what is this case???
A 30 year-year-old woman was admitted to the emergency department with a sudden onset of progressive paralysis involving four extremities. She denied having nausea, vomiting, diarrhea or the use of drugs, including diuretics and licorice. Her family history was un remarkable. One year ago she had presented to the hospital with muscle weakness and myalgias. Laboratory workup at that time revealed potassium level of 2.1 mEq/L (normal 3.5-5.5) but the cause of hypokalemia was not inves tigated in detail. During her current presentation blood pressure was 130/80 mmHg, she was a febrile with no respiratory distress. She had symmetric flaccid paralysis with areflexia in all extremities. Her muscle strength was 1/5 in the proximal muscle groups. Her laboratory tests revealed the following values: severe hypokalemia (1.51 mEq/L), metabolic alkalosis (pH 7.52), creatine kinase (CK) 6330 IU/L (16 190), lactic dehydrogenase (LDH) 886 IU/L (240-480), aspartate aminotransferase (AST) 192 IU/L (7-39), alanine aminotransferase (ALT) 101 IU/L (2-40), calcium 7.3 mg/dL (8.5 10.5), phosphorus 2.1 mg/dL (2.7-4.5), magnesium 0.57 mmol/L (0.85-1.15). 25(OH) vitamin D level was 7 IU/L (> 25). Urinary potassium excretion was 70 mEq/day. Transtubular potassium gradient was 5.2. Parathormone (PTH) level was 178 ng/mL (15-65). Normal or ne gative tests included sodium chloride, blood urea nitrogen, creatinine, glucose, total pro tein, albumin, thyroid function studies, and liver. Intravenous administration of potassium chloride (KCL) at the rate of 10 mmol/h progressively improved her muscle strength with concomitant increase in her potassium levels. Muscle biopsy and electroneuromyography were performed one week after resolution of hypokalemia. Metabolic alkalosis, hypocalcemia and hypomagnesaemia with hypokalemia prompted us to suspect of Gitelman’s syndrome. However, because this syndrome mostly appears in younger ages, a few other possible factors, such as mineralocorticoid excess syndrome, were taken into consideration. What do u people think of these case?
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Filed Under: Endocrine
Hypokalemic paralysis due to primary hyperaldosteronism simulating gitelman’s syndrome.
Also, Conn’s syndrome and Gitelman’s syndrome should be considered in a differential diagnosis of patients with hypokalemic paralysis due to occasional overlapping laboratory findings.
this is the case of conn,s disease…..in which aldosterone is increases that acts on distal convoluted tubules to reabsorption of sodium at the expense of potassium. During Na++ reabsorption water is also absorbed that leads to hypertension ……and the rest of the symptoms is due to lower serum potassium level…….
I think this is the case of Primary hyperaldosteronism,either it is due to 1)unilateral aldosterone-producing adenoma (APA) or Conn syndrome (50-60% of cases) and (2) idiopathic hyperaldosteronism (IHA) or bilateral adrenal hyperplasia (40-50% of cases).Because imaginary diagnostic major was not mention,the actual cause of primary hyperaldesteronism either by APA or by IHA can’t be differntiated.Increase in aldosterone increase renal distal tubular reabsorption of sodium, enhances secretion of potassium and hydrogen ions, causing hypernatremia, hypokalemia, and alkalosis.And alkalosis causes increase binding of free calcium with albumin results in hypocalcemia.