COVID-19 infection in 50 patients receiving lithium

Objectives. The aim of the study was a naturalistic observation of the occurrence and course of COVID-19 infection in fifty patients treated with lithium from March 2020 to March 2021 and not receiving the vaccination against COVID-19 during this period. Materials and methods. The study group included 23 men and 27 women aged 23–71 (mean 45) receiving lithium for 1–45 (mean 7) years. Bipolar disorder (BD) was diagnosed in 46 patients, including BD type 1 in 19 patients and BD type 2 in 26 patients, and recurrent depression in one patient. The patients were treated with lithium to prevent manic and depressive recurrences, of which six underwent lithium monotherapy. Four patients with schizophrenia receiving clozapine were administered with lithium to treat and prevent neutropenia. Results. In the study group, 37 patients (74%), including five patients receiving lithium monotherapy, did not develop the infection. The infection was mild in 8 patients and moderately severe in two. Two patients developed lithium intoxication. One patient died of COVID-19 related pneumonia. Conclusions. The observations made on the study group show that COVID-19 infection occurred in one-fourth of lithium-treated patients. In the majority of the subjects, the infection was benign. The results also suggest that COVID-19 infection and related circumstances may be a risk factor for lithium intoxication.

Sinus bradycardia with haemodynamic compromise following lithium intoxication

Lithium is a well-established treatment for mood disorders and considered first-line pharmacological therapy for bipolar disorder as per the American Psychiatric Association guidelines. However, lithium is associated with significant toxicity. Cardiotoxicity including sinus node dysfunction is a rare but clinically significant presentation of lithium intoxication. This case report describes an adult male presenting with unstable sinus bradycardia in the setting of acute kidney injury and elevated serum lithium levels. The patient required temporary management with inotropic support and transcutaneous pacing. The patient’s heart rate and hypotension improved in parallel with resolution of his acute kidney injury and elevated serum lithium level after treatment with intravenous fluids. Given the prevalence of bradycardia in both the outpatient and inpatient settings, a high index of suspicion is necessary for the prevention and identification of this clinical entity to guide appropriate management.

Hemodiafiltration for Intoxication with Lithium Unmasking Its Anti-Parkinsonian Effect

From lithium it is known that it exhibits an anti-Parkinson effect [1]. Accordingly, smokers develop less frequently Parkinson’s Disease (PD) than the non-smoking population [2]. This is because tobacco contains a significant amount of lithium [3]. The anti-PD effect of lithium is explained by increased autophagy and reduction of intracellular a-synuclein [3]. Lithium inhibits GSK-3ß and consequently increases the ß-catenine activity [4]. Development of a Parkinson crisis due to flushing out of lithium by Hemodiafiltration (HDF), as in the following case, has not been reported. The patient is a 63 years male (height 180cm, weight 75kg) who was living with his mother in a retirement home and developed fever since 4 days prior to admission. His previous history was positive for psychosis, bipolar disorder, arterial hypertension, chronic renal failure, chronic obstructive pulmonary disease, diabetes, bilateral hydrocele, prostate hypertrophy, polyneuropathy, lithium intoxication, and hyperlipidemia. He had the diagnosis of a questionable extra-pyramidal syndrome but no anti-Parkinson medication. His home medication included aripiprazole (400 mg/ once every 30 d), biperiden (8 mg/d), midazolam (0.25 mg/d), lithium (900 mg/d), quetiapine (50 mg/d), trazodone (75 mg/d), nebivolol (2.5 mg/d), metformin (850 mg/d), simvastatin (20 mg/d), tamsulosin (0.4 mg/d), fenoterol with ipratropium-bromid, and tiotropium plus olodaterol. On admission (hospital day-1 (hd1)) he was comatose, had spontaneous resting tremor, and arterial hypotension (80/40 mmHg). Blood tests revealed hypokaliemia, hypernatriemia, and renal insufficiency (Table 1). The swab test for SARS-CoV2 was negative. ECG showed AV-block-I, right bundle-branch-block, and QT-prolongation (501 ms). X-ray of the lung was normal. Clinical neurologic exam on hd2 revealed somnolence, pain upon maximal passive anteflexion of head, nuchal rigor, ptosis, ophthalmoparesis, spontaneous myocloni all over the body, mild rigor of all extremities, reduced tendon reflexes on the lower limbs, and clonus of the left lower leg (Table 1). Cerebral CT-scan was non-informative. He was treated with fluid substitution, cefuroxim, levetirazetam (LEV) (1000 mg/d), and discontinuation of all psychiatric medication.