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Background <p>Endocrine disturbances after organophosphate exposure are rarely emphasized in routine psychiatric care. In older inpatients, severe hyponatremia is often attributed to antidepressant-induced SIADH, which may delay recognition of relative hypocortisolemia. We report a hypothesis-generating case supporting a multifactorial ‘second-hit’ model.</p> Case presentation <p>A 67-year-old woman with long-standing major depressive disorder attempted suicide after an argument with family members by ingesting a suspected dimethoate emulsion (half a bottle found at the scene), approximately 20 estazolam tablets, and a small amount of detergent. She was transferred to a psychiatric ward for presumed depressive exacerbation. On day 1, serum sodium was 141.0 mmol/L (reference 137.0-147.0) but 8 AM cortisol was low at 112.4 nmol/L (reference 166-507). Influenza B was confirmed on day 2. After venlafaxine XR was initiated (75 mg/day) and up-titrated to 150 mg/day on day 4 because of apparent non-response, sodium progressively declined to 125.0 mmol/L on day 7, continued to fall to 120.2 mmol/L on day 8 and reached a nadir of 119.4 mmol/L on day 9, and remained low on day 10 (123.9 mmol/L) despite supplementation and fluid restriction. Repeat 8 AM cortisol was 122.0 nmol/L with an inappropriately normal ACTH of 24.4 pg/mL (reference 7.2-63.3) given systemic inflammation. Brain CT, adrenal ultrasound, and thyroid function were unremarkable. Urine sodium/osmolality and plasma osmolality were not measured. Oral prednisone acetate 5 mg twice daily was started on day 11 while venlafaxine was continued. Sodium rose to 130.0 mmol/L on day 12 and normalized by day 16 (141.0 mmol/L), accompanied by rapid improvement in appetite, spontaneous speech, and psychomotor activity.</p> Conclusions <p>Causality cannot be definitively established. However, this case highlights that medically stressed psychiatric inpatients may develop refractory hyponatremia from interacting factors (infection, SNRI up-titration, and relative HPA-axis insufficiency). Early-morning cortisol assessment should be considered when hyponatremia co-occurs with apparent antidepressant non-response, particularly in older, low-BMI patients.</p>

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Refractory hyponatremia mimicking worsening depression after suspected dimethoate exposure, influenza B infection, and venlafaxine up-titration: a case report

  • 期刊论文

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  • 发表日期：

    2026年3月28日

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  • Conghao Sun,
  • Guilan Sun,
  • Ke Chen,
  • Zheli Chen,
  • Zhixing Shen,
  • Yu Fang

摘要

Background

Endocrine disturbances after organophosphate exposure are rarely emphasized in routine psychiatric care. In older inpatients, severe hyponatremia is often attributed to antidepressant-induced SIADH, which may delay recognition of relative hypocortisolemia. We report a hypothesis-generating case supporting a multifactorial ‘second-hit’ model.

Case presentation

A 67-year-old woman with long-standing major depressive disorder attempted suicide after an argument with family members by ingesting a suspected dimethoate emulsion (half a bottle found at the scene), approximately 20 estazolam tablets, and a small amount of detergent. She was transferred to a psychiatric ward for presumed depressive exacerbation. On day 1, serum sodium was 141.0 mmol/L (reference 137.0-147.0) but 8 AM cortisol was low at 112.4 nmol/L (reference 166-507). Influenza B was confirmed on day 2. After venlafaxine XR was initiated (75 mg/day) and up-titrated to 150 mg/day on day 4 because of apparent non-response, sodium progressively declined to 125.0 mmol/L on day 7, continued to fall to 120.2 mmol/L on day 8 and reached a nadir of 119.4 mmol/L on day 9, and remained low on day 10 (123.9 mmol/L) despite supplementation and fluid restriction. Repeat 8 AM cortisol was 122.0 nmol/L with an inappropriately normal ACTH of 24.4 pg/mL (reference 7.2-63.3) given systemic inflammation. Brain CT, adrenal ultrasound, and thyroid function were unremarkable. Urine sodium/osmolality and plasma osmolality were not measured. Oral prednisone acetate 5 mg twice daily was started on day 11 while venlafaxine was continued. Sodium rose to 130.0 mmol/L on day 12 and normalized by day 16 (141.0 mmol/L), accompanied by rapid improvement in appetite, spontaneous speech, and psychomotor activity.

Conclusions

Causality cannot be definitively established. However, this case highlights that medically stressed psychiatric inpatients may develop refractory hyponatremia from interacting factors (infection, SNRI up-titration, and relative HPA-axis insufficiency). Early-morning cortisol assessment should be considered when hyponatremia co-occurs with apparent antidepressant non-response, particularly in older, low-BMI patients.