Hostname: page-component-848d4c4894-8kt4b Total loading time: 0 Render date: 2024-06-29T19:14:31.254Z Has data issue: false hasContentIssue false
  • English
  • Français

Hyperglycemia, Lumbar Plexopathy and Hypokalemic Rhabdomyolysis Complicating Conn's Syndrome

Published online by Cambridge University Press:  18 September 2015

Chi-Ping Chow ,
Christopher J. Symonds  and
Douglas W. Zochodne
Chi-Ping Chow
Affiliation:
Department of Clinical Neurosciences and The Neuroscience Research Group,The University of Calgary, Calgary.
Christopher J. Symonds
Affiliation:
Department of Clinical Neurosciences and The Neuroscience Research Group,The University of Calgary, Calgary.
Douglas W. Zochodne*
Affiliation:
Department of Clinical Neurosciences and The Neuroscience Research Group,The University of Calgary, Calgary.
*
The University of Calgary, Department of Clinical Neurosciences, Room 182A, 3330 Hospital Drive N.E., Calgary, Alberta, Canada T2N 4N1
Rights & Permissions [Opens in a new window]

Abstract:

Core share and HTML view are not available for this content. However, as you have access to this content, a full PDF is available via the ‘Save PDF’ action button.
Background:

Lumbosacral plexopathy is a complication of diabetes mellitus. Conn's syndrome from an aldosterone secreting adenoma may be associated with hypokalemia and rhabdomyolysis but mild hyperglycemia also usually occurs.

Methods:

Case description.

Results:

A 70-year-old male diagnosed as having Conn's syndrome, hypokalemia and mild hyperglycemia developed rhabdomyolysis and lumbar plexopathy as a presenting feature of his hyperaldosteronism. His rhadbdomyolysis rapidly cleared following correction of hypokalemia but recovery from the plexopathy occurred slowly over several months. Definite resection of the aldosterone secreting adenomas reversed the hyperglycemia.

Conclusion:

Our patient developed lumbar plexopathy resembling that associated with diabetes mellitus despite the presence of only mild and transient hyperglycemia.

Résumé:

RÉSUMÉ:Introduction:

La plexopathie lombosacrée est une complication du diabète. Le syndrome de Conn dû â un adénome sécréfant de l'aldostérone peut étre associe a une hypokaliemie et a un rhabdomyolyse, mais une legere hyperglycemic peut ussi etre présente.

Méthodes:

Description d'un cas.

Résultats:

Un patient âgè de 70 ans porteur d'un syndrome de Conn, d'une hypokaliémie et d'une légère hyperglycémic a développé une rhabdomyolyse et une plexopathie lombaire comme manifestation initiale de son hyperaldostéronisme. La rhabdomyolyse s'est résolue rapidement suite à la correction de l'hypokaliémie, mais la guérison de sa plexopathie a pris plusieurs mois. La résection définitive de l'adénome sécréfant de l'aldostérone a fait disparaître l'hyperglycémie.

Conclusions:

Notre patient a développé une plexopathie lombosacrée ressemblant à une plexopathie diabétique bien que son hyperglycémic n'ait été que légère et transitoire.

Type
Original Articles
Information
Canadian Journal of Neurological Sciences , Volume 24 , Issue 1 , February 1997 , pp. 67 - 69
Copyright
Copyright © Canadian Neurological Sciences Federation 1997

References

REFERENCES

1. Garland, H Diabetic amyotrophy. Br Med J 1955; 26: 1287–1290.Google Scholar
2. Vaughan, NJA Jowett, TP Slater, JDH et al. The diagnosis of primary hyperaldosteronism. Lancet 1981: 120–125.CrossRefGoogle ScholarPubMed
3. Melby, JC Spark, RF Dale, S et al. Diagnosis and localization of aldosterone-producing adenomas by adrenal vein catheterization. N Engl J Med 1967; 277: 1050–1056.Google Scholar
4. Conn, JW Hypertension, the potassium ion and impaired carbohydrate tolerance. N Engl J Med 1965; 273: 1135–1143.Google Scholar
5. Podolsky, S Melby, JC Improvement of growth hormone response to stimulation in primary aldosteronism with correction of potassium deficiency. Metabolism 1976; 25: 1027–1032.Google Scholar
6. Gorden, P Glucose intolerance and hypokalemia: failure of short term potassium depletion in normal subjects to reproduce the glucose and insulin abnormalities of clinical hypokalemia. Diabetes 1973; 22: 544–551.CrossRefGoogle ScholarPubMed
7. Gallai, M Myopathy with hyperaldosteronism. J Neurol Sci 1977; 32: 337–345.CrossRefGoogle ScholarPubMed
8. Bautista, J Gil-Neciga, E Gil-Peralta, A Hypokalemic periodic paralysis in primary hyperaldosteronism. Eur Neurol 1979; 18: 415–420.Google Scholar
9. Sambrook, MA Heron, JR Aber, GM Myopathy in association with primary hyperaldosteronism. J Neuro Neursurg Psychiatry 1972; 35: 202–207.CrossRefGoogle ScholarPubMed
10. Atsumi, T Ishikawa, S Miyatake, T Yoshida, M Myopathy and primary aldosteronism: electronmicroscopic study. Neurology 1979; 29: 1348–1353.Google Scholar
11. Raff, MC Sangalang, V Asbury, AK Ischemic mononeuropathy multiplex associated with diabetes mellitus. Arch Neurol 1968; 18: 487–499.Google Scholar
12. Weinberger, MH Grim, CE Hollifield, W et al. Primary aldosteronism: diagnosis, localization, and treatment. Ann Intern Med 1979; 90: 386–395.CrossRefGoogle ScholarPubMed
13. Dominic, JA Koch, M Guthrie, GP et al. Primary aldosteronism presenting as myoglobinuric acute renal failure. Arch Intern Med 1978; 138: 1433–1434.Google Scholar
14. Mijares, RP Hypokalemic rhabdomyolysis secondary to pseudohyperaldosteronism due to the use of a lotion containing 9-alphafluoroprednisolone. Nephron 1986; 43: 232–233.Google Scholar
15. Knochel, PL Schlein, EM On the mechanism of rhabdomyolysis in potassium depletion. J Clin Invest 1972; 51: 1750–1758.Google Scholar