Symptomatic Resistant Hypomagnesemia with Proton Pump Inhibitor Therapy in the Context of Vitamin D Deficiency

Program: Abstracts - Orals, Featured Poster Presentations, and Posters
Session: SUN 199-233-Bone Biology
Basic/Clinical
Sunday, June 16, 2013: 1:45 PM-3:45 PM
Expo Halls ABC (Moscone Center)

Poster Board SUN-232
Hazel K Turner*, Robert W Fowler and Nemanja D Stojanovic
Barking, Havering & Redbridge University Hospitals NHS Trust, United Kingdom
Background: Long term use of Proton Pump Inhibitors (PPIs) has been associated with hypomagnesemia, perhaps due to reduced gut absorption or increased renal excretion of magnesium.  Both hypomagnesemia and hypocalcemia can present with features of neuromuscular excitability which may be indistinguishable from each other.  Previous cases have identified a link between PPI induced hypomagnesemia and low serum calcium which does not stabilize despite calcium replacement, until serum magnesium is replete.  Whilst low magnesium may impair PTH secretion, this case demonstrates that serum calcium may be stabilized in a hypomagnesemic patient where there is an appropriately elevated PTH in conjunction with vitamin D deficiency, but that symptoms persist until the hypomagnesemia is addressed. 

Clinical Case: A 68 year old woman presented with a several month history of lethargy, diarrhoea and arthralgia. She had taken PPIs (rabeprazole, omeprazole, lansoprazole) for over a decade for dyspepsia.  Co-morbidities included hypertension, but there had been no use of diuretics or other drugs linked to hypomagnesemia. Following an episode of collapse with muscle cramps and palpitation, adjusted calcium was 1.81mmol/l (2.2-2.6), PTH 10.4pmol (1.3-6.8), serum 25-OH vitamin D 18nmol/l (30-200) and magnesium 0.25mmol/l (0.7-1). Treatment was with magnesium sulphate infusions, 10% calcium gluconate and vitamin D supplementation. With a similar presentation 2 months later she was calcium and vitamin D replete, but magnesium was 0.21mmol/l.  Trousseu’s and Chvostek’s signs remained positive.  On EKG QTc was normal (<440 msec) with frequent premature ventricular complexes.  Twenty-four hour urinary magnesium was low at 0.7mmol/24hr (2.4-6.5) which supports PPI induced decreased gut absorption rather than increased renal excretion, as the underlying mechanism for her hypomagnesemia.  PPIs were stopped and ranitidine 150 mg commenced.  Six months later she remains magnesium and calcium replete with no recurrence of her symptoms.    

Conclusion: Mild hypocalcemia in the presence of severe PPI induced hypomagnesemia may be fully corrected in the context of treated vitamin D deficiency with appropriately elevated PTH, independently of an ongoing hypomagnesemia.  However, the morbidity associated with the signs and symptoms of neuromuscular excitability may persist until serum magnesium is normalized by stopping PPIs.

Nothing to Disclose: HKT, RWF, NDS

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