Budesonide + Formoterol (Budesonidum + Formoterolum)

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Budesonide + Formoterol (Budesonidum + Formoterolum)

Formoterol and budesonide should be prescribed individually, at the minimum effective dose.

If the need for additional doses of formoterol ceases to be episodic (for example, becomes more often than 2 days a week), the patient should be advised to consult with a doctor about reviewing therapy, because this may indicate a worsening of the disease.

When control of bronchial asthma symptoms is achieved during formoterol therapy, it is necessary to consider the possibility of gradually reducing the dose of the drug. Reducing the dose of formoterol is carried out under regular medical supervision of the patient’s condition. Against the background of exacerbation of bronchial asthma, you should not start treatment with formoterol or change the dosage of the drug. Formoterol should not be used to relieve acute attacks of bronchial asthma.

To ensure proper use of medications, a doctor or other health care professional must show the patient how to use the inhaler.

In children and adolescents, inhalation of budesonide and formoterol should be carried out under adult supervision.

Not intended for initial selection of therapy in the first stages of treatment of bronchial asthma.

To minimize the possibility of developing fungal infections of the oropharynx, it is necessary to rinse your mouth with water after each inhalation.

There is no data on the use of the drug to relieve acute attacks of bronchial asthma. Patients should be strongly advised to carry emergency medications with them at all times.

Treatment should not be started during an exacerbation of bronchial asthma. As with any other inhalation therapy, paradoxical bronchospasm may occur (in this case, treatment tactics should be reconsidered and, if necessary, alternative therapy should be prescribed).

The occurrence of systemic effects during inhalation therapy is less likely than when using oral glucocorticosteroids. However, it can occur when taking any inhaled glucocorticosteroids, especially when using high doses over a long period of time (it is very important to use the lowest effective dose of inhaled glucocorticosteroids that provides optimal control of asthma symptoms).

Physicians should carefully monitor the growth of children and adolescents who take long-term glucocorticosteroids in any dosage form and evaluate the balance between the benefits of glucocorticosteroid therapy and the possible risk of growth retardation.

If adrenal function has been impaired due to previous systemic glucocorticosteroid therapy, precautions should be taken when transferring patients to inhaled treatment with the drug (in patients who stop therapy with oral glucocorticosteroids, insufficient adrenal function may persist for a long time). In stressful situations, it is always necessary to remember the possibility of residual adrenal dysfunction in such patients.

Its effectiveness is comparable to the combination of salmeterol + fluticasone.

During the treatment period, it is recommended to monitor the concentration of K+ in the blood serum, as well as glucose in patients with diabetes.

Contains lactose (less than 1 mg/dose). Typically this amount does not cause problems in patients with lactose intolerance.

Budesonide-native, 0.25 mg/ml, solution for inhalation, 2ml, 10 pcs.

Inhalation.

The dosage of Budesonide-native should be individual. The initial dose in adults for the treatment of bronchial asthma and COPD is 1–2 mg/day. The dose for maintenance treatment is 0.5–4 mg/day.

After obtaining the effect, the dose is reduced to the minimum effective dose necessary to maintain a stable condition. In some cases, in patients whose treatment requires achieving a rapid therapeutic effect, the dose of the drug may be increased.

If the patient took GCS orally, transfer to treatment with Budesonide-native should be carried out when the patient’s health condition is stable; inhalations and GCS taken orally are combined for 10–14 days.

For 10 days, it is recommended to take high doses of Budesonide-native while taking oral corticosteroids in a selected dose. Subsequently, the dose of oral corticosteroids should be gradually reduced (for example, 2.5 mg of prednisolone) to the minimum possible level. In many cases, it is possible to completely stop taking oral corticosteroids. There are no data on the use of budesonide in patients with renal failure or impaired liver function. Since budesonide is eliminated through biotransformation in the liver, an increase in the duration of action of the drug can be expected in patients with severe liver cirrhosis. When prescribed to patients with liver cirrhosis, more careful monitoring is required.

Children over 16 years of age - initial dose 0.25–0.5 mg/day. If necessary, the dose can be increased to 1 mg/day. The maintenance dose is 0.25–2 mg/day.

The drug is administered using a nebulizer. The bottle contains 1 single dose.

Instructions for use

Open the bottle with the drug. Fill the nebulizer through the top hole with the required amount of the drug. Nebulization should be carried out in accordance with the instructions for the type of nebulizer used.

The volume of budesonide solution delivered to the patient's lungs by nebulizer is variable and depends on several factors, including the following:

— inhalation time;

— chamber filling level;

— technical characteristics of the nebulizer;

— the ratio of the volume during inhalation/exhalation and the tidal volume of the patient;

- use of a mouthpiece or mask.

Note.

1. After each inhalation, rinse your mouth with water.

2. If the patient uses a mask, he should make sure that the mask fits tightly to his face when inhaling. After inhalation, wash your face.

Cleaning

The nebulizer chamber should be cleaned after each use.

Wash the nebulizer chamber and mouthpiece or mask with warm water, using a mild detergent, or according to the manufacturer's instructions.

Symbicort Turbuhaler is a fixed combination of the corticosteroid budesonide and the rapid-acting β2-agonist formoterol in a single inhaler. Based on the analysis of literature data, the author concludes that Symbicort Turbuhaler can be classified as a drug that represents the standard for the rational use of a single inhaler both for continuous anti-inflammatory therapy of a chronic disease and for on-demand therapy, i.e. rescue therapy.

Since the establishment of inflammation in the airways as one of the most important pathophysiological components of asthma, inhaled glucocorticosteroids (ICS) have firmly taken a leading place in the maintenance therapy of patients with asthma [1]. This becomes understandable if we consider that inflammation in asthma is chronic and is accompanied by eosinophilia, mast cell infiltration and activation of Th-2 lymphocyte cells expressing interleukins 4, 5, 13 (IL-4, 5, 13). In addition, structural changes are found in the bronchial wall, such as hyperplasia of the mucous glands, hypertrophy and hyperplasia of smooth muscles of the respiratory tract, and subepithelial fibrosis. They are more pronounced in patients with severe asthma, although they also occur in mild stages of the disease. These changes may contribute to the development of chronic airway obstruction and reduce the response to bronchodilators or inhaled corticosteroids [2].

It has been established that long-term treatment with inhaled corticosteroids has a positive effect on pulmonary function, reduces the frequency of exacerbations and the need for hospitalization, and improves quality of life. Typically, ICS doses have been adjusted according to asthma severity, suggesting that as disease severity increases, the ICS dose should be increased, as shown in Table 1 [3]

Table 1

Equipotential doses of inhaled corticosteroids for adults [3]

* - in patients with mild asthma, a single daily dose is possible

** - when asthma symptoms are controlled, titrate the dose downwards

Inhaled corticosteroids (iGCS): mechanism of action.

Traditionally, it was believed that the onset of action of inhaled corticosteroids in patients with asthma is slow. Moreover, for such manifestations of asthma as bronchial hyperreactivity, in order to minimize its severity, treatment with inhaled corticosteroids is required for many months and even years, and at the highest possible doses [4]. At the same time, the dynamics of symptoms and clinical indicators usually occurs quickly, within a few days. Currently, new aspects of the molecular mechanism of action of GCS have become known, proving the rapid manifestation of their anti-inflammatory effect, including in patients with exacerbation of asthma [5].

The mechanism of action of budesonide does not differ from other inhaled corticosteroids. It reversibly binds to the GCS receptor (GR), a type II receptor that is located in the cytoplasm and is expressed in all tissues and cells. After binding to GR, the GR + budesonide complex quickly moves to the cell nucleus. Some genes in their promoter part have regions for recognition of activated GR, known as GCS-responsive elements (GRE), which are activated upon interaction with GR. An example indicating gene activation under the influence of GCS is the ß2 receptor. An in vivo study in human lungs revealed a very rapid (within 2 hours) and significant increase in the number of ß2 receptors after exposure to corticosteroids [6]. GCS activate an important anti-inflammatory enzyme - phosphatase-1 - mitogen-activated protein kinase (MCP-1), which is an endogenous inhibitor of the pro-inflammatory pathways of mitogen-activated protein kinase (MAP). GCS quickly increase mRNA expression in MKP-1 tenfold within 2 hours after administration, and the protein level in MKP-1 increases within 4 hours, and this is accompanied by inhibition of MAP [7]. However, the main anti-inflammatory effects of GCS are due to the suppression of inflammatory genes activated by transcription of pro-inflammatory factors, such as the nuclear factor NFκB, which activates transcription by acetylation of the histone core around which DNA is wrapped. Activated GR connects the nuclear enzyme histone deacetylase-2 to a complex of activated inflammatory genes, resulting in deacetylation of the histone core and suppression of inflammatory genes [8]. Thus, the key action of histone deacetylase-2 is to deacetylate the acetylated form of GR so that it can inhibit the nuclear factor NFκB [9]. Time-lapse studies have shown that these effects of GCS appear very quickly, within minutes. Once inflammatory genes stop producing the proteins they encode, such as cytokines, they decay at a rate determined by the stability of their mRNA. For many inflammatory genes, such as granulocyte-macrophage colony-stimulating factor and chemokines, this breakdown occurs relatively quickly and therefore a significant decrease in cytokine or chemokine secretion occurs within 6-12 hours. This indicates that GCS have a relatively rapid anti-inflammatory effect in vitro.

Pharmacokinetics of iGCS.

Halogenation of CS led to the synthesis of unique drugs that retained high glucocorticosteroid activity when applied locally and changed pharmacokinetic parameters. ICS are rapidly absorbed from the cell membrane, for example, the peak concentration in the blood after inhalation of budesonide is reached after 20 minutes and is maintained for 1-2 hours. ICS quickly undergo a first-pass effect through the liver, leading to almost complete destruction of the ICS during the first passage through the liver (fluticasone, mometasone furoate, ciclesonide) (Table 2).

table 2

Pharmacological properties of ICS