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Hypokalemic paralysis revealing Sjögren’s syndrome
€ Hypokalemic paralysis revealing Sjogren’s syndrome
319
Hypokalemic paralysis € gren’s syndrome revealing Sjo
and the sensory system and consciousness remain unaffected.1 We report a case of acute hypokalemic paralysis as a consequence of underlying renal tubular acidosis as the presenting feature of primary Sj€ ogren’s syndrome.
I. Taylor
CASE REPORT
MBBS,
Mark Parsons FRACP
Department of Neurology, Royal Melbourne Hospital, Parkville, Vic. 3050, Australia
Summary A rare case of a lady with acute hypokalemic quadriparesis and underlying distal renal tubular acidosis manifesting as a presentation of Sj€ ogren’s syndrome is described. The case highlights the concept that acute hypokalemia due to unrecognized renal tubular acidosis may unmask Sj€ogren’s syndrome in patients without sicca symptoms and it may be a marker of more severe renal disease. Acute paralysis is a life threatening consequence of hypokalemia and when due to potassium wasting secondary to renal tubular acidosis may be easily prevented. Underlying Sj€ogren’s syndrome should be considered in all patients of either sex and at any age presenting with hypokalemic paralysis. ª 2003 Published by Elsevier Ltd. Journal of Clinical Neuroscience (2004) 11(3), 319–321 0967-5868/$ - see front matter ª 2003 Published by Elsevier Ltd. doi:10.1016/j.jocn.2003.04.004
Received 22 January 2003 Accepted 2 April 2003 Correspondence to: Mark Parsons FRACP, Department of Neurology, John Hunter Hospital, Hunter Region Mail Centre, Locked Bag 1, New South Wales 2310, Australia. Tel.: +61-3-9342-7000; Fax: +61-3-9342-7272; E-mail: [email protected]
INTRODUCTION The acute hypokalemic periodic paralyses are a heterogeneous potentially life threatening group of disorders caused by either intracellular shifts of potassium (familial hypokalemic paralyses, thyrotoxic periodic paralysis and barium poisoning) or by serum potassium deficits (renal and gastrointestinal losses).1 They present with acute generalized muscle weakness and associated reduced deep tendon reflexes in the setting of hypokalemia. The facial, bulbar and respiratory muscles are less commonly involved
Fig. 1
A 55 year old female kitchen hand presented to the emergency department with rapidly progressive quadriparesis. She had a past history of hysterectomy for carcinoma in situ of the cervix. Medications at admission were hormonal replacement therapy and flucloxacillin 500 mg tablets – (she had taken two tablets on the day prior to admission for axillary folliculitis). Two days prior to admission she experienced cramps and aches of her proximal arms and quadriceps bilaterally. On the day prior to admission she had difficulty climbing stairs, rising from chairs and lifting her arms above her head. On the day of admission she awoke at 2 am and could not move her limbs and was unable to walk. She denied any sensory, sphincter, bulbar, visual, respiratory, or language disturbance. There was no history of recent gastrointestinal or respiratory upset. She denied diuretic, laxative or excessive licorice intake. She had not had any recent vaccinations. She had never experienced a similar event in the past nor was there any significant family history. Examination findings Clinically she was haemodynamically stable, afebrile, pulse 65 beats/min and regular, blood pressure 90/60 mm Hg, respiratory rate 16 breaths per minute, peak expiratory flow rate 250 L/min and forced vital capacity was 2.6 L. Cardiovascular, respiratory and gastrointestinal examinations were otherwise unremarkable. Thyroid examination was normal. The cranial nerve examination was unremarkable. Head flexion and extension were mildly weak (4/5). Examination of the limbs did not reveal any evidence of fasciculations and tone was normal. On examination of the upper limbs there was profound proximal and distal weakness with a flicker of movement only on shoulder abduction, wrist flexion and extension, finger flexion, extension, abduction and adduction. The findings were bilateral and symmetrical. Elbow flexion and extension were preserved with only mild weakness evident. Reflexes were all present and symmetrical yet depressed. Sensory examination was unremarkable. Lower limb examination revealed a flicker of movement on hip flexion, knee flexion and ankle dorsiflexion and antigravity power on hip extension abduction and
ECG at admission: diffuse ST and T wave changes, prolonged PR interval, increased p wave amplitude, prolonged QRS complexes and U waves.
ª 2003 Published by Elsevier Ltd.
Journal of Clinical Neuroscience (2004) 11(3)
320 Taylor and Parsons
Fig. 2 EMG and NCS at admission EMG/NCS: CMAP amplitudes all markedly reduced, distal latencies and conduction velocities are normal. Needle EMG reveals reduced recruitment.
Fig. 3
ECG 24 h later after K corrected: normal.
Journal of Clinical Neuroscience (2004) 11(3)
ª 2003 Published by Elsevier Ltd.
€ Hypokalemic paralysis revealing Sjogren’s syndrome
adduction, knee extension and ankle plantar flexion. Knee jerks were normal, ankle jerks were absent and the plantar response was flexor bilaterally. Sensory examination was unremarkable as was examination of the sphincters.
Investigation findings Blood biochemical examination revealed the following. Na 142 mmol/L, K 2.1 mmol/L, chloride 117 mmol/L, HCO3 12 mmol/L, creatinine 0.11 mmol/L, urea 7.5 mmol/L, glucose 6.9 mmol/L, calcium 2.08 mmol/L, phosphate 0.37 mmol/L, magnesium 1.10 mmol/L, albumin 37 g/L, pH 7.26 L, pCO2 24 L, base excess – 15.7 L, pO2 172, CK 626IU/L. Liver function tests, thyroid functions tests, serum complement, serum protein electrophoresis, C-reactive protein, full blood picture, 25-OH vitamin D3, and cerebrospinal fluid examination were all within normal range. Urine. pH at the time was 7, K 51 mmol/L, CL 185 mmol/L, Na 146 mmol/L. Electrocardiograph (ECG). Diffuse ST and T wave changes, prolonged PR interval, increased p wave amplitude, prolonged QRS complexes and U waves (Fig. 1). Nerve conduction studies (NCS) and electromyography (EMG). The compound muscle action potential (CMAP) amplitudes were markedly reduced, the distal latencies and conduction velocities were normal. The CMAP amplitude did not increase following exercise or repetitive stimulation. Needle EMG revealed reduced recruitment. The upper extremity sensory nerve action potential (SNAP) were reduced in amplitude with a normal sural SNAP (Fig. 2). Autoantibodies. Antinuclear antibodies (ANA) positive, speckled titre 160, speck/Nuclr titre >640, extractable nuclear antigen (ENA) positive, anti Sm negative, anti RNP negative, anti Ro positive, anti La positive, anti Topo1 negative, anti Jo1 negative, anti PM/SCL negative anti KU negative, anti double stranded DNA (dsDNA) 1.6 IU/mL, anti-neutrophil cytoplasmic antibody (ANCA) pANCA and cANCA negative.
Progress Within 4 h despite replacing potassium at a rate or 10–15 mmol/h the serum potassium level fell to 1.7 mmol/L, pH fell to 6.96 and serum chloride and bicarbonate increased to 123 and 15 mmol/L, respectively. Our patient was admitted to a high dependency unit for intensive monitoring and ongoing potassium replacement. Within 24 h her potassium level normalized, limb power returned to normal, there was recovery of all reflexes and complete normalization of her ECG (Fig. 3). On the basis of positive immune markers she was diagnosed with Sj€ogren’s syndrome with underlying renal tubular acidosis presenting as acute hypokalemic paralysis. On further questioning she did not describe sicca symptoms, arthralgias or rash. She was then transferred under the care of the renal physicians for ongoing management and has been placed on long term potassium citrate replacement therapy.
DISCUSSION Sj€ogren’s syndrome is an autoimmune disease of the exocrine glands characterized by xerostomia and xerophthalmia, with possible involvement of other organs. It occurs at a mean age of 40 years and affects 0.2% of the adult population with a female predominance. The diagnosis is made by a number of criteria including subjective and objective symptoms, objective involvement of organs by lymphocytes (biopsy) and laboratory abnorª 2003 Published by Elsevier Ltd.
321
malities.2 Renal tubular acidosis is associated specifically with primary Sj€ ogren’s syndrome and occurs in 33%.3 It results in renal potassium wasting and disordered renal acidification with consequent serum hypokalemic hyperchloremic metabolic acidosis. Hypokalemic paralysis as a consequence of renal tubular acidosis is considered a marker for more severe renal disease in patients with primary Sj€ ogren’s syndrome.3;4 Hypokalemic paralysis is a rare and potentially life threatening presentation of Sj€ ogren’s syndrome.4–9 Both hypokalemic quad4–9 riplegia and respiratory arrest8;10 have been reported. Hypokalemic paralyses associated with Sj€ ogren’s syndrome have not only been recognized in middle aged women but also reported in an elderly male11 and a child6 hence the diagnosis should be considered at all ages and in both sexes. Hypokalemic paralysis in the setting of Sj€ ogren’s may precede the sicca symptoms4 therefore the Schirmer test may be negative.9 The diagnosis of imminent Sj€ ogren’s may be made on the basis of positive immune markers (positive ANA and ENA: anti Ro and anti La). Although these markers are not entirely specific for Sj€ ogren’s syndrome, in the absence of anti dsDNA antibody, anti cardiolipin antibody, ANCA and with a normal compliment they make the diagnosis of other systemic autoimmune diseases unlikely. In our patient presenting with hypokalemia it was straightforward to diagnose distal renal tubular acidosis on the basis of associated hyperchloremic metabolic acidosis (non anion gap acidosis) with concurrent abnormally acidified urine. Autoimmune tests revealed underlying Sj€ ogren’s syndrome. As our patient did not have sicca symptoms a Schirmer test and lip biopsy were not performed. She recovered rapidly with potassium replacement which is subsequently being continued long term. Her progress will be monitored by the renal and rheumatology units. Acute quadriparesis is a life threatening consequence of hypokalemia and may unveil underlying Sj€ ogren’s syndrome. When due to potassium wasting secondary to renal tubular acidosis it may be easily prevented. Underlying Sj€ ogren’s syndrome in spite of a lack of sicca symptoms should be considered in all patients of both sexes presenting with acute hypokalemic paralysis.
REFERENCES 1. Stedwell RE, Allen KM, Binder LS. Hypokalemic paralyses: a review of the etiologies, pathophysiology, presentation, and therapy. Am J Emerg Med 1992; 10(2): 143–148. 2. Vitali C, Bombardieri S, Moutsopoulos HM et al. Preliminary criteria for the classification of Sjogren’s syndrome. Results of a prospective concerted action supported by the European Community. Arthritis Rheum 1993; 36(3): 340–347. 3. Siamopoulos KC, Elisaf M, Drosos AA, Mavridis AA, Moutsopoulos HM. Renal tubular acidosis in primary Sj€ogren’s syndrome. Clin Rheumatol 1992; 11(2): 226–230. 4. Dowd JE, Lipsky PE. Sj€ogren’s syndrome presenting as hypokalemic periodic paralysis. Arthritis Rheum 1993; 36(12): 1735–1738. 5. Raskin RJ, Tesar JT, Lawless OJ. Hypokalemic periodic paralysis in Sj€ogren’s syndrome. Arch Intern Med 1981; 141(12): 1671–1673. 6. Chang YC, Huang CC, Chiou YY, Yu CY. Renal tubular acidosis complicated with hypokalemic periodic paralysis. Pediatr Neurol 1995; 13(1): 52–54. 7. Zimhony O, Sthoeger Z, Ben David D, Bar Khayim Y, Geltner D. Sj€ogren’s syndrome presenting as hypokalemic paralysis due to distal renal tubular acidosis. J Rheumatol 1995; 22(12): 2366–2368. 8. Poux JM, Peyronnet P, Le Meur Y, Favereau JP, Charmes JP, Leroux-Robert C. Hypokalemic quadriplegia and respiratory arrest revealing primary Sjogren’s syndrome. Clin Nephrol 1992; 37(4): 189–191. 9. Siamopoulos KC, Elisaf M, Moutsopoulos HM. Hypokalemic paralysis as the presenting manifestation of primary Sj€ogren’s syndrome. Nephrol Dial Transplant 1994; 9(8): 1176–1178. 10. Fujimoto T, Shiiki H, Takahi Y, Dohi K. Primary Sj€ogren’s syndrome presenting as hypokalaemic periodic paralysis and respiratory arrest. Clin Rheumatol 2001; 20(5): 365–368. 11. al-Jubouri MA, Jones S, Macmillan R, Harris C, Griffiths RD. Hypokalemic paralysis revealing Sj€ogren’s syndrome in an elderly man. J Clin Pathol 1999; 52(2): 157–158.
Journal of Clinical Neuroscience (2004) 11(3)
319
Hypokalemic paralysis € gren’s syndrome revealing Sjo
and the sensory system and consciousness remain unaffected.1 We report a case of acute hypokalemic paralysis as a consequence of underlying renal tubular acidosis as the presenting feature of primary Sj€ ogren’s syndrome.
I. Taylor
CASE REPORT
MBBS,
Mark Parsons FRACP
Department of Neurology, Royal Melbourne Hospital, Parkville, Vic. 3050, Australia
Summary A rare case of a lady with acute hypokalemic quadriparesis and underlying distal renal tubular acidosis manifesting as a presentation of Sj€ ogren’s syndrome is described. The case highlights the concept that acute hypokalemia due to unrecognized renal tubular acidosis may unmask Sj€ogren’s syndrome in patients without sicca symptoms and it may be a marker of more severe renal disease. Acute paralysis is a life threatening consequence of hypokalemia and when due to potassium wasting secondary to renal tubular acidosis may be easily prevented. Underlying Sj€ogren’s syndrome should be considered in all patients of either sex and at any age presenting with hypokalemic paralysis. ª 2003 Published by Elsevier Ltd. Journal of Clinical Neuroscience (2004) 11(3), 319–321 0967-5868/$ - see front matter ª 2003 Published by Elsevier Ltd. doi:10.1016/j.jocn.2003.04.004
Received 22 January 2003 Accepted 2 April 2003 Correspondence to: Mark Parsons FRACP, Department of Neurology, John Hunter Hospital, Hunter Region Mail Centre, Locked Bag 1, New South Wales 2310, Australia. Tel.: +61-3-9342-7000; Fax: +61-3-9342-7272; E-mail: [email protected]
INTRODUCTION The acute hypokalemic periodic paralyses are a heterogeneous potentially life threatening group of disorders caused by either intracellular shifts of potassium (familial hypokalemic paralyses, thyrotoxic periodic paralysis and barium poisoning) or by serum potassium deficits (renal and gastrointestinal losses).1 They present with acute generalized muscle weakness and associated reduced deep tendon reflexes in the setting of hypokalemia. The facial, bulbar and respiratory muscles are less commonly involved
Fig. 1
A 55 year old female kitchen hand presented to the emergency department with rapidly progressive quadriparesis. She had a past history of hysterectomy for carcinoma in situ of the cervix. Medications at admission were hormonal replacement therapy and flucloxacillin 500 mg tablets – (she had taken two tablets on the day prior to admission for axillary folliculitis). Two days prior to admission she experienced cramps and aches of her proximal arms and quadriceps bilaterally. On the day prior to admission she had difficulty climbing stairs, rising from chairs and lifting her arms above her head. On the day of admission she awoke at 2 am and could not move her limbs and was unable to walk. She denied any sensory, sphincter, bulbar, visual, respiratory, or language disturbance. There was no history of recent gastrointestinal or respiratory upset. She denied diuretic, laxative or excessive licorice intake. She had not had any recent vaccinations. She had never experienced a similar event in the past nor was there any significant family history. Examination findings Clinically she was haemodynamically stable, afebrile, pulse 65 beats/min and regular, blood pressure 90/60 mm Hg, respiratory rate 16 breaths per minute, peak expiratory flow rate 250 L/min and forced vital capacity was 2.6 L. Cardiovascular, respiratory and gastrointestinal examinations were otherwise unremarkable. Thyroid examination was normal. The cranial nerve examination was unremarkable. Head flexion and extension were mildly weak (4/5). Examination of the limbs did not reveal any evidence of fasciculations and tone was normal. On examination of the upper limbs there was profound proximal and distal weakness with a flicker of movement only on shoulder abduction, wrist flexion and extension, finger flexion, extension, abduction and adduction. The findings were bilateral and symmetrical. Elbow flexion and extension were preserved with only mild weakness evident. Reflexes were all present and symmetrical yet depressed. Sensory examination was unremarkable. Lower limb examination revealed a flicker of movement on hip flexion, knee flexion and ankle dorsiflexion and antigravity power on hip extension abduction and
ECG at admission: diffuse ST and T wave changes, prolonged PR interval, increased p wave amplitude, prolonged QRS complexes and U waves.
ª 2003 Published by Elsevier Ltd.
Journal of Clinical Neuroscience (2004) 11(3)
320 Taylor and Parsons
Fig. 2 EMG and NCS at admission EMG/NCS: CMAP amplitudes all markedly reduced, distal latencies and conduction velocities are normal. Needle EMG reveals reduced recruitment.
Fig. 3
ECG 24 h later after K corrected: normal.
Journal of Clinical Neuroscience (2004) 11(3)
ª 2003 Published by Elsevier Ltd.
€ Hypokalemic paralysis revealing Sjogren’s syndrome
adduction, knee extension and ankle plantar flexion. Knee jerks were normal, ankle jerks were absent and the plantar response was flexor bilaterally. Sensory examination was unremarkable as was examination of the sphincters.
Investigation findings Blood biochemical examination revealed the following. Na 142 mmol/L, K 2.1 mmol/L, chloride 117 mmol/L, HCO3 12 mmol/L, creatinine 0.11 mmol/L, urea 7.5 mmol/L, glucose 6.9 mmol/L, calcium 2.08 mmol/L, phosphate 0.37 mmol/L, magnesium 1.10 mmol/L, albumin 37 g/L, pH 7.26 L, pCO2 24 L, base excess – 15.7 L, pO2 172, CK 626IU/L. Liver function tests, thyroid functions tests, serum complement, serum protein electrophoresis, C-reactive protein, full blood picture, 25-OH vitamin D3, and cerebrospinal fluid examination were all within normal range. Urine. pH at the time was 7, K 51 mmol/L, CL 185 mmol/L, Na 146 mmol/L. Electrocardiograph (ECG). Diffuse ST and T wave changes, prolonged PR interval, increased p wave amplitude, prolonged QRS complexes and U waves (Fig. 1). Nerve conduction studies (NCS) and electromyography (EMG). The compound muscle action potential (CMAP) amplitudes were markedly reduced, the distal latencies and conduction velocities were normal. The CMAP amplitude did not increase following exercise or repetitive stimulation. Needle EMG revealed reduced recruitment. The upper extremity sensory nerve action potential (SNAP) were reduced in amplitude with a normal sural SNAP (Fig. 2). Autoantibodies. Antinuclear antibodies (ANA) positive, speckled titre 160, speck/Nuclr titre >640, extractable nuclear antigen (ENA) positive, anti Sm negative, anti RNP negative, anti Ro positive, anti La positive, anti Topo1 negative, anti Jo1 negative, anti PM/SCL negative anti KU negative, anti double stranded DNA (dsDNA) 1.6 IU/mL, anti-neutrophil cytoplasmic antibody (ANCA) pANCA and cANCA negative.
Progress Within 4 h despite replacing potassium at a rate or 10–15 mmol/h the serum potassium level fell to 1.7 mmol/L, pH fell to 6.96 and serum chloride and bicarbonate increased to 123 and 15 mmol/L, respectively. Our patient was admitted to a high dependency unit for intensive monitoring and ongoing potassium replacement. Within 24 h her potassium level normalized, limb power returned to normal, there was recovery of all reflexes and complete normalization of her ECG (Fig. 3). On the basis of positive immune markers she was diagnosed with Sj€ogren’s syndrome with underlying renal tubular acidosis presenting as acute hypokalemic paralysis. On further questioning she did not describe sicca symptoms, arthralgias or rash. She was then transferred under the care of the renal physicians for ongoing management and has been placed on long term potassium citrate replacement therapy.
DISCUSSION Sj€ogren’s syndrome is an autoimmune disease of the exocrine glands characterized by xerostomia and xerophthalmia, with possible involvement of other organs. It occurs at a mean age of 40 years and affects 0.2% of the adult population with a female predominance. The diagnosis is made by a number of criteria including subjective and objective symptoms, objective involvement of organs by lymphocytes (biopsy) and laboratory abnorª 2003 Published by Elsevier Ltd.
321
malities.2 Renal tubular acidosis is associated specifically with primary Sj€ ogren’s syndrome and occurs in 33%.3 It results in renal potassium wasting and disordered renal acidification with consequent serum hypokalemic hyperchloremic metabolic acidosis. Hypokalemic paralysis as a consequence of renal tubular acidosis is considered a marker for more severe renal disease in patients with primary Sj€ ogren’s syndrome.3;4 Hypokalemic paralysis is a rare and potentially life threatening presentation of Sj€ ogren’s syndrome.4–9 Both hypokalemic quad4–9 riplegia and respiratory arrest8;10 have been reported. Hypokalemic paralyses associated with Sj€ ogren’s syndrome have not only been recognized in middle aged women but also reported in an elderly male11 and a child6 hence the diagnosis should be considered at all ages and in both sexes. Hypokalemic paralysis in the setting of Sj€ ogren’s may precede the sicca symptoms4 therefore the Schirmer test may be negative.9 The diagnosis of imminent Sj€ ogren’s may be made on the basis of positive immune markers (positive ANA and ENA: anti Ro and anti La). Although these markers are not entirely specific for Sj€ ogren’s syndrome, in the absence of anti dsDNA antibody, anti cardiolipin antibody, ANCA and with a normal compliment they make the diagnosis of other systemic autoimmune diseases unlikely. In our patient presenting with hypokalemia it was straightforward to diagnose distal renal tubular acidosis on the basis of associated hyperchloremic metabolic acidosis (non anion gap acidosis) with concurrent abnormally acidified urine. Autoimmune tests revealed underlying Sj€ ogren’s syndrome. As our patient did not have sicca symptoms a Schirmer test and lip biopsy were not performed. She recovered rapidly with potassium replacement which is subsequently being continued long term. Her progress will be monitored by the renal and rheumatology units. Acute quadriparesis is a life threatening consequence of hypokalemia and may unveil underlying Sj€ ogren’s syndrome. When due to potassium wasting secondary to renal tubular acidosis it may be easily prevented. Underlying Sj€ ogren’s syndrome in spite of a lack of sicca symptoms should be considered in all patients of both sexes presenting with acute hypokalemic paralysis.
REFERENCES 1. Stedwell RE, Allen KM, Binder LS. Hypokalemic paralyses: a review of the etiologies, pathophysiology, presentation, and therapy. Am J Emerg Med 1992; 10(2): 143–148. 2. Vitali C, Bombardieri S, Moutsopoulos HM et al. Preliminary criteria for the classification of Sjogren’s syndrome. Results of a prospective concerted action supported by the European Community. Arthritis Rheum 1993; 36(3): 340–347. 3. Siamopoulos KC, Elisaf M, Drosos AA, Mavridis AA, Moutsopoulos HM. Renal tubular acidosis in primary Sj€ogren’s syndrome. Clin Rheumatol 1992; 11(2): 226–230. 4. Dowd JE, Lipsky PE. Sj€ogren’s syndrome presenting as hypokalemic periodic paralysis. Arthritis Rheum 1993; 36(12): 1735–1738. 5. Raskin RJ, Tesar JT, Lawless OJ. Hypokalemic periodic paralysis in Sj€ogren’s syndrome. Arch Intern Med 1981; 141(12): 1671–1673. 6. Chang YC, Huang CC, Chiou YY, Yu CY. Renal tubular acidosis complicated with hypokalemic periodic paralysis. Pediatr Neurol 1995; 13(1): 52–54. 7. Zimhony O, Sthoeger Z, Ben David D, Bar Khayim Y, Geltner D. Sj€ogren’s syndrome presenting as hypokalemic paralysis due to distal renal tubular acidosis. J Rheumatol 1995; 22(12): 2366–2368. 8. Poux JM, Peyronnet P, Le Meur Y, Favereau JP, Charmes JP, Leroux-Robert C. Hypokalemic quadriplegia and respiratory arrest revealing primary Sjogren’s syndrome. Clin Nephrol 1992; 37(4): 189–191. 9. Siamopoulos KC, Elisaf M, Moutsopoulos HM. Hypokalemic paralysis as the presenting manifestation of primary Sj€ogren’s syndrome. Nephrol Dial Transplant 1994; 9(8): 1176–1178. 10. Fujimoto T, Shiiki H, Takahi Y, Dohi K. Primary Sj€ogren’s syndrome presenting as hypokalaemic periodic paralysis and respiratory arrest. Clin Rheumatol 2001; 20(5): 365–368. 11. al-Jubouri MA, Jones S, Macmillan R, Harris C, Griffiths RD. Hypokalemic paralysis revealing Sj€ogren’s syndrome in an elderly man. J Clin Pathol 1999; 52(2): 157–158.
Journal of Clinical Neuroscience (2004) 11(3)