Mepolizumab — side effects, herpes, infections, and consequences of long-term treatment

EFFECTIVE | TOXIC

What names the drug is known by

The international nonproprietary name of the drug is mepolizumab. The Latin spelling is mepolizumab. English-language prescribing information and medical documents may use the terms mepolizumab injection, mepolizumab for injection, and anti-IL-5 monoclonal antibody. The main trade name is Nucala. Mepolizumab is a recombinant humanized IgG1κ monoclonal antibody that binds to interleukin-5. It is a large protein molecule, so the drug has no salts, esters, or other low-molecular-weight derivatives.

Dosage forms include a lyophilized powder in a vial for preparation of a solution, a ready-to-use solution in a prefilled syringe, and a solution in an autoinjector. Depending on age and disease, doses of 40, 100, or 300 mg are administered subcutaneously once every four weeks. The 300 mg dose is given as three separate 100 mg injections. There are no combination medicines containing mepolizumab together with another active substance. Unintentional duplicate dosing may occur through accidental repeat administration, use of several devices instead of one, or confusion between the 100 mg and 300 mg regimens.

Mepolizumab is used as add-on maintenance therapy for severe eosinophilic asthma. Depending on national approval, the drug is also used for chronic rhinosinusitis with nasal polyps, the eosinophilic phenotype of chronic obstructive pulmonary disease, eosinophilic granulomatosis with polyangiitis, and hypereosinophilic syndrome. Age restrictions vary by indication, so a pediatric dosing regimen for one disease must not automatically be applied to another.

Why the drug is considered harmless and where the real risk begins

The main danger of mepolizumab is not classic chemical toxicity to the liver or kidneys, but systemic hypersensitivity reactions and prolonged interference with IL-5-dependent regulation of eosinophils. After an injection, anaphylaxis, angioedema, bronchospasm, generalized urticaria, widespread rash, and a drop in blood pressure may occur. Such reactions may develop immediately, after several hours, or with a delay of several days, when the patient may no longer associate the deterioration with the administered drug.

A false sense of safety can arise after several well-tolerated injections. Mepolizumab does not usually cause liver pain, changes in urine color, or other obvious signs of organ toxicity, so the patient may assume that the body is not reacting to treatment at all. However, each dose suppresses the maturation, activation, and survival of eosinophils for several weeks. This is the intended therapeutic effect in eosinophilic disease, but at the same time it interferes with the physiological functions of eosinophils, including their role in antiparasitic defense.

A confirmed infectious safety signal is herpes zoster associated with reactivation of Varicella zoster virus. This does not mean that mepolizumab automatically causes cold sores, genital herpes, or any viral infection. However, a painful unilateral vesicular rash, particularly on the face, head, chest, or back, requires early diagnosis. Delayed antiviral therapy increases the likelihood of postherpetic neuralgia and complications involving the eye, ear, or nervous system.

Mepolizumab must not be used as an emergency treatment. It does not immediately dilate the bronchi and is not intended to relieve an acute asthma attack, status asthmaticus, or sudden worsening of chronic obstructive pulmonary disease. A repeat injection because breathlessness persists will not restore breathing, but it will increase systemic exposure to the antibody for the following weeks.

No confirmed direct interaction with alcohol has been established. However, alcohol can impair coordination during self-injection, reduce critical assessment of symptoms, and mask dizziness, weakness, or developing hypotension. Drinking alcohol at the same time can also make it more difficult to determine the cause of a deterioration in well-being.

Side effects after the first dose and during the first weeks of treatment

Common reactions include headache, pain, redness, swelling, itching, or burning at the injection site, fatigue, and back pain. Muscle pain or spasms, itchy skin, eczema, dizziness, nausea, and upper abdominal pain may also occur. Some of these complaints occur almost as frequently in patients who are not receiving mepolizumab, so an isolated nonspecific symptom does not by itself prove a toxic effect of the drug.

More informative signs are recurrence of the reaction after each injection, its temporal relationship to administration, and the combination of several symptoms. For example, a headache without other manifestations may be incidental, whereas a headache accompanied by urticaria, swelling of the lips, stridor, or a drop in blood pressure requires immediate assessment for systemic hypersensitivity.

Clinically significant allergic reactions may present with generalized itching, widespread rash, urticaria, flushing, swelling of the face, lips, or tongue, a sensation of tightness in the throat, increasing shortness of breath, bronchospasm, dizziness, and reduced blood pressure. A higher dose consisting of three injections is used in eosinophilic granulomatosis with polyangiitis, so the patient should be particularly alert to systemic symptoms after administration.

A life-threatening reaction is anaphylaxis with laryngeal edema, severe bronchospasm, marked hypotension, fainting, or impaired consciousness. Good tolerance of previous doses does not guarantee that a reaction will not occur after the next injection. Waiting for spontaneous improvement when there is tongue swelling, stridor, or a fall in blood pressure increases the risk of respiratory and cardiovascular decompensation.

Herpes zoster requires particular attention. Early symptoms may include burning, tingling, skin pain, and increased sensitivity to touch, followed only later by the appearance of grouped vesicles. Involvement of the face, eyelid, tip of the nose, external auditory canal, or scalp requires urgent assessment because of the risk of ophthalmic and neurological complications.

There is no convincing evidence that the risk of ordinary herpes simplex is increased. Therefore, recurrence of cold sores or genital herpes should not automatically be regarded as a side effect of mepolizumab. Herpes simplex must be distinguished from herpes zoster, contact dermatitis, bacterial skin infection, and drug-induced rash.

Side effects with long-term and repeated use

Long-term treatment has not revealed a characteristic pattern of cumulative hepatotoxicity, nephrotoxicity, cardiotoxicity, neurotoxicity, bone marrow suppression, or hormonal toxicity. Mepolizumab does not cause physiological dependence, euphoria, or a typical withdrawal syndrome. This allows the drug to be classified as non-toxic by the criterion of classic organ toxicity, but it does not make it completely risk-free.

The terminal half-life is approximately 16–22 days. When administered once every four weeks, the drug concentration gradually reaches steady state. After treatment is stopped, the antibody does not disappear from the body on the day a scheduled injection is missed; its effect gradually diminishes over several weeks.

Long-term suppression of IL-5 does not cause universal immunodeficiency, but it alters one component of immune regulation. Therefore, in cases of recurrent infections, unusually severe herpes zoster, or helminth infection, it is necessary to assess not only mepolizumab but also the total immunopharmacological burden: systemic glucocorticosteroids, cytostatics, immunosuppressants, age, and comorbid conditions.

Antibodies to mepolizumab are detected in a small proportion of patients. Neutralizing antibodies are rare, and their clinical significance remains limited. Loss of efficacy is more often associated not with immunogenicity of the drug, but with inappropriate patient selection, a change in the disease phenotype, poor adherence to background therapy, or development of irreversible airway remodeling.

Dedicated long-term carcinogenicity studies have not been performed for mepolizumab. Clinical observations have not identified a consistent tumor signal, but the role of eosinophils in antitumor immune surveillance is complex. Therefore, there is no basis for claiming that the drug causes tumors, although it is also premature to declare this question definitively resolved.

The absence of early adverse reactions does not mean that treatment should continue indefinitely without assessment of benefit. The need for therapy should be reassessed according to the frequency of exacerbations, the need for systemic steroids, symptom control, lung function, and activity of the underlying disease. If there is no objective response, continuing biological therapy solely because the drug is well tolerated is not pharmacologically justified.

Contraindications and higher-risk groups

An absolute contraindication is previously established hypersensitivity to mepolizumab or its excipients. After anaphylaxis, angioedema, severe bronchospasm, or marked hypotension, re-administration creates a risk of recurrence and requires reconsideration of treatment.

Active helminth infection should be excluded before therapy is started. Eosinophils participate in the antiparasitic immune response, and patients with known helminth infections were generally not included in the main clinical trials. If a parasitic infection develops during treatment and does not respond to antiparasitic therapy, mepolizumab is temporarily discontinued until the infection resolves.

Parasitological risk is particularly important for patients who live in or spend prolonged periods in tropical regions where strongyloidiasis, toxocariasis, and other tissue helminth infections are prevalent. Suppression of eosinophilia may reduce a laboratory marker of infection without eliminating the parasite itself, so normalization of the eosinophil count after administration of the drug must not be mistakenly regarded as evidence of cure.

A previous episode of herpes zoster is not an absolute contraindication. However, before treatment begins, indications for vaccination against herpes zoster should be assessed, especially in older patients, people with immunodeficiency, and patients receiving systemic glucocorticosteroids or other immunosuppressants.

During pregnancy, controlled data are insufficient for a definitive assessment of risk. Monoclonal antibodies cross the placenta more actively during the second and third trimesters. At the same time, severe uncontrolled asthma increases the risk of hypoxia, preeclampsia, fetal growth restriction, and preterm birth. Therefore, automatically discontinuing effective therapy may be more dangerous than continuing treatment.

Age restrictions depend on the disease. In severe eosinophilic asthma, the drug may be used in children, whereas for some other indications it is approved only for adults or adolescents. An adult dose and device must not be used in a child without checking the regimen appropriate to the specific diagnosis and age.

Mepolizumab is not intended to relieve acute bronchospasm. This restriction is not because the drug worsens an attack, but because it has no rapid bronchodilator action. Replacing a rescue medication with mepolizumab creates a direct risk of severe respiratory failure.

Dangerous interactions

Formal drug interaction studies have been limited. Mepolizumab is not metabolized by the cytochrome P450 system and is degraded by proteolytic enzymes, so classic interactions through CYP3A4, CYP2D6, or CYP2C9 are unlikely.

Re-administration after confirmed severe hypersensitivity is contraindicated. This is not a metabolic interaction, but it is the most dangerous situation involving repeat exposure of a sensitized individual.

Abrupt discontinuation of systemic or inhaled glucocorticosteroids after starting mepolizumab is strongly undesirable. Sudden withdrawal of a systemic steroid can cause adrenal insufficiency, profound weakness, hypotension, nausea, muscle pain, hypoglycemia, and recurrence of the previously suppressed disease. These symptoms may mistakenly be interpreted as a side effect of mepolizumab.

Combination with cytostatics, systemic immunosuppressants, and other biological medicines requires individualized monitoring. No direct pharmacokinetic conflict has been established, but the overall immunosuppressive burden may increase the risk of infections and make it difficult to determine the cause of an allergic reaction.

No confirmed interaction with food, caffeine, nicotine, or alcohol has been established. This means there is no known mechanism by which these substances alter the concentration of mepolizumab; it does not prove that every combination is safe. Starting several medicines, dietary supplements, and herbal products at the same time makes it more difficult to determine the cause of rash, edema, bronchospasm, hypotension, or dyspepsia.

There are no combination medicines containing mepolizumab. Unintentional overdose does not arise from tablets, nasal preparations, or inhalers, but from repeat injections, confusion between devices, and accidentally using three syringes instead of one.

Patient errors

The most dangerous mistake is expecting immediate relief of breathlessness. Mepolizumab is a maintenance biological therapy and does not replace a rapid-acting bronchodilator. Attempting to wait out a worsening attack in the expectation that previously administered Nucala will work may lead to status asthmaticus.

During home administration, errors may include giving a repeat injection because of uncertainty about whether the autoinjector worked, shortening the four-week interval, using another person's medication, using a damaged device, or injecting the solution into inflamed, hardened, painful, or injured skin. If the patient is uncertain whether the full dose was received, the injection must not be repeated without professional advice.

A common error is confusion between dosing regimens. A dose of 100 mg is used for most respiratory indications. A dose of 300 mg is used for eosinophilic granulomatosis with polyangiitis and hypereosinophilic syndrome and is administered as three separate injections. It is not a universal intensified dose for inadequately controlled asthma.

If a dose is missed, a double dose must not automatically be administered. Shortening the interval without medical guidance increases the duration of excessive exposure, which cannot be rapidly reversed once the injection has been given.

It is dangerous to discontinue prednisolone or an inhaled glucocorticosteroid immediately after improvement without medical supervision. Mepolizumab may reduce the need for steroids, but it does not eliminate the need for gradual dose reduction or monitoring of adrenal function after prolonged systemic therapy.

A painful unilateral vesicular rash must not be ignored. It may be herpes zoster. Swelling of the lips or tongue, stridor, widespread urticaria, increasing shortness of breath, profound weakness, dizziness, and fainting may indicate anaphylaxis.

The everyday assumption that an injectable medication prescribed by a specialist cannot be overdosed at home is incorrect. An autoinjector simplifies administration but does not protect against repeated use of multiple devices, use of the wrong dose, or shortening of dosing intervals.

Overdose and poisoning

A toxic single dose and a critical cumulative dose of mepolizumab have not been established. No characteristic dose-dependent poisoning syndrome has been described, and there is no specific antidote. After excessive administration, breathing, blood pressure, consciousness, skin manifestations, and signs of systemic hypersensitivity should be monitored.

Administration of 300 mg does not by itself mean poisoning, because this is a therapeutic dose for certain diseases. Overdose occurs when three 100 mg injections are mistakenly given to a patient who was prescribed one injection, or when a dose is repeated because of uncertainty about whether the autoinjector functioned correctly.

Impaired liver or kidney function does not usually cause hidden accumulation of mepolizumab. The drug is not eliminated primarily by the kidneys and does not undergo conventional hepatic metabolism. Standard dose adjustment for renal or hepatic impairment is not предусмотрена. However, severe comorbid disease may reduce tolerance of anaphylaxis, bronchospasm, or hypotension.

The classic course of poisoning consisting of early nausea followed by liver or kidney injury is not characteristic of mepolizumab. The main observed danger is an allergic reaction, which may develop immediately or several hours and even days later.

Because the half-life is 16–22 days, an antibody that has already been administered remains in the body for weeks. Gastric lavage, sorbents, and forced diuresis are meaningless because the drug is given subcutaneously and is a large protein molecule. Hemodialysis is likewise not considered an effective method for removing a monoclonal antibody.

Emergency care is required for swelling of the face, tongue, or larynx, stridor, severe bronchospasm, widespread urticaria, a sharp fall in blood pressure, fainting, or impaired consciousness. It is not appropriate to wait for a complete picture of poisoning to develop: delaying treatment of anaphylaxis directly worsens the prognosis.

An integrative alternative with a lower toxicological burden

For stable allergic or eosinophilic inflammation of the airways, a multi-target combination has been selected: Nigella sativa, Boswellia serrata, Punica granatum, Atractylodes lancea, and Scutellaria baicalensis. Punica granatum is represented by an industrially standardized 10% extract. The formula has not undergone a clinical trial as a single five-component preparation, so the proposed synergy is based on pharmacological data for the individual components.

Nigella sativa is the most clinically substantiated component of the combination. In controlled studies, black seed preparations improved asthma control and were associated with a reduction in eosinophil counts. The main potentially relevant mechanisms include reduction of Th2 inflammation, effects on IL-4, IL-5, and IL-13, inhibition of mast-cell degranulation, reduced leukotriene formation, and a moderate bronchodilator effect.

Boswellia serrata complements the formula through its effect on the 5-lipoxygenase pathway. Cysteinyl leukotrienes contribute to bronchospasm, vascular permeability, mucus hypersecretion, and recruitment of eosinophils. In small clinical studies, Boswellia preparations reduced asthma symptoms and improved selected measures of respiratory function. These data support pharmacological promise, but they do not establish equivalence to modern biological therapy.

Punica granatum is included because a standardized industrial preparation is available and human data exist in allergic asthma. Pomegranate extract may reduce oxidative stress, the activity of pro-inflammatory mediators, and cellular infiltration of the airways. A clinical study reported reductions in certain daytime and nighttime symptoms and a decrease in eosinophil counts. Its action is less selective than IL-5 neutralization, but it broadens the anti-inflammatory and antioxidant components of the formula.

Atractylodes lancea provides the most targeted preclinical effect on initiation of Th2 inflammation. Atractylodin reduced airway hyperresponsiveness, production of IL-4, IL-5, and IL-13, allergen-specific immunoglobulins, and activation of dendritic cells. Clinical efficacy of Atractylodes lancea in severe eosinophilic asthma in humans has not yet been demonstrated, so this component should be regarded as a pharmacologically justified adjunct rather than an independent replacement for mepolizumab.

Scutellaria baicalensis complements the combination through effects on eosinophilic infiltration, Th2 cytokines, mast cells, histamine, mucus hypersecretion, and bronchial remodeling. Baicalin, baicalein, and wogonin possess antiallergic and anti-inflammatory activity. The main evidence base in asthma remains preclinical, so efficacy should be assessed according to the patient's actual response rather than mechanistic expectations alone.

Mepolizumab is superior to the herbal combination in speed and predictability of effect. It directly binds IL-5, rapidly reduces eosinophil counts, and has a standardized dosing regimen. The herbal formula acts on multiple targets, but its effect develops gradually, depends on standardization of each extract, and does not guarantee a defined reduction in eosinophils.

An independent integrative strategy may be discussed for mild or moderate stable allergic asthma, allergic rhinitis, and chronic rhinosinusitis without recurrent hospitalizations, systemic eosinophilia, vasculitis, or internal-organ involvement. In these conditions, mepolizumab is generally not a first-line medicine, so it is more appropriate to discuss the possibility of not progressing to biological therapy without sufficient indications rather than discontinuing biological therapy that is genuinely necessary.

In a patient already receiving mepolizumab, the herbal combination should initially be introduced as a controlled adjunct. Starting all five extracts at the same time while discontinuing biological therapy creates both a methodological and clinical error: if the condition worsens, it becomes impossible to determine whether this is due to recurrence of the disease, failure of the alternative treatment, or an allergic reaction to one of the components.

In severe eosinophilic asthma with recurrent exacerbations, dependence on systemic glucocorticosteroids, eosinophilic granulomatosis with polyangiitis, hypereosinophilic syndrome, eosinophilic myocarditis, neuropathy, vasculitis, or internal-organ involvement, the selected combination is not an equivalent replacement for mepolizumab. In such conditions, the decision to reduce or discontinue biological therapy is made by the treating specialist.

Plant origin does not mean absence of adverse effects. Allergic reactions, dyspepsia, decreased blood pressure, changes in glycemia, and interactions with concomitant medicines are possible. It is advisable to introduce the components sequentially so that the source can be identified if a reaction occurs.

Real-world efficacy of mepolizumab

Mepolizumab is genuinely effective in diseases in which IL-5-dependent eosinophil activity plays a leading role. In severe eosinophilic asthma, the drug reduces the frequency of clinically significant exacerbations by approximately half, reduces the need for hospitalization, and allows some patients to lower their dose of systemic glucocorticosteroids.

The main clinical value of mepolizumab lies not in immediately eliminating shortness of breath, but in reducing future risk. The drug lowers the likelihood of severe exacerbations, courses of prednisolone, and hospitalization. Improvement in FEV1 is usually moderate and does not always reach a clinically meaningful magnitude. This is because suppression of eosinophilic inflammation does not reverse established bronchial remodeling or fixed airflow limitation.

In chronic rhinosinusitis with nasal polyps, mepolizumab can reduce polyp size, nasal obstruction, loss of smell, and the need for systemic steroids or surgical treatment. The effect develops gradually and does not guarantee complete disappearance of the polyps.

In the eosinophilic phenotype of chronic obstructive pulmonary disease, the effect is more modest than in severe eosinophilic asthma. The drug can reduce the frequency of moderate and severe exacerbations, but it does not restore destroyed lung tissue, eliminate emphysema, or replace smoking cessation, bronchodilators, and maintenance inhaled therapy.

In eosinophilic granulomatosis with polyangiitis, mepolizumab increases the duration of remission, reduces the number of relapses, and allows the steroid burden to be reduced. However, a substantial proportion of patients do not achieve complete sustained remission. The drug suppresses the eosinophilic component of the disease but does not always fully control the vasculitic component.

In hypereosinophilic syndrome, mepolizumab reduces the frequency of exacerbations and lowers eosinophil counts. It is particularly important when there is a risk of involvement of the heart, lungs, nervous system, or other organs, where the slow and unpredictable action of herbal products may be insufficient.

Mepolizumab does not eliminate the primary cause of the disease and does not restore already established organ damage. Its main purpose is to suppress the activity of eosinophilic inflammation, prevent new exacerbations, and reduce the steroid burden.

Medical errors include prescribing the drug without confirmation of an eosinophilic phenotype, failing to check inhaler technique and adherence to background therapy, using it in ordinary non-eosinophilic asthma, expecting a rapid bronchodilator effect, ignoring parasitic risk, and continuing ineffective treatment without an objective assessment of benefit.

Prescribing the drug solely on the basis of a single elevated eosinophil count without determining its cause is particularly questionable. Eosinophilia may be associated with parasitic infection, a drug reaction, allergic disease, a hematological disorder, or systemic vasculitis. Reducing eosinophils with a monoclonal antibody does not replace diagnostic evaluation.

Safety monitoring during treatment

Before therapy begins, the diagnosis should be confirmed, the eosinophilic phenotype should be established, and the frequency of exacerbations during the previous year, need for systemic glucocorticosteroids, inhaler technique, adherence to treatment, and pulmonary function should be assessed. In marked eosinophilia, parasitic infections, drug reactions, eosinophilic granulomatosis with polyangiitis, hypereosinophilic syndrome, and hematological disease should be excluded.

The first assessment of efficacy is performed after three to four months. Daytime and nighttime symptom frequency, use of a rapid-acting bronchodilator, number of exacerbations, courses of prednisolone, hospitalizations, results of asthma-control questionnaires, FEV1, and the impact of the disease on everyday activity are taken into account. In the case of a partial response, observation may be extended, but indefinite continuation of ineffective treatment is not justified.

The eosinophil count predictably decreases during treatment, but the dose of mepolizumab is not changed after each blood test. An excessively low eosinophil count is not by itself a reason to reduce the dose because the regimen is determined by the disease and the approved dosing schedule, not by individualized titration according to cell counts.

Routine monitoring of liver enzymes, creatinine, electrocardiography, or drug concentrations solely because of mepolizumab is not required. These investigations are performed as indicated by comorbid conditions, systemic glucocorticosteroid treatment, and other medicines.

Mepolizumab is discontinued immediately in the event of anaphylaxis, angioedema, generalized urticaria, severe bronchospasm, or hypotension. If a helminth infection does not respond to antiparasitic therapy, the drug is temporarily stopped until the infection resolves.

A painful unilateral vesicular rash requires early exclusion of herpes zoster. Involvement of the face, eye, or ear, high fever, severe headache, weakness of the limbs, impaired coordination, or altered consciousness requires urgent medical assessment.

Sudden worsening of breathlessness, inability to speak in full sentences, cyanosis, confusion, or failure to respond to a rapid-acting bronchodilator are signs of a severe asthma exacerbation. It is not appropriate to wait for mepolizumab to take effect in this situation.

Correct discontinuation of the drug

Mepolizumab does not cause physiological dependence and does not require gradual dose reduction. Injections may be stopped immediately, but the pharmacological effect will diminish gradually because of the long half-life.

The absence of a withdrawal syndrome does not mean that there is no risk of disease worsening. After treatment is discontinued, eosinophil counts gradually recover and the frequency of exacerbations may increase. This is not toxic rebound, but the return of IL-5-dependent inflammation after the antibody effect wears off.

A trial discontinuation may be considered in a carefully selected patient with sustained long-term disease control, no severe exacerbations, and continued use of necessary maintenance therapy. After mepolizumab is stopped, symptoms, need for bronchodilator medication, peak-flow or spirometry measurements, eosinophil counts, and frequency of exacerbations should be monitored.

Mepolizumab, systemic glucocorticosteroids, and inhaled therapy must not all be stopped at the same time. In that situation, it becomes impossible to determine the cause of deterioration, while the risks of severe exacerbation and adrenal insufficiency increase.

If, after discontinuation, the need for rescue medication increases, nighttime symptoms appear, peak expiratory flow falls, eosinophil counts rise, or an exacerbation develops, effective therapy should be restored promptly. Waiting for a severe attack to confirm that discontinuation has failed is not pharmacologically justified.

A rational approach to treatment

Mepolizumab is justified when a patient has severe eosinophilic asthma with recurrent exacerbations, dependence on systemic glucocorticosteroids, severe chronic rhinosinusitis with nasal polyps, active eosinophilic granulomatosis with polyangiitis, hypereosinophilic syndrome, or a risk of eosinophilic organ damage. In these situations, selective, rapid, and predictable suppression of IL-5 has a clinical advantage over less standardized interventions.

An integrative formula consisting of Nigella sativa, Boswellia serrata, Punica granatum, Atractylodes lancea, and Scutellaria baicalensis may be considered in stable mild to moderate allergic or eosinophilic asthma without systemic organ involvement. Its purpose is to provide multi-target reduction of Th2 inflammation, leukotriene activity, eosinophil migration, mast-cell degranulation, mucus hypersecretion, and bronchial hyperresponsiveness.

Combined use is possible as a stage of integrative therapy, but the components should be introduced sequentially without simultaneously changing the doses of mepolizumab and glucocorticosteroids. This approach makes it possible to assess the effectiveness of each intervention and promptly identify the source of an allergic or other adverse reaction.

The aim of integrative pharmacology is not to abandon effective treatment at any cost. Mepolizumab should be used where its selectivity, potency, and predictability are genuinely necessary. In stable and less severe disease, a multi-target herbal strategy may be considered when it can reduce the medication burden without creating an unjustified risk of disease progression.

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