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LETTER TO EDITOR
Year : 2013  |  Volume : 54  |  Issue : 4  |  Page : 283-284  

Hypokalemia- induced myopathy and massive creatine kinase elevation as first manifestation of Conn's syndrome


1 Department of Internal Medicine, Sakarya University Faculty of Medicine, Sakarya, Turkey
2 Department of Radiology, Sakarya University Faculty of Medicine, Sakarya, Turkey

Date of Web Publication9-Oct-2013

Correspondence Address:
Selcuk Yaylaci
Department of Internal Medicine, Sakarya University Faculty of Medicine 54100
Turkey
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0300-1652.119658

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How to cite this article:
Olt S, Yaylaci S, Tatli L, Gunduz Y, Garip T, Tamer A. Hypokalemia- induced myopathy and massive creatine kinase elevation as first manifestation of Conn's syndrome. Niger Med J 2013;54:283-4

How to cite this URL:
Olt S, Yaylaci S, Tatli L, Gunduz Y, Garip T, Tamer A. Hypokalemia- induced myopathy and massive creatine kinase elevation as first manifestation of Conn's syndrome. Niger Med J [serial online] 2013 [cited 2024 Mar 29];54:283-4. Available from: https://www.nigeriamedj.com/text.asp?2013/54/4/283/119658

Sir,

Primary hyperaldosteronism is characterized by hypersecretion of aldosterone from the adrenal cortex. If the aldosterone-producing pathology is adenoma then the disease is called Conn's syndrome. Hypertension, hypokalemia and metabolic alkalosis are developed in excessive secretion of aldosterone. [1] In this article, it is aimed to present a case diagnosed as myopathy caused by hypokalemia and elevated creatin kinase developed secondary to the primary hyperaldosteronism in a 43-year-old female patient, who has admitted with symptoms of muscle weakness, exhaustion, fatigue, dry mouth, frequent urination and drinking a lot of water.

A 43-year-old female patient has admitted to our endocrinology clinic with the complaints of muscle weakness, exhaustion, fatigue, dry mouth, frequent urination and drinking a lot of water, which were present for approximately 1 year and increased recently. The patient's blood pressure was 150/90 mm Hg, pulse was 80 per min., and fever was 37.2°C. System examination was normal except for 3/5 muscle weakness in both the upper and lower extremities. Laboratory tests revealed hypokalemia and elevation of massive CK [Table 1]. The patient had history of hypertension and was using Olmesartan 20 mg 1 × 1; and since her potassium was 1.7 mmol/L, the causes of secondary hypertension were investigated. 1 mg of dexamethasone suppression test has revealed that cortisol level was 1.3 mg/dl. Plasma aldosterone and Plasma Aldosterone/Plasma Renin activity was increased. Vanil mandelic acid, metanephrine and normetanephrine were normal in 24-hour urinary. Saline infusion test was performed and plasma aldosterone was found as 980 ng/dl [Table 1]. Adrenal Computed Tomography revealed an adenoma-related nodular lesion of 32 × 20 mm in diameter in the right adrenal [Figure 1] and [Figure 2]. The patient was diagnosed with Conn's syndrome, presented with hypokalemic myopathy and elevation of massive CK. After medical treatment, muscle weakness and laboratory parameters were completely normal in line with the normalized potassium levels. The patient's initial symptoms were thought to be connected to hypokalemia developed secondarily to Conn's syndrome. The patient was referred for adrenal surgery with the diagnosis of Conn's syndrome, and histopathology result was reported adenomas.
Figure 1: In axial contracted CT section in the right adrenal gland hypodense nodular lesion (white arrow) can be seen size in diameter 32 × 20 mm

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Figure 2: In axial cross‑section dynamic contrast‑enhanced CT,anterior part of the right adrenal gland showing the minimal contrast enhancement (white arrow) 20 HU density well‑defined in diameter 32 × 20 mm nodular lesions observed

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Table 1: Laboratory values of patient

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Severe muscle weakness may be present due to hypokalemia seen in Conn's syndrome. [2],[3] It is also reported that elevation of CK may be present in Conn's syndrome. [4],[5] In our patient, there was an ongoing and increasing muscle weakness. The measured value of potassium was 1.7 mmol/L, and CK was 4267 U/L. There was a dramatic improvement in the patient's clinical and laboratory values after potassium supplementation. Our patient was diagnosed as Conn's syndrome as a result of the tests performed considering the secondary hypertension due to the symptoms of hypokalemia, hypertension, and high levels of massive CK, and the patient underwent surgery. And in the result of the operation, adenoma was reported in accordance with the radiological imaging.

As a result, it should be kept in mind that hypokalemia-related myopathy and elevated massive CK may be the first presentation of Conn's syndrome in a patient followed up due to hypertension.

 
   References Top

1.Mattsson C, Young WF Jr. Primary aldosteronism: Diagnostic and treatment strategies. Nat Clin Pract Nephrol 2006;2:198-208.  Back to cited text no. 1
[PUBMED]    
2.Huang YY, Hsu BR, Tsai JS. Paralytic myopathy: A leading clinical presentation for primary aldosteronism in Taiwan. J Clin Endocrinol Metab 1996;81:4038-41.  Back to cited text no. 2
[PUBMED]    
3.Kotsaftis P, Savopoulos C, Agapakis D, Ntaios G, Tzioufa V, Papadopoulos V, et al. Hypokalemia induced myopathy as first manifestation of primary hyperaldosteronism-an elderly patient with unilateral adrenal hyperplasia: A case report. Cases J 2009;2:6813.  Back to cited text no. 3
[PUBMED]    
4.Crawhall JC, Tolis G, Roy D. Elevation of serum creatine kinase in severe hypokalemic hyperaldosteronism. Clin Biochem 1976;9:237-40.  Back to cited text no. 4
[PUBMED]    
5.Steinfurt J, Müller MC, Seidel A, Salm R, Ochs A. Pareses, myalgias, and massive CK elevation: A severe neurological disorder?. Med Klin (Munich) 2010;105:496-500.  Back to cited text no. 5
    


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