Drugs Effects on Nutritional Status

Loop Diuretics (furosemide):
-Excretion of sodium, chloride, potassium, hydrogen ion, calcium, magnesium, ammonium, bicarbonate and possibly phosphate is enhanced.
-After 4 weeks of furosemide use, thiamin concentrations and transketolase activity was significantly reduced.

Thiazide Diuretics (hydrochlorthiazide) :
-Excretion of sodium, chloride, potassium, bicarbonate, magnesium, phosphate and iodine are enhanced.
-Calcium excretion is decreased.

Triamterene containing diuretics (Dyazide, Dyrenium, Maxzide):
-Triamterene is potassium sparing, supplementation could result in potassium overload.
-Folic acid deficiency is possible.

Histamine H2. Antagonists (Tagamet, Zantac, Pepcid, Axid):
-Reduction of gastric acid secretion resulting in mal digestion of protein.
-decreased vitami
B12 gastric acid is required for B12 absorption.
-Tagamet inhibits cytochrome P-450 pathways.

Biquanides (Metforman):
-Interferes with glucose absorption.
-Decreases absorption of B12.

Potassium Chloride:
-Interferes with the absorption of B12

Sulfasalazine:
-Interferes with folic acid metabolism

Oral Contraceptives:
-Oral contraceptives have significantly increased plasma vitami
A levels. This is thought to be mediated by steroid induced alterations in the rate of retinal-binding protein synthesis and release, depletion of reserves may result.
-Vitamin B6 deficiencies due to alteration in B6 arid tryptophan metabolism.
-Interference with folate absorption.
-Reduced serum B12 levels.
-Increased serum copper as a result of increased plasma ceruloplasm, clinical importance has not been determined.
-Increased serum iron and increased total iron-binding capacity along with increased incidence of iron deficiency anemia.
-Increased serum magnesium and zinc, clinical importance has not been determined.

Corticosteroids ( hyrocortisone, prednisone, dexamethasone etc..):
-Corticosteroids increase the rate of vitami
A transport from the liver, resulting in elevated serum levels and depletion of reserves.
-Negative nitrogen balance due to increased protein catabolism.
-Increased calcium excretion (increased catabolism).
-Sodium retention (mineralocorticoid activity).
-Increased potassium excretion ( sodium is exchanged for potassium).
-May deplete B6, B12 and folic acid.
-May deplete D3.

Bile acid sequestrants (Questran):
-Interference with absorption of fats and fat soluble vitamins.
-Enhanced absorption of chloride ions in exchange for bicarbonate ions which may lead to acidosis.
-Increased urinary calcium excretion.
-Increased urinary magnesium excretion.
-Altered absorption of phosphate and nitrogen.
-Vitamin K deficiency
-Reduced folic acid absorption.
-Reduced absorption of Vitamin E and iron are possible.

HMG-CoA reductase inhibitors (Zocor, Mevacor, Pravachol ):
-block the biosynthesis of Coenzyme Q-10

Levodopa:
-Pyridoxine reverses the effects of levodopa, although this does not occur when levodopa is given with carbadopa.( Pyridoxine stimulates decarboxylation of levodopa in the periphery, carbadopa inhibits decarboxylation.)

Phenytoin(Dilantin):
-Folate deficiency ( increased folate catabolism or utilization as a result of enzyme induction is considered to be the mechanism. However, supplementation may decrease the effectiveness of the phenytoin).
-Interference with vitami
D metabolism.

Folic acid analogues (methotrexate, pyrimethamine, trimethoprin):
-These antagonists inhibit the enzyme dihydrofolate reductase which can lead to a functional folate deficiency. Supplementation can antagonize the effect of these drugs.

NSAIDS (Motrin, Naprosyn, Tylenol,ASA etc...) :
-Reduce night time melatonin secretion ( related to prostaglandin inhibition).

Isoniazid:
-Increases excretion of pyridoxine into the urine resulting in deficiency.
-Inhibits tryptophan to niacin pathway resulting in increased need for niacin and tryptophan. n