Rapid Responses to:
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Rapid Responses: Rapid Responses published:
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Box 2
- Piero Baglioni (31 March 2007)
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Corticosteroids cause hypokalemia, not hyperkalemia
- Shirwan A. Mirza (4 April 2007)
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what about bananas?
- jessica harris (5 April 2007)
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Curiosity of spurious hyperkalemia
- Kenneth S Wilson (12 April 2007)
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Pontefract and potassium
- Andrew Clegg (15 April 2007)
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Re: Corticosteroids cause hypokalemia, not hyperkalemia
- W Stuart A Smellie (16 April 2007)
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Re: Curiosity of spurious hyperkalemia
- W Stuart A Smellie (20 April 2007)
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The "C" word again
- Diane-Marie Campbell (29 April 2007)
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Re: The "C" word again
- W Stuart A Smellie (30 April 2007)
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Piero Baglioni, Consult Physician Prince Charles Hospital Merthyr Tydfil Mid Glamorgan CF47 9DT
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I am surprised to read that corticosteroids may cause raised serum potassium [usually the opposite is true). I understand that Movicol contains potassium but usually the effect is to cause diarrhea which is usually associated with reduced serum potassium. I am uncertain if "blockers" refers to BETA blockers [whcih can indeed cause hyperkalaemia via inhibition of renin release]. Competing interests: None declared |
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Shirwan A. Mirza, Private practice Auburn, NY 13021
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In his review, Dr. W Stuart A Smellie lists corticosteroids as one of the medications that might cause hyperkalemia. This is probably an oversight. Corticosteroids are well known to cause hypokalemia. Hyperkalemia is a manifestation of adrenal insufficiency. Hypokalemia is also a manifestation of Cushing's syndrome, which is a corticosteroid excess condition. Competing interests: None declared |
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jessica harris, gp bacon road medical centre, 16 bacon road, norwich NR2 3QX
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I was always taught to ask if patients were eating lots of bananas or liquorice if I found a patient to have hyperkalaemia. Is this old hat or still relevant? Competing interests: None declared |
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Kenneth S Wilson, Consultant Medical Oncologist BC Cancer Agency, Vancouver Island Centre, Victoria, BC,V8R 6V5, Canada
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As a Registrar in Medicine in Edinburgh, I had a case report in a sister journal on this subject in 1976 (Postgrad Med J Vol 52, 470-472). The report of "critical" hyperkalemia (7.3 mEq/L) caused great consternation when the laboratory called. The patient had sustained a spontaneous splenic rupture due to chronic lymphatic leukemia. The total white cell count was 496,000/mm3, of which 98% were lymphocytes. ECG showed no confirmatory signs of hyperkalemia. Fortunately our junior lecturer recognised the scenario. The anxiety was promptly relieved when a further plasma sample was tested after immediate centrifugation and a normal plasma potassium level reported. Once seen, never forgotten.
The previous respondent referred to excess liquorice leading to hyperkalemia. It can also correct hypokalemia. Again, in Edinburgh, we had a case of "glycyrrhizinophilia". A patient with undiagnosed Addison's disease had found that eating plenty pontefract cakes relieved the symptoms. Competing interests: None declared |
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Andrew Clegg, SpR Geriatrics Yorkshire Deanery
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In response to Jessica Harris (1) liquorice tends to cause hypo- rather than hyperkalaemia. This is due to a particluarly interesting mechanism. Revision of adrenal biochemistry reveals aldosterone to be the primary minaralocorticoid, responsible for sodium (and associated water) retention at the expense of potassium and hydrogen ions. Acting as the hormone at the endpoint of the renin-angiotensin system (and in direct response to hyperkalaemia) aldosterone acts on its own receptor at the distal convuluted tubule (DCT) to promote Na+ (and hence fluid) retention. As sodium is retained, K+ and H+ travel in the opposite direction to maintain electroneutrality. The hypertensive, hypokalaemic alkalosis of Conn's syndrome is therefore explained. Cortisol is best known for its glucocorticoid activity. It actually possesses intrinsic mineralocorticoid properties that are generally not appreciated in normal human physiology. This is due to the action of an enzyme, 11-B Hydroxysteroid Dehydrogenase (11B HSD) which is found in the region of the DCT. This functions to convert cortisol to the inactive cortisone (and vice versa). Circulating cortisol is therefore unable to manifest its potential mineralocorticoid activity at the aldosterone receptor due to the action of 11B HSD. Liquorice, as you may have surmised, acts to inhibit 11B HSD. Cortisol is therefore now able to exhibit its mineralocorticoid activity, in tandem with aldosterone, at the aldosterone receptor in the region of the DCT. In a sense, liquorice produces a temporary Conn's-like syndrome, explaining the potential for hypertension, hypokalaemia (and associated consequences) and metabolic alkalosis. This may also explain why liquorice is able to alleviate some of the symptoms (hypotension, electrolyte disturbance, etc) of Addison's by potentiating the action of the suppressed levels of cortisol. The rare genetic deficiency of 11B HSD leads to a similar endocrine/biochemical state. Pontefract cakes are not actually cakes at all but small, round sweets made entirely from liqourice. I personally find liquorice revolting. Apologies to Bertie Bassett... 1. J Harris. What about bananas? BMJ Rapid Response. 5th April 2007. Competing interests: I live near to Pontefract, where the eponymous cakes are manufactured. |
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W Stuart A Smellie, Consultant Bishop Auckland Hospital DL14 6 AD
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Thank you to both Drs Baglioni and Mirza for pointing out the confusing reference to corticosteroids in box 2. Both corticosteroids and mineralosteriods do indeed classically cause hypokalaemia. Hyperkalaemia may occur in patients with adrenal supression resulting from high dose or long term corticosteriod use, if for example these are stopped although the box entry does not make this clear. A better wording would be: 'patients with primary or corticosteroid induced adrenal insufficiency' Competing interests: None declared |
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W Stuart A Smellie, Consultant Chemical Pathologist Bishop Auckland Hospital DL14 6AD
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An excellent example- the typical advice is to obtain an anticoagulated sample (using lithium heparin and not a potassium EDTA (full blood count) sample (!)although immediate centrifugation should have the same effect. As you say, once seen never forgotten but in reality many are not fortunate enough to have seen a case. 'Factitious' hyperkalaemia remains one of the biggest problems in critical lab results and although usually due to time-deteriorated or cold samples, it is important to be aware of the other causes. I would also agree entirely with your comments on liquorice. I am not personally aware of hyperkalaemia from liquorice and certainly the classical presentation is of a pseudo-Conn's syndrome with hypertension and hypokalaemia. To pick up on a second comment from the same responder, high potassium foods certainly do merit consideration, although are unlikely to produce true hyperkalaemia in someone with 'normal' renal function. They are of clear relevance in patients with decreased renal function or taking potassium sparing drugs. Competing interests: None declared |
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Diane-Marie Campbell, itinerant emergency physician Western Australia, 6230
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I had believed that New Zealand had progressed with the rest of the developed world. Did the doctor in the first case really find a "casualty" or was the patient referred to a Department of Emergency Medicine? Competing interests: None declared |
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W Stuart A Smellie, Consultant Bishop Auckland Hospital DL14 6 AD
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Apologies for the abbreviation. Out of courtesy for my New Zealand colleagues, however, I must point out that this underdeveloped author in fact lives in Bishop Auckland, County Durham, England Competing interests: None declared |
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