Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0015672 (fatigue)
 51,768 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 27-year-old Turkish male presented with fatigue, long lasting hypertension, hyperkalemia, hyperchloremic metabolic acidosis and normal glomerular filtration rate. His brother also showed hyperkalemia with no other features of the disease. Plasma renin levels were low and serum aldosterone levels were inappropriately low-normal to his hyperkalemia. Plasma cortisol levels were normal. Plasma renin aldosterone levels responded appropriately to postural changes, salt restriction and saline infusion. Fludrocortisone was ineffective in his hyperkalemia. The conditions were consistent with Type II pseudohypoaldosteronism (PHA). Furosemide and sodium bicarbonate were effective to control his hyperchloremia, metabolic acidosis and hypertension but partly effective for his hyperkalemia. dDAVP alone did not control the situation and hypertension and metabolic derangement reoccurred. Adding dDAVP to furosemide and sodium bicarbonate successfully controlled hyperkalemia, hyperchloremic acidosis and hypertension. The patient stayed normotensive with normal metabolic and biochemical parameters after 6 months with furosemide and dADVP although sodium bicarbonate had been discontinued after the first month of therapy. dDAVP is a useful adjunct to furosemide and non chloride anions which altogether successfully reverse the metabolic derangement in Type II PHA.
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PMID:Furosemide and dDAVP for the treatment of pseudohypoaldosteronism type II. 949 9

Adrenal insufficiency is a rare disease, but its prevalence is increasing. The most frequent cause of primary adrenal insufficiency in western countries is autoimmune adrenalitis, whereas secondary adrenal insufficiency is most often caused by pituitary tumours and their treatment (e.g., surgery). Chronic glucocorticoid replacement consists of hydrocortisone 15-25 mg/day in divided doses and dose monitoring is largely based on clinical judgement. Fludrocortisone 0.05-0.2 mg/day is given for substitution in mineralocorticoid deficiency aiming at normotension, normokalaemia and a plasma renin activity in the upper normal range. It has recently been shown that, despite adequate glucocorticoid and mineralocorticoid replacement well being in patients with adrenal insufficiency is still impaired. Several studies have demonstrated that dehydroepiandosterone 25-50 mg/day p.o. may improve mood, fatigue, well-being and, in women, also sexuality, suggesting that dehydroepiandosterone should become part of the standard treatment regime. However, large Phase III trials of dehydroepiandosterone for adrenal insufficiency are still lacking and it has not yet been approved for the treatment of this disease. Patients with adrenal insufficiency are at risk of adrenal crisis, usually precipitated by major stress, such as severe infection or surgery. Early dose adjustments are required to cover the increased glucocorticoid demand in stress. Careful and repeated education of patients and their partners is the best strategy to avoid this life-threatening emergency. Some recent studies suggest that during sepsis some patients with intact adrenal function may develop transient relative adrenal insufficiency and benefit from administration of hydrocortisone plus fludrocortisone. However, the pathophysiology and diagnosis criteria of relative adrenal insufficiency and its treatment remain unsettled issues.
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PMID:Management of adrenal insufficiency in different clinical settings. 1625 72

Hypokalemia associated with aldosterone-producing adenomas (APA) are almost corrected following successful unilateral adrenalectomy. Prolonged hyperkalemia after unilateral adrenalectomy is rarely reported and may be overlooked. We describe a 62-year-old man who presented with fatigue and dizziness 2 weeks after unilateral adrenalectomy for aldosterone-producing adenomas. Physical examination showed decreased skin turgor and postural hypotension. Laboratory studies revealed hyperkalemia (6.3 mmol/l) with a low transtubular potassium gradient of 5. A relatively low plasma aldosterone concentration and high plasma renin activity in the setting of normal plasma cortisol and adrenocorticotropic hormone levels lead to a diagnosis of functional hypoaldosteronism. Fludrocortisone 0.2 mg/day for one week completely corrected his hyperkalemia which recurred after cessation of fludrocortisone. Long-term suppression of contralateral aldosterone synthesis by APA and/or chronic untreated hypokalemia may have accounted for the development of prolonged hyperkalemia after unilateral adrenalectomy. Serum potassium concentration following unilateral adrenalectomy must be meticulously monitored to avoid life-threatening hyperkalemia.
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PMID:Prolonged hyperkalemia following unilateral adrenalectomy for primary hyperaldosteronism. 2042 Aug 1