Rhabdomyolysis
BMJ 2003; 327 doi: https://doi.org/10.1136/bmj.327.7407.115 (Published 17 July 2003) Cite this as: BMJ 2003;327:115All rapid responses
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Sir,
In my opinion, as regards pathophysiological mechanisms underlying
rhabdomyolysis, we have to take into account particularly Co Q10
deficiency syndrome, that can nowadays be recognized in a quantitative
manner at the bed side by means of biophysical semeiotics (1, 2) (See
HONCode site http://digilander.libero.it/semeioticabiofisica). In fact,
among the numerous causes inducing rhabdomyolysis there are statins, which
are moreover of particular concern because of their widespread and
increasing use.
Statins can bring about, to some extent, rhabdomyolysis,
but exclusively in patients affected already by ubidecarenone deficiency,
since these drugs impaire normally also Co Q10 synthesis with subsequent
functional, mitochondrial damage, as I discussed in previous article, as
far as cerivastatine is concerned (3). As a matter of fact, drug
interactions particularly with fibrates or drugs that interfere with
cytochrome p450, the main isoenzyme involved in the metabolism of statins,
seem to account for most instances, but only in individuals with Co Q10
deficiency syndrome, diagnosed clinically, as stated above.
1) Stagnaro-Neri M., Stagnaro S., Sindrome clinica percusso-
ascoltatoria da carenza di Co Q10. Medic. Geriatr. XXIV, 239, 1993.
2) Stagnaro-Neri M., Stagnaro S., Carenza di Co Q10 secondaria a terapia
ipolipidemizante diagnosticata con la Percussione Ascoltata. Settimana
Italiana di Dietologia, 9-13 Aprile 1991, Merano. Atti, pg. 65. Epat. 37,
17, 1990
3) Stagnaro-Neri M., Stagnaro S., La sindrome percusso-ascoltatoria da
carenza di Carnitina. Clin. Ter. 145, 135 [Pub-Med indexed for MEDLINE]
4) Stagnaro Sergio Statine e Cerivastatina. www.piazzetta.sfera.net.
URL:
http://digilander.libero.it/piazzettamedici/professione/professione.htm
Competing interests:
None declared
Competing interests: No competing interests
Pheochromocytoma producing rhabdomyolysis and secondary diabetes mellitus, with asymptomatic primary
Pheochromocytoma producing rhabdomyolysis and secondary diabetes
mellitus, with asymptomatic primary hyperparathyroidism
Lane and Phillips in their well documented editorial about
rhabdomyolisis emphasize the absence of ?prospective studies of the
incidence of rhabdomyolisis? and the multiple cases that could go
undiagnosed.1 I am sure you would like to know about a peculiar clinical
experience.
My report refers to a case of a previously healthy 22 years old woman
who presented with polyuria, polydipsia, weight loss and also complained
of severe headache, sweating, tachycardia, nausea and vomit, with
myalgias, fatigue and rest discomfort. Accordingly, laboratory evidence of
diabetes mellitus was confirmed with the finding of plasma glucose of 232
milligrams/deciliter (mg/dL), glycosylated hemoglobin of 7.3%, and,
without renal function damage, a marked increase of serum level of
creatine kinase was detected (1759 IU/L). Common causes of rhabdomyolysis
were ruled out so we decided to start insulin replacement and to
hospitalize her for study.
During hospitalization the symptoms became more manifested in
association with severe episodic hypertension and blood pressure readings
as high as 240/140 mmHg. A workup for pheochromocytoma started and the
presence of a left adrenal tumor was suggested by computed tomography. A
plasmatic catecholamines level and free catecholamines in a 24-hour urine
sample collected for measurement disclosed the following convincing
values: plasma norepinephrine 12211 picograms/ml (normal <750 pg/ml)
and urinary excretion of catecholamine metabolites (metanephrines) 6400
micrograms (mg) per 24 hours (normal <900 mg/24 hrs). We suspect a
secondary etiology for the diabetes in relation with this tumor, however
we ruled out the possibly of an autoimmune origin with negative islet cell
CF-ICA auto-antibodies; besides, islet cell Ig-G auto-antibodies, insulin
antibodies and glutamic acid decarboxylase auto-antibodies were also
negative.
After surgical removal, the pheochromocytoma was histologically
confirmed. The patient?s biochemical abnormalities eventually returned to
normal, with correction of the serum creatine kinase (63 IU/L) seven days
after removal of the pheochromocytoma. The blood pressure readings
improved to 110/80 mmHg and glycemic control also was reached (85 mg/dL)
without insulin therapy. She can leave hospitalization ten days after
surgery to continue her evaluation in the external consultation.
As it is known, in multiple endocrine neoplasia (MEN) syndrome the
hyperparathyroidism often remains without clinical manifestations so we
search this possibility once the biochemical and histological diagnosis of
pheochromocytoma was confirmed. Certainly, the result of the intact
parathyroid hormone concentration was moderately elevated, 86 pg/ml
(normal range <59 pg/ml). Correspondingly, the measurement of 24-hour
urine calcium excretion was elevated, 386 mg/day (normal range <250
mg/day). Parathyroid isotope scintigraphy with 99 m-technetium sestamibi
exhibit a solitary left inferior parathyroid adenoma and probably a right
inferior parathyroid hyperplasia. The results of plasmatic calcium and
phosphorus were always between normal ranges. We also complemented her
study with biochemical screening of medullar thyroid cancer with serum
calcitonin. The result was negative.
Fisrt of all, I want to notice that it was quite evident the
association of rhabdomyolysis secondary to muscular ischemia for severe
catecholamines release from the pheochromocytoma. As far as we know, this
particular event was reported in the British Medical Journal for the first
time in 1984 by Oristrell and colleagues2, and we also know of another
case reported, in 1990, by Sheimin et al.3 Secondly, the association of
pheochromocytoma with secondary diabetes mellitus usually reflects the
impaired glucose tolerance originated by a decreased insulin secretion, as
it was fully confirmed in the clinical evolution and laboratory findings
of this young woman.4, 5 Finally, we want to emphasize the wide variety of
symptoms presented by this particular pheochromocytoma plus an
asymptomatic primary hyperparathyroidism, although without reaching a MEN
syndrome. As Lane and Phillips rightly stress: ?The prognosis should be
excellent providing the causative mechanism for the rhabdomyolysis is
identified and reversed where possible?.1
References:
1. Lane, R, Phillips, M. Rhabdomyolysis. BMJ 2003;327:115-116(19
July).
2. Oristrell-Salvá J, Mirada-Canals A. Phaechromocytoma and
rhabdomyolysis. Br Med J 1984;288:1198.
3. Shemin D, Cohn PS, Steven BZ. Pheochromocytoma presenting as
rhabdomyolysis and acute myoglobinuric renal failure. Arch Intern Med
1990;150:2384-2385.
4. Tumbull DM, Johnston DG, Alberti KG, Hall R: Hormonal and
metabolic studies in a patient with phaeochromocytoma. J Clin Endocrinol
Metabo 1980;51:930-933.
5. Michael Bluher, Matthias Windgassen, Ralf Paschke. Improvement of
Insulin Sensitivity after Adrenalectomy in Patients with Pheochromocytoma.
Diabetes Care 2000;23:1591-1592.
Author:
Daniel Cuevas-Ramos, MD, resident of Internal Medicine.
Instituto Nacional de Ciencias Médicas y Nutrición "Salvador
Zubirán". Department of Internal Medicine.
Calle Vasco de Quiroga # 15. Deleg. Tlalpan, CP 14000, México, D. F.
México.
www.innsz.mx
Competing interests:
None declared
Competing interests: No competing interests