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. 2023 May 5;11:79–86. doi: 10.5414/CNCS110994

Table 1. Ten case series of primary Sjögren’s syndrome with renal tubular acidosis and central pontine myelinolysis.

Bruns et al. [23] Abdulla et al. [24] Maturu et al. [8] Nagashima et al. [25] Saxena et al. [26] KH Yoon et al. [10] Watson et al. [27] Rubo, S et al. [9] Index Case
Germany India India Japan India Singapore London China South Africa
Age 17 28 33 42 45 47 64 75 42
Sex Female Female Female Female Female Female Female Female Female
Sicca symptoms No Yes - Yes Yes No Yes Yes Yes
Diagnosis type I RTA On index CPM admission Occurred prior to CPM diagnosis Occurred 1 year after CPM diagnosis On index CPM admission On index CPM admission Occurred prior to CPM diagnosis On index CPM admission On index CPM admission On index CPM admission
On presentation Muscular weakness with leg pain. Later developed bilateral 6th nerve palsies, dysarthria and dizziness;

Additional Hashimoto thyroiditis, vitiligo, celiac disease
Jaundice, hepatic encephalopathy, generalized tonic clonic seizures;

Additional hepatitis A infection
Sudden onset, rapidly progressive quadriplegia, severe dysarthria, bilateral facial palsies, bulbar palsy Periodic weakness from hypokalemia for 9 years prior to index presentation Progressive weakness of all 4 limbs, difficulty with respiration and swallowing, dysarthria and altered sensorium Obtunded with quadriplegia; previous history of hypokalemic weakness and small vessel vasculitis of the bowel 3-month history of fatigue, nausea and vomiting, hypercalcemia; later developed bilateral 6th nerve palsies with generalized weakness Rapid, progressive quadriplegia, hypersomnia, dysphagia Progressive global quadriplegia, ophthalmoplegia, and encephalopathy
Admission serum sodium 137 mmol/L Hypernatremia; no history of hyponatremia with rapid sodium correction Hypernatremia Hypernatremia
(154 mmol/L)
Reported normal 140 mmol/L
Admission serum potassium 1.8 mmol/L 2.6 mmol/L 2.2 mEq/L Low 1.9 meq/L Low 2.0 mmol/L 1.4 mmol/L 1.6 mmol/L
ANA Positive Positive Positive Positive Positive Positive Positive
Anti SSA +/Anti SSB + Anti SSA +/anti SSB + Anti SSA +/anti SSB + Anti SSA +/anti SSB + Anti SSA +/anti SSB - Anti SSA +/anti SSB - Anti SSA +/anti SSB– Anti SSA +/anti SSB– Anti SSA +/anti SSB + Anti SSA +/anti SSB +
Serum IgG and IgA Elevated Elevated
Salivary gland biopsy Yes Yes No
Treatment Electrolyte and acid-base balance correction, steroids Electrolyte and acid-base balance correction Electrolyte and acid-base balance correction, steroids Electrolyte and acid-base balance correction, steroids, CYC Steroids, CYC, and IVIG;

After relapse required PE and IVIG
Electrolyte and acid-base balance correction, hydroxychloroquine Electrolyte and acid-base balance correction, steroids, CYC Electrolyte and acid-base balance correction, steroids, CYC
Short-term neurological outcome Response seen within 2 weeks:
by 4 weeks the muscle weakness had resolved
Neurology improved within 1 month Within a week, motor power recovered Within 2/52 recovery to walking Complicated course post-treatment – neutropenic sepsis, PE;

Able to ambulate independently at 1 month
Good neurological recovery Over several days: LOC and cranial muscle strength improved;
within 2 weeks, neurology significantly improved
Improved neurology within days
Long-term neurological outcome Occasional dizziness, 6th nerve palsies persistent Complete neurological recovery Asymptomatic at 6 months Residual right lateral rectus palsy Recurrent relapsing disease Persistent diplopia Mild residual truncal ataxia Complete neurological recovery

CPM = central pontine myelinolysis; Anti-SSA = anti-Sjogren’s syndrome-related antigen A autoantibodies; Anti SSB = anti-Sjogren’s syndrome-related antigen B autoantibodies; CYC = cyclophosphamide; IVIG = intravenous immunoglobulin; PE = plasma exchange; LOC = level of consciousness.