Interactions : אינטראקציות

4.5     Interaction with other medicinal products and other forms of interaction

Drugs leading to an increased vasopressin effect
The below listed drugs increase the vasopressin effect, leading to reduced renal electrolyte free water excretion and may increase the risk of hospital acquired hyponatraemia following inappropriately balanced treatment with i.v. fluids (see sections 4.2, 4.4 and 4.8).
• Drugs stimulating vasopressin release include: Chlorpropamide, clofibrate, carbamazepine, vincristine, selective serotonin reuptake inhibitors, 3.4- methylenedioxy-N-methamphetamine, ifosfamide, antipsychotics, narcotics
• Drugs potentiating vasopressin action include: Chlorpropamide, NSAIDs, cyclophosphamide
• Vasopressin analogues include: Desmopressin, oxytocin, terlipressin 
Other medicinal products increasing the risk of hyponatraemia also include diuretics in general and antiepileptics such as oxcarbazepine.

Interaction related to the presence of sodium:
-       Corticoids/Steroids and carbenoxolone, which are associated with the retention of sodium and water (with oedema and hypertension).

Interaction related to the presence of potassium:
The following combinations increase the concentration of potassium in the plasma and may lead to potentially fatal hyperkalaemia notably in case of renal failure increasing the hyperkalaemic effects:
-      Potassium-sparing diuretics (amiloride, potassium canreonate, spironolactone, triamterene, alone or in combination) (see 4.4),
-      Angiotensin converting enzyme inhibitors (ACEi) and, by extrapolation, angiotensin II receptor antagonists: hyperkalaemia potentially lethal (see 4.4), Tacrolimus, cyclosporin (see 4.4)
Administration of potassium in patients treated with such medications can produce severe and potentially fatal hyperkalaemia, particularly in patients with severe renal insufficiency.

Interaction related to the presence of magnesium:
Neuromuscular blockers such as tubocurarine, suxamethonium, and vecuronium whose effects are enhanced by the presence of magnesium.
Acetylcholine whose release and effects are reduced by magnesium salts what may contribute to neuromuscular blockade.
Aminoglycoside antibacterials and nifedipine that have additive effects with parenteral magnesium and enhanced the neuromuscular blocking.

Interaction related to the presence of acetate and gluconate (which are metabolised into bicarbonate):
Caution is advised when administering Plasma-Lyte 148 (pH 7.4) to patients treated with drugs for which renal elimination is pH dependent. Due to its alkalinizing effect (formation of bicarbonate), Plasma-Lyte 148 (pH 7.4) may interfere with the elimination of such
drugs.Renal clearance of acidic drugs such as salicylates, barbiturates and lithium may be increased because of the alkalinisation of urine by the bicarbonate resulting from acetate and gluconate metabolism.
Renal clearance of alkaline drugs such as sympathomimetics (e.g. ephedrine, pseudoephedrine) and stimulants (e.g. dexamphetamine sulphate, phenfluramine hydrochloride) may be decreased.