The syndrome of inappropriate antidiuresis after vaccination against COVID-19: case report

Background The Syndrome of Inappropriate Antidiuresis (SIADH) has been described to be associated with a multitude of conditions and medications, including the severe acute respiratory syndrome coronavirus 2. We describe the case of a patient with newly diagnosed and symptomatic SIADH after receiving the second COVID-19 vaccination not explained otherwise. Case presentation A 79-year-old male person was admitted to the emergency department due to a worsening of his general health state expressed by weakness, fatigue and anorexia. Vital signs and clinical findings were normal, in particular the patient was considered to be euvolemic. Laboratory investigations revealed a serum sodium of 117 mmol/L, a serum osmolality of 241 mosm/kg and a urea of 1.2 mmol/L with creatinine within normal range. Urine chemistry showed a urine osmolality of 412 mosm/kg and urine sodium of 110 mmol/L. TSH, C-reactive protein, and basal cortisol levels were normal. Under therapy with balanced crystalloid fluids, hyponatremia worsened and in absence of diuretic medications, diagnosis of SIADH was made. Since fluid restriction was not sufficiently effective, oral urea was administered. Under this therapy regimen hyponatremia resolved. Conclusions Local as well as systemic reactions have been described for the new mRNA-based vaccines including pain and fever. Therefore, it is imaginable that the vaccine might trigger SIADH in some patients.

Tolvaptan Use in SIAD (Syndrome of Inappropriate Antidiuresis)

Background: SIAD (Syndrome of Inappropriate Antidiuresis) is the commonest cause of hyponatraemia in hospital inpatients. Hyponatraemia is associated with increased length of stay and worse primary clinical outcomes. Our study aimed to evaluate the effectiveness of Tolvaptan, a selective, non-peptide, Vasopressin receptor antagonist, treatment in hospitalised patients with SIAD. Method and Baseline Characteristics: A Retrospective analysis of 9 patients treated with Tolvaptan for a confirmed diagnosis of SIAD was carried out. Information was collected from the inpatient records and biochemical test results. Serum Sodium levels on admission ranged between 104- 124mmol/ L (Normal range 136 -145 mmol/L). Average inpatient days solely due to hyponatraemia was 24 days. The number of in-patient days on fluid restriction ranged from 8-22 days depending on timing of referral to endocrine department. Tolvaptan was only started at a stable serum sodium at 118 mmol/L or greater. Four patients also had a prior trial of demeclocycline. Tolvaptan was started at its smallest dose of 7.5mg OD under strict monitoring of serum sodium with locally agreed protocol. Aetiology of SIAD included lung malignancy, acute demyelinating polyneuropathy, listeria meningitis, autoimmune encephalitis, SSRI (Selective Serotonin Reuptake inhibitor) use, Aspergillosis and Idiopathic (n=3). Results: Serum sodium level improved to >128 mmol/L in 2 days of starting Tolvaptan in all cases. After discharge, there was remote virtual clinic monitoring from the endocrinology team at 2 weeks, 4- 6 weeks and 3 months with a view to stop the medication. No adverse events were observed during use of Tolvaptan in the patient population. Tolvaptan 7.5mg OD was either stopped completely after 4-6 weeks or switched to 7.5mg alternate days depending on the clinical course of underlying pathology. Average duration of Tolvaptan treatment was 4.5 months excluding one patient with chronic lung pathology. 3 patients had further hospital admission on stopping Tolvaptan treatment and treatment with Tolvaptan had to be re-initiated. Conclusion: This study confirms the efficacy of Tolvaptan use in SIAD related hyponatremia. Tolvaptan serves as a cost effective treatment option for hospitalised patients who have either failed to respond to demeclocycline or fluid restriction. In our case cohorts, cost comparison of Low dose Tolvaptan with retrospective calculation of total inpatient days of fluid restriction and use of demeclocycline showed a better outcome and clinical effectiveness with low dose Tolvaptan. We recommend earlier use of Tolvaptan in SIAD under guidance from specialist team as a safe, cost effective and in some cases, as a hospital admission-avoidance strategy.

Syndrome of Inappropriate Antidiuresis Associated with Pancreatic Neuroendocrine Tumor: Case Report

BackgroundFunctional pancreatic neuroendocrine tumors (pNETs) rarely produce vasopressin. To the best of our knowledge, only one case of an ADH-producing pNET has been reported thus far. Here, we report a case of pNET producing vasopressin in a 78-year-old man with hyponatremia.Case presentationThe patient presented with anorexia 4 years ago, and the lowest serum sodium level was 121 mmol/L. Upon admission, serum osmolarity was 277 mOsm/kg·H2O, urine osmolarity was 465 mOsm/kg·H2O, urine sodium level was 82.5 mmol/L, and 24-hour urine sodium level was 140.25 mmol. There was no evidence of adrenal insufficiency or hypothyroidism. Syndrome of inappropriate antidiuresis (SIAD) was diagnosed on the basis of laboratory and clinical findings. The serum sodium level was maintained within the normal range after the oral administration of tolvaptan 7.5 mg. 68Ga-tetraazacyclododecanetetraacetic acid–DPhe1-Tyr3-octreotate positron emission tomography-computed tomography (68Ga-DOTATATE PET-CT) showed a high uptake lesion measuring approximately 1 cm in diameter in the pancreatic body, and the possibility of the pNET was considered. The patient underwent surgery, and the immunohistochemical study showed that the tumor cells were positive for somatostatin receptors 2 (SSTR2) and vasopressin. The patient was weaned from tolvaptan post-surgery, and low-dose corticosteroids were started due to signs of relative adrenal insufficiency, which was probably related to heart failure and surgery. Serum sodium level was maintained within the normal range.ConclusionsThis case illustrates the potential ectopic production of vasopressin resulting in SIAD in pNETs, highlighting the adoption of 68Ga-DOTATATE PET-CT and vasopressin immunohistochemical staining in the evaluation of the etiology of SIAD.