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Hyponatremia Associated with Prophylactic Low-Dose Trimethoprim during Systemic Corticosteroid Therapy for AQP4-Positive Optic Neuritis in a Diabetic Patient
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 impairmen...
Autores principales: | , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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MDPI
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7235834/ https://www.ncbi.nlm.nih.gov/pubmed/32340132 http://dx.doi.org/10.3390/antibiotics9040201 |
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author | Takubo, Masahiro Tanaka, Sho Kushimoto, Masaru Ikeda, Jin Ogawa, Katsuhiko Suzuki, Yutaka Abe, Masanori Ishihara, Hisamitsu Fujishiro, Midori |
author_facet | Takubo, Masahiro Tanaka, Sho Kushimoto, Masaru Ikeda, Jin Ogawa, Katsuhiko Suzuki, Yutaka Abe, Masanori Ishihara, Hisamitsu Fujishiro, Midori |
author_sort | Takubo, Masahiro |
collection | PubMed |
description | 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. |
format | Online Article Text |
id | pubmed-7235834 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-72358342020-05-22 Hyponatremia Associated with Prophylactic Low-Dose Trimethoprim during Systemic Corticosteroid Therapy for AQP4-Positive Optic Neuritis in a Diabetic Patient Takubo, Masahiro Tanaka, Sho Kushimoto, Masaru Ikeda, Jin Ogawa, Katsuhiko Suzuki, Yutaka Abe, Masanori Ishihara, Hisamitsu Fujishiro, Midori Antibiotics (Basel) Case Report 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. MDPI 2020-04-23 /pmc/articles/PMC7235834/ /pubmed/32340132 http://dx.doi.org/10.3390/antibiotics9040201 Text en © 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/). |
spellingShingle | Case Report Takubo, Masahiro Tanaka, Sho Kushimoto, Masaru Ikeda, Jin Ogawa, Katsuhiko Suzuki, Yutaka Abe, Masanori Ishihara, Hisamitsu Fujishiro, Midori Hyponatremia Associated with Prophylactic Low-Dose Trimethoprim during Systemic Corticosteroid Therapy for AQP4-Positive Optic Neuritis in a Diabetic Patient |
title | Hyponatremia Associated with Prophylactic Low-Dose Trimethoprim during Systemic Corticosteroid Therapy for AQP4-Positive Optic Neuritis in a Diabetic Patient |
title_full | Hyponatremia Associated with Prophylactic Low-Dose Trimethoprim during Systemic Corticosteroid Therapy for AQP4-Positive Optic Neuritis in a Diabetic Patient |
title_fullStr | Hyponatremia Associated with Prophylactic Low-Dose Trimethoprim during Systemic Corticosteroid Therapy for AQP4-Positive Optic Neuritis in a Diabetic Patient |
title_full_unstemmed | Hyponatremia Associated with Prophylactic Low-Dose Trimethoprim during Systemic Corticosteroid Therapy for AQP4-Positive Optic Neuritis in a Diabetic Patient |
title_short | Hyponatremia Associated with Prophylactic Low-Dose Trimethoprim during Systemic Corticosteroid Therapy for AQP4-Positive Optic Neuritis in a Diabetic Patient |
title_sort | hyponatremia associated with prophylactic low-dose trimethoprim during systemic corticosteroid therapy for aqp4-positive optic neuritis in a diabetic patient |
topic | Case Report |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7235834/ https://www.ncbi.nlm.nih.gov/pubmed/32340132 http://dx.doi.org/10.3390/antibiotics9040201 |
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