressed patients were treated with salbutamol, a beta-2 adrenergic agonist, and beta-2 adrenergic receptor sensitivity was evaluated by measuring the plasma cyclic AMP rise after an iv dose of salbutamol. Salbutamol treatment induced subsensitivity of the beta-adrenergic adenylate cyclase with a time course paralleling the antidepressant effects. In the present study nine patients who were depressed despite treatment with lithium were treated with salbutamol plus lithium. Subsensitivity of the beta-adrenergic adenylate cyclase developed in the presence of lithium to the same degree as in patients treated with salbutamol alone. These results represent the first human study of the theory that lithium stabilizes receptor sensitivity changes. Lithium's failure to prevent subsensitivity agrees with reports that lithium fails to prevent impramine-induced subsensitivity of beta-adrenergic receptors in rat cortex. Lithium stabilization of receptor sensitivity of beta-adrenergic receptors in rat cortex. Lithium stabilization of receptor sensitivity would therefore appear to be unidirectional, preventing supersensitivity but not subsensitivity.

Adenylyl Cyclases↗
PubMed1984

Treatment of acute lithium toxicity.

Although accurate epidemiological data is not available, it is generally agreed that acute lithium toxicity is becoming a more frequent problem. Consequently recognition and treatment of lithium toxicity has also become more important. Acute lithium toxicity is generally subdivided into three grades: mild, moderate, and severe. Mild toxicity can often be managed successfully with minimal intervention; often only cessation or reduction of lithium doses is sufficient. Moderate and severe toxicity both require more aggressive approaches. Initial general anti-poisoning measures, such as gastric lavage, may be helpful, but the ultimate success of treatment depends upon the elimination of lithium from the body. Hemodialysis, and, to a lesser extent, peritoneal dialysis, will both rapidly eliminate lithium from the body. Sodium administration, and the maintenance of high-normal sodium levels, may also reduce the severity of lithium toxicity by removing the dangerous intracellular fraction of lithium from inside excitable cells.

Acute Disease↗
PubMed1982

Is lithium bad for the kidneys?

Lithium alters renal physiology (e.g. polyuria) and is nephrotoxic in severe intoxications. With proper precautions, lithium was otherwise presumed safe through the mid-1970's. In 1977, the controversial question arose whether lithium may induce a chronic renal disease documented by biopsy. Later, similar lesions were demonstrated in affective disturbance patients never exposed to lithium. The possible role of lithium as an inducer of kidney damage is undetermined; but concern for the kidney in lithium patients is expressed. Better pre-lithium patient selection and renal work-up, lower serum lithium levels, and closer clinical and laboratory follow-up are advised.

Biopsy↗
PubMed1981

Influence of lithium on proliferation of hematopoietic stem cells.

We studied the effect of lithium on normal marrow hematopoiesis by determining the numbers of pluripotential (CFUS) and committed stem cells (CFUC, CFUE and BFUE) after in vitro and in vivo exposure to lithium. In the presence of 1 meq/L lithium in vitro, marrow CFUS and CFUC were increased; higher concentrations (greater than or equal to 5 meq/L) were inhibitory. Marrow CFUE and BFUE were decreased at concentrations of lithium greater than or equal to 0.5 meq/L. In vivo (0.5-5.0 meq/L i.p.), lithium produced similar results to those obtained in vitro with striking CFUC enhancement. Serum from these lithium-treated mice contained increased colony stimulating factor (CSF). In the Dexter continuous marrow culture system, lithium stimulated increased CFUC production from the non-adherent fraction. These in vitro nd vivo studies document lithium's ability to modulate hematopoiesis by influencing pluripotential and committed stem cell proliferation and differentiation towards granulopoiesis, apparently at the expense of erythropoiesis. Mechanisms of this modulation are discussed.

Animals↗
PubMed1980

Aftereffects of lithium-conditioned stimuli on consummatory behavior in the presence or absence of the drug.

Drinking is increased by prior exposure to lithium-conditioned stimuli. Experiment 1 showed that this phenomenon is not an artifact of testing subjects with a novel, palatable drinking fluid and also showed that lithium-conditioned olfactory stimuli produce a biphasic change in drinking, with drinking suppressed at the start of exposure to the conditioned stimulus (CS) and enhanced a long time after CS onset or exposure. Experiment 2 showed that the increased drinking aftereffect of lithium-conditioned stimuli is not a result of the instrumental reinforcement of the drinking response by the scheduling of water access following drug injections during conditioning, and Experiments 3, 4, and 5 showed that the increased drinking effect occurs even if subjects are injected with lithium prior to the test session. The results of Experiments 3 and 5 alos showed that lithium administration and exposure to lithium-conditioned stimuli have independent and opposite aftereffects: Lithium disrupts drinking, whereas prior exposure to lithium-conditioned stimuli increases consumption. The relevance of conditioned opponent and compensatory processes to the findings is discussed.

Animals↗
PubMed1981

Effect of lithium on the myelosuppressive and chemotherapeutic activities of vinblastine.

Serum concentrations of lithium after i.p. administration to normal mice declined with biphasic kinetics. Treatment of mice bearing ascitic L1210 leukemia with lithium resulted in a modest protection against the myelosuppressive effects of vinblastine. Lithium as a single agent was without effect on the survival times of mice bearing either the L1210 or P388 leukemia. Similarly, there was no evidence of significant antiproliferative or cytotoxic activity when cultured L1210 leukemia and murine neuroblastoma cells were exposed to lithium at levels comparable to those observed in the serum of lithium-treated mice. The therapeutic activity of vinblastine against the L1210 and P388 leukemias was not significantly altered by either simultaneous or subsequent administration of lithium. Lithium did not antagonize the antiproliferative or cytotoxic action of vinblastine against L1210 leukemia or murine neuroblastoma cells and was without effect in experiments with neuroblastoma cells that assessed vinblastine inhibition of a biological function dependent on formation of cytoplasmic microtubules (neurite formation induced by serum deprivation). The results obtained suggest that administration of lithium to reduce myelosuppression is not likely to counteract the tumoricidal activity of vinblastine.

Animals↗
PubMed1995

A further prospective evaluation of an equation to predict daily lithium dose.

BACKGROUND: Recently, one prospective study confirmed the safety and accuracy of a lithium-dose prediction equation created by Zetin et al., but no definitive conclusion on the reliability of the equation has been established as yet. METHOD: The authors applied the Zetin et al. equation to 18 chronic male schizophrenic inpatients. Predicted doses to reach the serum lithium concentration of 0.4 mmol/L were calculated and prescribed in the form of lithium capsules. At Weeks 1 and 3 after treatment initiation, morning blood samples were collected about 12 hours after the last lithium dose for the measurement of serum lithium concentrations. RESULTS: None of the 18 patients achieved the desired concentration (0.4 mmol/L) exactly. The mean +/- SD of serum lithium concentrations at Week 1 was 1.01 +/- 0.29 mmol/L (range, 0.2-1.5) and at Week 3 was 0.94 +/- 0.35 mmol/L (range, 0.2-1.8). Lithium concentrations were lower than 0.4 mmol/L in only 1 patient and were higher than 0.4 mmol/L in the other 17 patients. The deviations from the unexpected value were significantly correlated with the renal function (blood urea nitrogen and serum creatinine levels) but not with the neuroleptic doses administered to the patients. Moreover, our patients were relatively older and weighed relatively less than the patients described in the previous prospective study. CONCLUSION: The Zetin et al. equation cannot always accurately predict a required lithium dose. Renal function data, even when they range within normal values, may be useful to improve the accuracy of the equation, particularly in patients who are older or weigh less than the norm.

Adult↗
PubMed1975

[Methodological experiences in the treatment supervision of lithium prophylaxis of manic-depressive illnesses].

During lithium treatment it was observed that a larger evening dose, due to the definite increase of lithium in the blood, leads to a slight drop of the blood level during the night; and that to maintain a therapeutically defined serum lithium level during the day a smaller dose of lithium is sufficient, particularly in more elderly patients. By plotting a 24-hour the profile best individual dosage can be arranged and a reduction in side-effects thereby achieved. This profile provides numerous advantages for the further strictly organized out-patient care for patients under lithium therapy. By filling out a proforma comparing the amount of serum lithium administered at each set time of the day with the appropriate daily profile, the point where lithium prophylaxis is indicated can be extended even to patients with a slight renal insufficiency, and above all to more elderly patients, for whom a therapeutic serum lithium level can be achieved with a very low dose of 4--4--8 mval/die. After a set period of supervision other fellow specialists can at first be drawn into the system of treatment, and later the general practitioner as well.

Adult↗
PubMed1993

Evaluation of lithium treatment in alcoholism.

In psychiatric practice, lithium prevents manic depressives recidivism. Lithium could also be useful in non-manic-depressive conditions with a reduction of aggression and impulsivity. From the observation that alcoholics often present mood swings and impulsivity, several authors studied the effects of maintenance doses of lithium on alcohol intake and the depressive symptoms of alcoholics. This article reviews all the published controlled and uncontrolled studies on the effects of lithium in chronic alcoholics. Wren, Kline and colleagues firs demonstrated that lithium treatment could significantly decrease the number of disabling alcoholic episodes and that its effect was independent of an effect on the depressive symptoms. These initial optimistic conclusions were not confirmed by later controlled studies involving a larger number of patients. Most of the recent studies failed to demonstrate a significant effect of lithium on the depressive symptoms of alcoholics. Thus, it is now established that lithium is not an effective treatment of affective disorders in alcoholics. The latest published studies also suggest that lithium treatment does not decrease alcohol intake or craving for alcohol in either depressed or non-depressed alcoholics.

Alcoholism↗
PubMed1977

On the mechanism of lithium-induced renal tubular acidosis.

The effect of lithium chloride administration on urinary acidification was studied in dogs. Lithium-treated dogs developed hyperchloremic metabolic acidosis with alkaline urine. Bicarbonate loading resulted in a normal increase in urinary Pco2 in normal dogs but failed to produce the same response in lithium-treated dogs. The bicarbonate titration curve of lithium-treated dogs revealed a small leak of bicarbonate at low plasma levels of bicarbonate; at high plasma levels bicarbonate reabsorption was significantly higher in lithium-treated dogs. This pattern of bicarbonate reabsorption is identical to that described in classic distal renal tubular acidosis. Sodium sulfate administration resulted in a normal urinary acidification ilithium-treated dogs. It is possible that lithium administration induces distal renal tubular acidosis by allowing excessive back-diffusion of acid. This excessive back-diffusion of acid would result in a low urinary Pco2 during bicarbonate loading. Sodium sulfate administration, by increasing the negative intratubular potential, would restrict back-diffusion of hydrogen ion and thereby result in a normal acidification in lithium-treated dogs. We previously demonstrated that postureteral obstruction of the kidney fails to increase urinary Pco2 during bicarbonate loading and to lower urinary pH with sodium sulfate. It is possible that a low urinary Pco2 during HCO3 loading can occur as a consequence of either diminished hydrogen ion secretion (postobstructed kidney) or excessive back-diffusion of acid (lithium administration). Further studies are indicated to determine whether both mechanisms may be found in patients with distal renal tubular acidosis.

Absorption↗
PubMedDate not supplied

[Mediation of the lithium increase in rat liver tryptophan pyrrolase activity by 11-hydroxycorticosteroids].

After a single intraperitoneal administration lithium carbonate (50 and 100 mg per kg of body weight) caused an increase in the tryptophane pyrrolase activity in rat liver tissue by 50-80% within 5 hrs and did not affect the enzyme within 1, 3 and 20 hrs. Content of lithium was quite unaltered in rat blood serum after administration of lithium carbonate at a dose of 50 mg/kg; it slightly exceeded the therapeutic level at a dose of 100 mg/kg. Addition of the lithium preparation (7-10(-3)-7-10(-5) M) to liver homogenates did not change the tryptophane pyrrolase activity in vitro. The same doses of lithium (50 and 100 mg/kg) caused a 2.5-fold increase in content of 11-hydrocorticosteroids in rat blood plasma; the effect was prevented by previous administration of dexamethasone. In experiments with adrenalectomized rats lithium did not affect the enzymatic activity. Repeated administration of lithium (50 mg/kg) within 10 days did not affect the tryptophane pyrrolase activity and did not alter the content of 11-hydroxycorticosteroids in rat blood plasma. The data obtained suggest that the increase in the tryptophane pyrrolase activity, caused by lithium, is mediated through the elevation in content of 11-hydroxycorticosteroids in blood.

11-Hydroxycorticosteroids↗
PubMed1996

Pharmacokinetic interactions and side effects resulting from concomitant administration of lithium and divalproex sodium.

BACKGROUND: Valproic acid is added to the lithium regimens of many patients with bipolar disorder, especially those with mania refractory to lithium treatment. METHOD: We evaluated the pharmacokinetic effects and safety of coadministration of lithium and valproate in 16 healthy volunteers in this randomized, placebo-controlled, two-period (12 days each) crossover trial. Valproate or placebo was given twice daily. On Days 6-10, lithium was added. Blood samples drawn on Days 5 and 10 were analyzed for valproate by high-pressure liquid chromatography (HPLC) and for lithium by atomic absorption spectrophotometry. RESULTS: Lithium pharmacokinetics were unchanged by valproate, but valproate C(max), C(min), and AUC rose slightly during lithium coadministration. Adverse events did not change significantly. CONCLUSION: Concomitant administration of lithium and valproate appears to be safe in patients with bipolar disorder.

Adult↗
PubMedDate not supplied

[Calcium antagonists and lithium in preventive treatment of manic-depressive disorder].

Recent advances in knowledge about calcium's role as an intracellular regulator allow to broaden understanding of possible pathophysiologic mechanisms in affective disorders. An hypothesis emerge that bipolar illness arise from disorders in calcium-regulated functions. Given this hypothesis, some authors propose to describe the common profiles of action of the different mood-stabilizers: all the neural mechanisms that are hypothesized to explain various psychopharmacological treatments of bipolar illness involve functions that are critically controlled by calcium. Moreover, in every instance, a known action of lithium on calcium-dependent processes could account for lithium's prophylactic results. Similarities exist between the action of lithium and calcium antagonists like verapamil and nimodipine. From these considerations the hypothesis emerge that calcium antagonists could be an alternative pharmacological agent in the maintenance treatment of bipolar illness. Calcium antagonists have been found useful in this indication by a number of investigators. Given the safety and relative lack of side effects of calcium channel blocking agents, their potential efficacy in mood disorders, it is concluded that calcium antagonists may be an alternative choice in prophylactic treatment for bipolar illness, especially in patients who cannot be treated with lithium or carbamazepine. There is evidence for using verapamil at 240 to 320 mg a day, in 2 to 4 times. Some studies suggest that the association of lithium with calcium antagonist resulted more effective than lithium alone or calcium antagonist alone in the reduction of episodes of affective disorders. However, concomitant administration of a calcium channel antagonist and lithium present adverse interactions (lithium toxicity, cardiovascular accidents), probably because of synergistic toxic effects. Therefore, authors advise care in monitoring patients receiving the combination of these medications.

Antimanic Agents↗
PubMedDate not supplied

Does acyclovir increase serum lithium levels?

A 42-year-old woman was admitted to the hospital to receive intravenous acyclovir for a herpes zoster infection. At the time she was taking lithium carbonate 450 mg twice/day. Six days after starting acyclovir she exhibited signs of lithium toxicity. When measured, the serum lithium level had increased 4-fold during acyclovir therapy. Both agents are excreted by the kidneys, raising the possibility that acyclovir at high serum concentrations may interfere with the renal excretion of lithium. A MEDLINE search did not identify any citation describing the possibility of an interaction between the drugs. This case suggests that acyclovir when given intravenously in doses of 10 mg/kg may result in increased serum lithium concentrations. Until additional data are available, if intravenous acyclovir is administered concurrently with lithium, we recommend closely monitoring patients for signs of lithium toxicity and measuring serum lithium levels every second or third day.

Acyclovir↗