Lordestin, 5 mg 10 pcs.

Lordestin is an anti-allergic.

Pharmacodynamics

H₁-histamine receptor blocker, is the primary active metabolite of loratadine. Suppresses the release of histamine and LT C4 from mast cells. Prevents the development and facilitates the course of allergic reactions. It has anti-allergic, antipruritic and antiexudative effects. Reduces capillary permeability, prevents the development of tissue edema. It has practically no sedative effect and when used in therapeutic doses it does not influence the speed of psychomotor reactions.

Pharmacokinetics

Intake

After oral administration desloratadine is well absorbed from the GI tract, with detectable plasma concentrations of desloratadine being reached within 30 minutes. After a single dose of 5 or 7.5 mg, C_max is reached after approximately 3 h (2-6 h). The bioavailability of desloratadine is proportional to the dose (in the dose range of 5-20 mg).

Distribution

The binding of desloratadine to plasma proteins is 83-87% and that of 3-hydroxydesloratadine is 85-89%. When used in dose from 5 mg to 20 mg once a day for 14 days no signs of clinically significant cumulation of desloratadine were found. Concomitant intake of food or simultaneous consumption of grapefruit juice does not affect bioavailability and distribution of desloratadine (when administered at a dose of 7.5 mg once daily). It does not penetrate through the HEB.

Metabolism and excretion

It is extensively metabolized in the liver to 3-hydroxydesloratodine, which is then glucuronized. The main route of dezloratadine metabolism is hydroxylation. It is not an inhibitor of CYP3A4 and CYP2D6 isoenzymes and is not a substrate or inhibitor of P-glycoprotein. Desloratadine is excreted as a glucuronide compound and in small amounts in unchanged form (less than 2% by the kidneys and less than 7% through the intestine). T_1/2 for both desloratadine and 3-hydroxydesloratadine is 20-30 h (average – 27 h).

Cronic renal failure (CKD). C_max and AUC of desloratadine increase from 1.2 to 1.7 times and from 1.9 to 2.5 times, respectively (compared with data of healthy volunteers). Concentration of 3-hydroxydesloratadine changes insignificantly. Binding of desloratadine and 3-hydroxydesloratadine to plasma proteins in CKD does not change. Desloratadine and 3-hydroxydesloratadine are poorly excreted by hemodialysis.

Hepatic failure. In patients with hepatic impairment AUC is increased by 2.4 times compared to data of healthy volunteers. Total clearance of desloratadine when administered orally in patients with mild, moderate and severe hepatic impairment is 37, 36 and 28% respectively (as compared to data of healthy volunteers). There is an increase in T_1/2 of desloratadine in patients with hepatic impairment. The C_max and AUC of 3-hydroxydesloratadine in patients with hepatic impairment are not different from those in healthy subjects with normal liver function.

Indications

Seasonal allergic rhinitis (to relieve the following symptoms – sneezing, rhinorrhea, itching, nasal congestion, itchy eyes, lacrimation, red eyes, itching in the palate, cough); chronic idiopathic urticaria (skin itching and rash).

Pharmacological effect

Lordestin is antiallergic.

Pharmacodynamics

H1-histamine receptor blocker, is the primary active metabolite of loratadine. Suppresses the release of histamine and LT C4 from mast cells. Prevents the development and facilitates the course of allergic reactions. It has antiallergic, antipruritic and antiexudative effects. Reduces capillary permeability, prevents the development of tissue edema. It has virtually no sedative effect and, when taken in therapeutic doses, does not affect the speed of psychomotor reactions.

Pharmacokinetics

Suction

After taking the drug orally, desloratadine is well absorbed from the gastrointestinal tract, and detectable concentrations of desloratadine in the blood plasma are achieved within 30 minutes. After a single dose of 5 or 7.5 mg, Cmax is achieved in approximately 3 hours (2–6 hours). The bioavailability of desloratadine is dose proportional (dose range 5–20 mg).

Distribution

Plasma protein binding of desloratadine is 83–87%, and 3-hydroxydesloratadine is 85–89%. When used in a dose of 5 mg to 20 mg 1 time per day for 14 days, no signs of clinically significant accumulation of desloratadine were detected. Concomitant food intake or simultaneous consumption of grapefruit juice does not affect the bioavailability and distribution of desloratadine (when taken at a dose of 7.5 mg 1 time per day). Does not penetrate the BBB.

Metabolism and excretion

It is extensively metabolized in the liver to 3-hydroxydesloratodine, which is then glucuronidized. The main route of metabolism of desloratadine is hydroxylation. It is not an inhibitor of CYP3A4 and CYP2D6 isoenzymes and is not a substrate or inhibitor of P-glycoprotein. Desloratadine is excreted from the body in the form of a glucuronide compound and in small amounts unchanged (by the kidneys – less than 2% and through the intestines – less than 7%). T1/2 for both desloratadine and 3-hydroxydesloratadine is 20–30 hours (average 27 hours).

Chronic renal failure (CRF). Cmax and AUC of desloratadine increase from 1.2 to 1.7 times and from 1.9 to 2.5 times, respectively (compared to data from healthy volunteers). The concentration of 3-hydroxydesloratadine changes slightly. The binding of desloratadine and 3-hydroxydesloratadine to plasma proteins does not change in chronic renal failure. Desloratadine and 3-hydroxydesloratadine are poorly excreted by hemodialysis.

Liver failure. In patients with liver failure, AUC increases 2.4 times compared to healthy volunteers. The overall oral clearance of desloratadine in patients with mild, moderate and severe hepatic impairment is 37, 36 and 28%, respectively (compared with data in healthy volunteers). There is an increase in T1/2 of desloratadine in patients with liver failure. The Cmax and AUC of 3-hydroxydesloratadine in patients with hepatic impairment do not differ from those in healthy subjects with normal liver function.

Special instructions

Impact on the ability to drive vehicles and operate machinery

There was no observed effect of Lordestin when used in recommended doses on the ability to drive vehicles and operate machinery.

However, given that patients may experience drowsiness, caution is recommended if central nervous system side effects occur.

Active ingredient

Desloratadine

Composition

Active ingredient:

desloratadine hemisulfate 5.788 (equivalent to 5 mg desloratadine);

Excipients:

MCC – 39 mg;

calcium hydrogen phosphate dihydrate – 46.712 mg;

pregelatinized starch – 7 mg;

colloidal silicon dioxide (Aerosil) – 0.5 mg;

magnesium stearate – 1 mg;

Film casing:

Opadry AMB yellow 80W22099 (partially hydrolyzed polyvinyl alcohol, titanium dioxide, talc, lecithin, aluminum varnish based on quinoline yellow dye, xanthan gum, iron oxide yellow, aluminum varnish based on indigo carmine dye)

Pregnancy

The drug is contraindicated during pregnancy.

Since desloratadine is excreted in breast milk, the use of the drug during lactation (breastfeeding) is contraindicated.

Contraindications

hypersensitivity to the components of the drug;
pregnancy;
lactation period;
children’s age up to 12 years.

With caution: severe renal failure.

Side Effects

The most common side effects: fatigue (1.2%), dry mouth (8%), headache (0.6%).

Side effects according to post-marketing studies.

From the central nervous system: dizziness, hallucinations, psychomotor hyperreactivity, insomnia, drowsiness.

From the cardiovascular system: tachycardia, palpitations.

From the digestive system: abdominal pain, dyspepsia (including nausea, vomiting, diarrhea), hyperbilirubinemia, increased activity of liver enzymes, hepatitis.

Allergic reactions: skin rash, itching, urticaria, angioedema, anaphylactic shock.

Other: dysmenorrhea, increased fatigue, myalgia.

Interaction

When used together with ketoconazole, erythromycin, azithromycin, fluoxetine and cimetidine, no clinically significant changes in plasma concentrations of desloratadine were detected.

Lordestin does not enhance the inhibitory effect of ethanol on psychomotor function.

Overdose

Symptoms: drowsiness.

Treatment: gastric lavage, activated carbon, symptomatic therapy. The drug is not eliminated by hemodialysis. The effectiveness of peritoneal dialysis has not been established.

Storage conditions

At a temperature not exceeding 25 °C

Shelf life

4 years

Manufacturer

Gedeon Richter, Hungary