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The level of digoxin for treatment is typically 0.5-2 ng/mL. [8] Since this is a narrow therapeutic index, digoxin overdose can happen. A serum digoxin concentration of 0.5-0.9 ng/mL among those with heart failure is associated with reduced heart failure deaths and hospitalizations. [9]
An unusual side effect of digoxin is a disturbance of color vision (mostly yellow and green) called xanthopsia. Vincent van Gogh's "Yellow Period" may have somehow been influenced by concurrent digitalis therapy. Other oculotoxic effects of digoxin include generalized blurry vision, as well as seeing a "halo" around each point of light.
This disease is encountered typically after the 1st decade of life, i.e., during adolescence or adulthood. However, it can occur in the neonatal period. Heterozygous carriers of the SLC12A3 gene mutations are 1% of the population. [16] A person with Gitelman syndrome has a low probability of passing the disease to their offspring.
Digoxin increased the risk of death in women by 23%. There was no difference in the death rate for men in the study. [38] Digoxin is also used as a standard control substance to test for P-glycoprotein inhibition. [39] Digoxin appears to be a peripherally selective drug due to limited brain uptake caused by binding to P-glycoprotein. [40] [41]
They are due to elevated cytosolic calcium concentrations, classically seen with digoxin toxicity. [ 5 ] [ 6 ] The overload of the sarcoplasmic reticulum may cause spontaneous Ca 2+ release after repolarization, causing the released Ca 2+ to exit the cell through the 3Na + /Ca 2+ -exchanger.
Causes of hypokalemia include vomiting, diarrhea, medications like furosemide and steroids, dialysis, diabetes insipidus, hyperaldosteronism, hypomagnesemia, and not enough intake in the diet. [1] Normal potassium levels in humans are between 3.5 and 5.0 mmol/L (3.5 and 5.0 mEq/L ) with levels below 3.5 mmol/L defined as hypokalemia.
Hypokalemic periodic paralysis is a condition that causes episodes of extreme muscle weakness typically beginning in childhood or adolescence. Most often, these episodes involve a temporary inability to move muscles in the arms and legs. Attacks cause severe weakness or paralysis that usually lasts from hours to days.
Fanconi syndrome or Fanconi's syndrome (English: / f ɑː n ˈ k oʊ n i /, / f æ n-/) is a syndrome of inadequate reabsorption in the proximal renal tubules [1] of the kidney.The syndrome can be caused by various underlying congenital or acquired diseases, by toxicity (for example, from toxic heavy metals), or by adverse drug reactions. [2]