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Hypokalemic paralysis; an unusual presentation of Conn's Syndrome

INTRODUCTION: Primary aldosteronism (PA) is the most common cause of secondary hypertension. It is caused by excessive aldosterone secretion in adrenal cortex. The typical presentation of PA at young patients, is resistant hypertension and hypokalemia. In recently published series, potassium levels...

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Detalles Bibliográficos
Autores principales: Güller, Pınar Üzgeç, Şahin Alak, Zehra Yağmur, Güçlü, Metin, Kıyıcı, Sinem
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Oxford University Press 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10653182/
http://dx.doi.org/10.1210/jcemcr/luac014.006
Descripción
Sumario:INTRODUCTION: Primary aldosteronism (PA) is the most common cause of secondary hypertension. It is caused by excessive aldosterone secretion in adrenal cortex. The typical presentation of PA at young patients, is resistant hypertension and hypokalemia. In recently published series, potassium levels are frequently reported normal. Normotension is also rare in these patients. We report a case of PA, presenting with hypokalemic paralysis and normal blood pressure, atypically. CLINICAL CASE: A 33-year-old female patient with fatigue, muscle weakness and difficulty walking, was admitted to the emergency department. She had muscle weakness and numbness, especially in the arms and hands for two months. Flaccid paralysis of the limbs was observed at the time of admission. She did not report vomiting, diarrhea, abdominal pain or drug use such as diuretics. There was no history of hypertension. None of her family had hypertension or sudden death at younger age. On physical examination, her blood pressure was less than 140/90 mmHg in repetitive measurements with a manual sphygmomanometer. Lower extremity motor strength was 2/5 and deep tendon reflexes were absent. Biochemical tests revealed that hypokalemia (2 mmol/L) with metabolic alkalosis (pH: 7.47 HCO3:30 mmol/L) and kaliuresis (24-h urinary potassium 87.89 mmol). Serum magnesium level and thyroid function tests were within the reference ranges. After the treatment of hypokalemia, neuromuscular symptoms regressed. Extremely high aldosterone levels (58.5 ng/dL) with suppressed renin activity (0.3 uIU/mL) were detected in blood tests. The diagnosis of PA was confirmed by unsuppressed aldosterone levels (44 ng/dL) after the saline infusion test. Adrenal contrast-enhanced CT identified a solid mass in the right adrenal gland which was 18×10 mm in size, consistent with adenoma (Figure 1). She was referred to surgery. Postoperatively, serum potassium and plasma aldosterone levels returned to normal without medication. Her home blood pressures remained between 110/70 and 120/80 mmHg. [Figure: see text] CONCLUSION: Aldosterone-producing adenoma (APA) is one the most common cause of PA. In APA, aldosterone levels and blood pressures tend to be high. It has been reported that only 28% of patients with hyperaldosteronism have had hypokalemia and 3.1% may be normotensive. We described a patient with PA who presented with flaccid paralysis due to hypokalemia, moreover, she was normotensive. It is a rare condition for primary aldosteronism to present with hypokalemic paralysis. Delayed diagnosis and treatment can be life threatening. In conclusion, we should consider primary aldosteronism in the differential diagnosis of severe hypokalemia and to keep in mind that patients may rarely be normotensive.