Syndrome of inappropriate antidiuretic hormone (SIADH) is a disorder of the posterior pituitary gland where vasopressin (ADH) is secreted even when plasma osmolality is normal or low. SIADH, or Schwartz-Barter syndrome, occurs when ADH is secreted in the presence of a low plasma osmolality. This alteration results in increased levels of anti-diuretic hormone. High levels of ADH results in excretion of sodium. The incidence is unknown but might be related to cancers, viral and bacterial pneumonia, lung abscesses, tuberculosis, chronic obstructive pulmonary disease, mycoses, positive pressure ventilators, pneumothorax, brain tumors, head trauma, certain medications, and infectious diseases. Signs and symptoms include nausea, vomiting, muscle twitching, changes in level of consciousness, and low sodium levels with increased urine sodium. The treatment for SIADH includes fluid restrictions because fluid further dilutes the serum sodium levels, gradual replacement of sodium, and administration of demeclocycline (Declomycin) and intravenous hypertonic sodium.
Following single oral doses of mg to mg given to 12 healthy adult volunteers, mean peak plasma levels of 30 to 70 picograms (pg)/mL of cabergoline were observed within 2 to 3 hours. Over the -to-7 mg dose range, cabergoline plasma levels appeared to be doseproportional in 12 healthy adult volunteers and nine adult parkinsonian patients. A repeat-dose study in 12 healthy volunteers suggests that steady-state levels following a once-weekly dosing schedule are expected to be twofold to threefold higher than after a single dose. The absolute bioavailability of cabergoline is unknown. A significant fraction of the administered dose undergoes a first-pass effect. The elimination half-life of cabergoline estimated from urinary data of 12 healthy subjects ranged between 63 to 69 hours. The prolonged prolactin-lowering effect of cabergoline may be related to its slow elimination and long half-life.