indication

For the treatment of infections caused by susceptible strains of microorganisms, such as Rocky Mountain spotted fever, typhus fever and the typhus group, Q fever, rickettsial pox and tick fevers caused by Rickettsiae, upper respiratory tract infections caused by Streptococcus pneumoniae and for the treatment of asymptomatic carriers of Neisseria meningitidis.

pharmacology

Minocycline, the most lipid soluble and most active tetracycline antibiotic, is, like doxycycline, a long-acting tetracycline. Minocycline's effects are related to the inhibition of protein synthesis. Although minocycline's broader spectrum of activity, compared to other members of the group, includes activity against Neisseria meningitidis, its use as a prophylaxis is no longer recomended because of side effects (dizziness and vertigo). Current research is examining the possible neuroprotective effects of minocycline against progression of Huntington's Disease, an inherited neurodegenerative disorder. The neuroprotective action of minocycline may include its inhibitory effect on 5-lipoxygenase, an inflammatory enzyme associated with brain aging.

mechanism of action

Minocycline passes directly through the lipid bilayer or passively diffuses through porin channels in the bacterial membrane. Tetracyclines like minocycline bind to the 30S ribosomal subunit, preventing the binding of tRNA to the mRNA-ribosome complex and interfering with protein synthesis.

toxicity

Minocycline has been observed to cause a dark discoloration of the thyroid in experimental animals (rats, minipigs, dogs and monkeys). In the rat, chronic treatment with minocycline has resulted in goiter accompanied by elevated radioactive iodine uptake and evidence of thyroid tumor production. Minocycline has also been found to produce thyroid hyperplasia in rats and dogs. LD₅₀=2380 mg/kg (rat, oral), LD₅₀=3600 mg/kg (mouse, oral)

biotransformation

Hepatic.

absorption

Rapidly absorbed from the gastrointestinal tract and absorption is not significantly impaired by ingestion of food or milk. Oral bioavailability is 100%.

half life

11-22 hours

drug interactions

Acenocoumarol: The tetracycline, minocycline, may increase the anticoagulant effect of acenocoumarol.

Acitretin: Increased risk of intracranial hypertension.

Aluminium: Formation of non-absorbable complexes

Amoxicillin: Possible antagonism of action

Ampicillin: Possible antagonism of action

Anisindione: The tetracycline, minocycline, may increase the anticoagulant effect of anisindione.

Attapulgite: Formation of non-absorbable complexes

Azlocillin: Possible antagonism of action

Aztreonam: Possible antagonism of action

Bacampicillin: Possible antagonism of action

Bexarotene: Tetracycline derivatives like minocycline may enhance the adverse/toxic effect of Retinoic Acid Derivatives. Due to the risk of developing pseudotumor cerebri (also known as intracranial hypertension), avoid this combination of drugs if possible. If used concomitantly, monitor for evidence of this interaction (eg, dizziness, diplopia, headache).

Bismuth Subsalicylate: Formation of non-absorbable complexes

Calcium: Formation of non-absorbable complexes

Calcium Acetate: Calcium salts such as calcium acetate may decrease the serum concentration of tetracycline derivatives such as minocycline. In general, the coadministration of oral calcium salts and oral tetracycline derivatives should be avoided. Interactions may be able to be minimized by administering oral calcium preparations several hours before or after the dose of the oral tetracycline derivatives. Even with dose separation, therapy may still be compromised. Monitor for decreased therapeutic effect of oral tetracycline derivatives.

Calcium Chloride: Calcium salts such as calcium chloride may decrease the serum concentration of tetracycline derivatives such as minocycline. In general, the coadministration of oral calcium salts and oral tetracycline derivatives should be avoided. Interactions may be able to be minimized by administering oral calcium preparations several hours before or after the dose of the oral tetracycline derivatives. Even with dose separation, therapy may still be compromised. Monitor for decreased therapeutic effect of oral tetracycline derivatives.

Carbenicillin: Possible antagonism of action

Clavulanate: Possible antagonism of action

Cloxacillin: Possible antagonism of action

Colesevelam: Bile acid sequestrants such as colesevelam may decrease the absorption of Tetracycline Derivatives. Monitor for decreased therapeutic effects of tetracycline derivatives if coadministered with a bile acid sequestrant. If these agents are used concomitantly, separate doses 2 or more hours to minimize the interaction. The manufacturer of colesevelam suggests that drugs should be administered at least 1 hour before or 4 hours after colesevelam.

Cyclacillin: Possible antagonism of action

Dicloxacillin: Possible antagonism of action

Dicumarol: The tetracycline, minocycline, may increase the anticoagulant effect of dicumarol.

Ethinyl Estradiol: This anti-infectious agent could decrease the effect of the oral contraceptive

Etretinate: Increased risk of intracranial hypertension

Flucloxacillin: Possible antagonism of action

Hetacillin: Possible antagonism of action

Iron: Formation of non-absorbable complexes

Iron Dextran: Formation of non-absorbable complexes

Isotretinoin: Increased risk of intracranial hypertension

Magnesium: Formation of non-absorbable complexes

Magnesium oxide: Formation of non-absorbable complexes

Magnesium salicylate: Formation of non-absorbable complexes

Mestranol: This anti-infectious agent could decrease the effect of the oral contraceptive

Methicillin Acyl-Serine: Possible antagonism of action

Methoxyflurane: The tetracycline, minocycline, may increase the renal toxicity of methoxyflurane.

Mezlocillin: Possible antagonism of action

Nafcillin: Possible antagonism of action

Oxacillin: Possible antagonism of action

Penicillin G: Possible antagonism of action

Penicillin V: Possible antagonism of action

Piperacillin: Possible antagonism of action

Pivampicillin: Possible antagonism of action

Pivmecillinam: Possible antagonism of action

Tazobactam: Possible antagonism of action

Ticarcillin: Minocycline may reduce the effect of Ticarcillin by inhibiting bacterial growth. Ticarcillin exerts its effects on actively growing bacteria. To achieve synergism, Ticarcillin should be administered at least 2 hours prior to using Minocycline.

Tretinoin: Minocycline may increase the adverse effects of oral Tretinoin. Increase risk of pseudotumour cerebri. Concurrent therapy should be avoided.

Trisalicylate-choline: Formation of non-absorbable complexes

Warfarin: The tetracycline, minocycline, may increase the anticoagulant effect of warfarin.

Zinc: Formation of non-absorbable complexes