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Dear all,

We did a little audit in 2007 in reply to Dr. Smellie's article in BMJ
Cases in primary care laboratory medicine: Pitfalls of testing and summary of guidance on safety monitoring with amiodarone and digoxin BMJ 2007;334:312 doi:10.1136/bmj.39090.709537.47. 

We collected our data regarding the digoxin level requests (n=967) from 01/02/06 to 29/01/07. There were 82 samples with high digoxin (>2.6 mmol/L), of which 6 samples had low potassium (<3.5 mmol/L), 3 had high corrected calcium (>2.5 mmol/L); 5 had low magnesium (<0.7mmol/L) and 3 had both low potassium and low magnesium.There were 203 samples with digoxin in the upper 3rd of the reference range (1.9-2.6nmol/L), of which 10 had low potassium, 3 had high corrected calcium; 3 had low magnesium, and 3 had both low potassium and low magnesium.

Of the samples with high digoxin (n=82); 57 were from stages 3-5 Chronic Kidney Disease, in whom 6 had low potassium (all the low potassium patients were CKD stage 3-5) and 49 had normal or high potassium, 14 did not have any electrolyte checked.

Of the 68 patients with high digoxin in whom serum electrolytes were measured, 15 (22%) had electrolyte abnormalities which could cause arrhythmia. Please find details at:

http://www.bmj.com/content/334/7588/312/reply

Dr Mehdi Mirzazadeh

SpR in Chemical Pathology ( metabolic medicine)

Oxford



On 22 Jun 2011, at 13:52, Ian Young wrote:

Apologies for the truncated message!  Full version below.


There is a high degree of awareness around the effect of hypokalaemia on dogixin toxicity (abstract below), but much less awareness of the effect of hypomagnesaemia.  Many years ago I published a sort paper suggesting this was the most common electrolyte abnormality in patients with evidence of digoxin toxicity (which is a clinical diagnosis).  I think it is under-recognised because Mg is not measured routinely in these patients, but it is something clinicians and labs should be more aware of.

Best wishes

Ian Young


Prof.Ian S. Young

Professor of Medicine and Director of The Centre for Public Health
Queen's University Belfast

1st Floor ICS B Block
Royal Victoria Hospital
Grosvenor Road
Belfast
BT12 6BJ
Northern Ireland

tel: +44 (0) 2890 632743
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Br J Clin Pharmacol. 1991 Dec;32(6):717-21.
Magnesium status and digoxin toxicity.

Young IS, Goh EM, McKillop UH, Stanford CF, Nicholls DP, Trimble ER.

Department of Clinical Biochemistry, Royal Victoria Hospital, Belfast.


Abstract

1. Eighty-one hospital patients receiving digoxin were separated into groups with and without digoxin toxicity using clinical criteria. Serum digoxin, sodium, potassium, calcium, creatinine, magnesium and monocyte magnesium concentrations were compared. 2. Subjects with digoxin toxicity had impaired colour vision (P less than 0.0001, Farnsworth-Munsell 100 hue test) and increased digoxin levels (1.89 (1.56-2.21) vs 1.34 (1.20-1.47) nmol l-1, P less than 0.01) (mean (95% confidence limits], though there was considerable overlap between two groups. 3. Subjects with digoxin toxicity had lower levels of serum magnesium (0.80 (0.76-0.84) vs 0.88 (0.85-0.91) mmol l-1, P less than 0.01) and monocyte magnesium (6.40 (5.65-7.16) vs 8.76 (7.81-9.71) mg g-1 DNA, P less than 0.01), but there were no significant differences in other biochemical parameters. A greater proportion of toxic subjects were receiving concomitant diuretic therapy (20/21 vs 37/60, P less than 0.05). 4. Magnesium deficiency was the most frequently identified significant electrolyte disturbance in relation to digoxin toxicity. In the presence of magnesium deficiency digoxin toxicity developed at relatively low serum digoxin concentrations.

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