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      Hyponatremia Associated with Prophylactic Low-Dose Trimethoprim during Systemic Corticosteroid Therapy for AQP4-Positive Optic Neuritis in a Diabetic Patient

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          Abstract

          Hyponatremia associated with low-dose trimethoprim in patients on concomitant systemic corticosteroid therapy has rarely been reported. Here, we describe a 57-year-old woman with a history of diabetes mellitus and hypertension treated with telmisartan, who presented with progressive visual impairment of the left eye due to anti-aquaporin-4 antibody-positive optic neuritis. The patient received pulsed intravenous methylprednisolone followed by oral prednisolone at 30 mg/day and trimethoprim–sulfamethoxazole prophylaxis (160 mg and 800 mg daily). Her serum sodium level steadily decreased, and the potassium level was slightly elevated despite well-preserved renal function. This state persisted even after telmisartan discontinuation. In addition to hypotonic hyponatremia (125 mEq/L) with natriuresis, hyperkalemic renal tubular acidosis was diagnosed based on normal anion gap metabolic acidosis and hyperkalemia with low urinary potassium excretion. After trimethoprim–sulfamethoxazole cessation, electrolytes and acid–base imbalances swiftly recovered. We can conclude that caution must be exercised when treating such patients, because even low-dose trimethoprim may cause hyponatremia concomitant with hyperkalemic renal tubular acidosis, despite the mineralocorticoid effects of systemic corticosteroids.

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          Most cited references21

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          Neuromyelitis optica brain lesions localized at sites of high aquaporin 4 expression.

          Neuromyelitis optica (NMO)-IgG is a specific autoantibody marker for NMO. It binds selectively to aquaporin 4 (AQP4), which is highly concentrated in astrocytic foot processes at the blood-brain barrier and is not restricted to optic nerve and spinal cord. Although it is conventionally believed that the brain is spared, brain imaging abnormalities are not uncommon in patients with NMO. To investigate the location of brain lesions that are distinctive for NMO with respect to the localization of AQP4 in mammalian brain. Observational, retrospective case series. Clinical serologic cohort of patients tested for NMO-IgG for whom brain MRI images were available. We identified 120 patients seropositive for NMO-IgG for whom brain magnetic resonance images were available. Magnetic resonance imaging abnormalities. In 8 patients we observed recurring and distinctive magnetic resonance imaging abnormalities in the hypothalamic and periventricular areas that corresponded to brain regions of high AQP4 expression. The distribution of NMO-characteristic brain lesions corresponds to sites of high AQP4 expression.
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            The molecular basis of water transport in the brain.

            Brain function is inextricably coupled to water homeostasis. The fact that most of the volume between neurons is occupied by glial cells, leaving only a narrow extracellular space, represents an important challenge, as even small extracellular volume changes will affect ion concentrations and therefore neuronal excitability. Further, the ionic transmembrane shifts that are required to maintain ion homeostasis during neuronal activity must be accompanied by water. It follows that the mechanisms for water transport across plasma membranes must have a central part in brain physiology. These mechanisms are also likely to be of pathophysiological importance in brain oedema, which represents a net accumulation of water in brain tissue. Recent studies have shed light on the molecular basis for brain water transport and have identified a class of specialized water channels in the brain that might be crucial to the physiological and pathophysiological handling of water.
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              A review of drug-induced hyponatremia.

              Hyponatremia (defined as a serum sodium level < 134 mmol/L) is the most common electrolyte abnormality in hospitalized patients. Certain drugs (eg, diuretics, antidepressants, and antiepileptics) have been implicated as established causes of either asymptomatic or symptomatic hyponatremia. However, hyponatremia occasionally may develop in the course of treatment with drugs used in everyday clinical practice (eg, newer antihypertensive agents, antibiotics, and proton pump inhibitors). Physicians may not always give proper attention in time to undesirable drug-induced hyponatremia. Effective clinical management can be handled through awareness of the adverse effect of certain pharmaceutical compounds on serum sodium levels. Here, we review clinical information about the incidence of hyponatremia associated with specific drug treatment and discuss the underlying pathophysiologic mechanisms.
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                Author and article information

                Journal
                Antibiotics (Basel)
                Antibiotics (Basel)
                antibiotics
                Antibiotics
                MDPI
                2079-6382
                23 April 2020
                April 2020
                : 9
                : 4
                : 201
                Affiliations
                [1 ]Division of Diabetes and Metabolic Diseases, Department of Internal Medicine, Nihon University School of Medicine, Tokyo 173-8610, Japan
                [2 ]Department of Internal Medicine, Nihon University Hospital, Tokyo 101-8309, Japan
                [3 ]Division of Nephrology, Hypertension and Endocrinology, Department of Internal Medicine, Nihon University School of Medicine, Tokyo 173-8610, Japan
                [4 ]Division of Neurology, Department of Medicine, Nihon University School of Medicine, Tokyo 173-8610, Japan
                Author notes
                [* ]Correspondence: tanaka.sho@ 123456nihon-u.ac.jp (S.T.); fujishiro.midori@ 123456nihon-u.ac.jp (M.F.); Tel.: +81-3-3972-8111 (S.T.); +81-3-3972-8111 (M.F.)
                Author information
                https://orcid.org/0000-0003-0091-7284
                https://orcid.org/0000-0002-9156-5415
                Article
                antibiotics-09-00201
                10.3390/antibiotics9040201
                7235834
                32340132
                33df702c-513d-449b-b684-00af1e6956f3
                © 2020 by the authors.

                Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license ( http://creativecommons.org/licenses/by/4.0/).

                History
                : 18 March 2020
                : 20 April 2020
                Categories
                Case Report

                acidosis,aquaporin 4,hyperkalemia,hyponatremia,steroids,trimethoprim

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