Drug-induced edema: Certain medications can induce edema by enhancing sodium and water reabsorption by the kidneys. Potent vasodilators such as minoxidil and diazoxide are good examples. Other drugs that can cause edema include calcium channel blockers, which lead to capillary leakage due to dilation of the precapillary sphincter,13 and the NSAIDs, which induce edema formation through different mechanisms by inhibiting renal prostaglandin synthesis. They can also exacerbate edema in patients with underlying HF or cirrhosis.14 Antidepressants, estrogens, corticosteroids, and COX-2 inhibitors can also cause peripheral edema.
Nippon Rinsho. 2005 Jan;63(1):102-6.
Kaizu K, Abe M.
It is well known that there are many drugs which induce edema. Drug-induced edema can be divided into three types by the mechanism as follows, 1) sodium overload, 2) renal dysfunction and 3) hyperpermeability of blood vessel.
Ann Intern Med. 1989 Nov 15;111(10):859.
Vitamin E deficiency and peripheral edema.
Peripheral edema due to increased vascular permeability: a clinical appraisal
Comp Biochem Physiol C. 1992 Jun;102(2):325-7.Links
Effects of copper, iron and zinc on oedema formation induced by phospholipase A2.
Ferrer X, Moreno JJ.
1. Intradermal or subplantar injection of soluble snake venom phospholipase A2 (PLA2) evoked a brisk inflammatory response, with cutaneous vascular permeability increase and paw oedema. 2. These inflammatory processes are mainly the result of arachidonic acid cascade activation and mast cell degranulation. 3. Copper, iron and zinc have an inhibitory effect on vascular permeability increase and paw oedema induced by PLA2. 4. Copper and iron could have not only a direct effect on PLA2 but on enzymes of arachidonic acid cascade. 5. However, zinc have a moderate antiinflammatory activity. This effect could be the result to inhibit PLA2 induced mast cell degranulation.
The adverse events most strongly associated with TYSABRI therapy compared to placebo in AFFIRM were fatigue and allergic reaction. Adverse events in SENTINEL associated with add-on therapy compared to AVONEX alone were anxiety, pharyngitis, sinus congestion and peripheral edema.
For instance, phosphorus and zinc have both left-sided cell receptors, so if either level is low in ratio to calcium, calcification would only take place on the left side of the body, whereas the cell receptors of manganese or magnesium are right-sided, as a result, any calcification would develop on the right side of the body only.
Many therapeutic agents cause renal Mg wasting and subsequent deficiency. These include loop and thiazide diuretics, aminoglycosides, cisplatin, pentamidine, and foscarnet... Refractory hypokalemia [jl: low potassium] and hypocalcemia can be caused by concomitant hypomagnesemia and can be corrected with Mg therapy. The dose and route of administration of Mg in the treatment of hypomagnesemia is dictated by the clinical presentation, the degree of Mg deficiency, and the renal function.
Magnesium affects blood pressure by modulating vascular tone and reactivity. It acts as a calcium channel antagonist, it stimulates production of vasodilator prostacyclins and nitric oxide and it alters vascular responses to vasoactive agonists. Magnesium deficiency has been implicated in the pathogenesis of hypertension with epidemiological and experimental studies demonstrating an inverse correlation between blood pressure and serum magnesium levels.
A small pilot study suggests that magnesium may prevent or delay progression of vascular calcification in hemodialysis patients without a detrimental effect on bone, researchers reported here at the 2008 Annual Dialysis Conference...
When used as the principal phosphate binder for 18 months, Dr. Spiegel concluded, magnesium carbonate/calcium carbonate provided excellent control of serum phosphorus, prevented progression of vascular calcification and did not worsen BMD.
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