RESUMEN
BACKGROUND: Lithium is known to cause certain neurological deficits. However, reports of aphasia secondary to lithium toxicity are scant. We report the case of a 70 year old African American woman with a history of schizoaffective disorder and mild dementia who developed transient intermittent aphasia secondary to lithium toxicity. METHODS: Patient was admitted because of agitation, delusional behavior, and pressured speech. Her previous medications included divalproex sodium 500 mg po bid, valproic acid 250 mg po qd, risperidone 3.5 mg po bid, lorazepam 1 mg po bid, amlodipine besylate 5 mg po qd, levothyroxine sodium 25 mcg po qd, gabapentin 300 mg po qd, amantadine HCl 100 mg po bid, and aspirin 81 mg po qd. Since patient's symptoms have not improved, she was started on lithium 300mg po bid and titrated up to 300 mg po bid and 450 mg po qhs over 7-8 days. Her lithium levels ranged from 0.4 mEq/L on 11/11/16 to 1.5 mEq/L on 11/22/16. Patient was observed to have aphasia symptoms intermittently at lithium level of 1.5 mEq/L. CT scan of head and neurology consultations were unremarkable. The Naranjo Adverse Drug Reaction Probability Scale score was 8 in the probable range for an adverse drug reaction. Patient's sodium was also found to be high at 148 mmol/L. RESULTS: Lithium was discontinued and patient rehydrated with intravenous fluids. Patients aphasia resolved completely in 2-3 days. CONCLUSION: Clinicians should be aware of this rarely reported side effect of lithium particularly in patients at risk for volume depletion and closely monitor fluid intake, lithium level, and potential side effects.
Asunto(s)
Antimaníacos/efectos adversos , Afasia de Broca/inducido químicamente , Afasia de Broca/diagnóstico , Compuestos de Litio/efectos adversos , Anciano , Femenino , Humanos , Litio/efectos adversos , Trastornos Psicóticos/diagnóstico , Trastornos Psicóticos/tratamiento farmacológicoRESUMEN
In primary cell cultures of the avian (Gallus gallus) renal proximal tubule parathyroid hormone and cAMP activation generate a Cl(-)-dependent short circuit current (I(SC)) response, consistent with net transepithelial Cl(-) secretion. In this study we investigated the expression and physiological function of the Na-K-2Cl (NKCC) transporter and CFTR chloride channel, both associated with Cl(-) secretion in a variety of tissues, in these proximal tubule cells. Using both RT-PCR and immunoblotting approaches, we showed that NKCC and CFTR are expressed, both in proximal tubule primary cultures and in a proximal tubule fraction of non-cultured (native tissue) fragments. We also used electrophysiological methods to assess the functional contribution of NKCC and CFTR to forskolin-activated I(SC) responses in filter grown cultured monolayers. Bumetanide (10 µM), a specific blocker of NKCC, inhibited forskolin activated I(SC) by about 40%, suggesting that basolateral uptake of Cl(-) is partially mediated by NKCC transport. In monolayers permeabilized on the basolateral side with nystatin, forskolin activated an apical Cl(-) conductance, manifested as bidirectional diffusion currents in the presence of oppositely directed Cl(-) gradients. Under these conditions the apical conductance appeared to show some bias towards apical-to-basolateral Cl(-) current. Two selective CFTR blockers, CFTR Inhibitor 172 and GlyH-101 (both at 20 µM) inhibited the forskolin activated diffusion currents by 38-68%, with GlyH-101 having a greater effect. These data support the conclusion that avian renal proximal tubules utilize an apical CFTR Cl(-) channel to mediate cAMP-activated Cl(-) secretion.