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This group of diseases can include bronchial asthma and diseases with a leading broncho-asthmatic syndrome, which are based on other etiological factors.

These diseases include:

1. Allergic bronchopulmonary aspergillosis.

2. Tropical pulmonary eosinophilia.

3. Pulmonary eosinophilia with systemic manifestations.

4. Hyperereosinophilic myeloproliferative syndrome.

5. Nodular periarteritis.

Aspergillus can cause several types of respiratory damage:

• atonic IgE-dependent bronchial asthma, mediated by mediators of labocytes;

• exogenous allergic alveolitis - in non-atopic patients who inhaled a large number of aspergillus spores;

• allergic bronchopulmonary aspergillosis;

• the formation of aspergillomas in pre-existing pulmonary cavities;

• invasive aspergillosis, which develops in patients with immunodeficiency.

Allergic bronchopulmonary aspergillosis can be assumed in every patient with bronchial asthma, combined with pulmonary infiltrates and eosinophilia. Its distinctive features are: pulmonary infiltrates, high peripheral eosinophilia, recurrent asthma attacks, proximal bronchiectasis, determined radiographically or tomographically (bronchography is contraindicated!), High total IgE content, detection of precipitating antibodies to aspergillus antigen.

The key to the diagnosis of allergic bronchopulmonary aspergillosis is the doctor’s view of the frequent possibility of this disease. Its presence can be assumed in patients with asthma, with a history of pulmonary infiltrates with a steroid-dependent course of bronchial asthma. Treatment with glucocorticoids gives a good effect.

Tropical pulmonary eosinophilia (syn: Weingarten syndrome), caused by invasion of various microfilariae - transmissible nematodosis. The clinical picture is characterized by the development of acute allergosis in response to the migration of larval forms of microfilariae helminths with a slow progression of the disease: moderate (up to 38 ° C) increase in body temperature, intoxication, cough, abdominal pain, anorexia, weight loss. Attacks of bronchial asthma, up to severe asthmatic status, are combined with focal, infiltrative, often miliary changes in the lungs, which leads to mixed respiratory failure. As the disease progresses, the fibrous process progresses in the lungs. Microfilariae possess tropism not only to the respiratory system, but also to the lymphatic system (vuchereriosis, brugiosis), connective tissue (onchocerciasis, loiasis, dipetalonematosis). In this regard, one can observe exanthema, lymphadenopathy, splenomegaly, damage to the gastrointestinal tract. In peripheral blood, high (60-80%) eosinophilia, a false positive Wasserman reaction, an increase in the total IgE content.

In diagnostics, great importance is attached to collecting an epidemiological history (staying in the countries of Southeast Asia, India, Pakistan), identifying microfilariae in a thick drop of blood, taking into account the microfilariaemia rhythm (nighttime is typical for vuchereriosis, daytime for loiasis), detection of antifilarial complement in the binding reaction antibodies. Treatment with a specific drug diethylcarbamazine (ditrazine) gives a good clinical effect, but in advanced cases, changes in the lungs persist.

Pulmonary eosinophilia with systemic manifestations.
To this group

independent diseases are included, which along with pulmonary eosinophilia are characterized by the involvement of many organs and systems in the process.

Hyperereosinophilic myeloproliferative syndrome (syn: HES syndrome, Leffler II syndrome, fibroblastic parietal endocarditis) is a rare disease from the group of systemic allergic vasculitis of unknown etiology. In the development of the disease, great importance is attached to tissue damage caused by degranulapia of eosinophils and, primarily, the endothelium of blood vessels and the endocardium. The disease begins, as a rule, with lung damage in the form of infiltrates, accompanied by high eosinophilia of the blood, fever, arthralgia, myalgia, polymorphic skin rashes. Subsequently, lymphadenopathy, hepatolienal syndrome, damage to the central nervous system (Gordon's phenomenon), and kidneys (proteinuria, hematuria) join. An examination of the bone marrow reveals its hyperplasia with a high content of eosinophils.

The most clinically significant is heart damage in the form of parietal fibroplastic endocarditis with the development of restrictive heart failure. The heart is small, congestive heart failure develops early.

Treatment is carried out with glucocorticosteroids (average daily dose of 30-40 mg in terms of prednisone) or their combination with cytostatics (azathioprine 100-150 mg per day).

In 20% of cases, periarteritis nodosa begins with one of the most typical syndromes - bronchial asthma, often combined with high blood eosinophilia, or Charge-Strauss syndrome (allergic necrotizing arteritis with extravasular granulomatosis and eosinophilic tissue infiltrates). Clinically, it is manifested by rhinitis, asthma attacks, eosinophilic pneumonia, signs of systemic vasculitis.

The course of the syndrome can be divided into three phases:

1) prodromal - phase of allergic diseases (allergic rhinitis, bronchial asthma);

2) the phase of blood and tissue eosinophilia (joining Leffler's syndrome or chronic eosinophilic pneumonia with relapse of lung infiltrates for several years);

3) the phase of systemic vasculitis (weight loss, fever, diarrhea, myalgia, arthralgia, hemorrhagic exanthema, abdominal pain, pericarditis, asymmetric polyneuritis, coronaryitis, kidney damage with the development of hematuria, persistent hypertension and chronic renal failure).

The diagnosis of asthmatic variant of periarteritis nodosa (Charge-Strauss syndrome) becomes reliable if hypereosinophilic bronchial asthma is combined with at least two of the four classic signs of Kussmaul-Meyer disease: kidney damage with persistent hypertension, asymmetric polyneuritis, abdominal syndrome, coronaritis.

As with hypereosinophilic myeloproliferative syndrome, the prognosis for periarteritis nodosa depends on extrapulmonary manifestations and in most cases is poor. Treatment is carried out with large doses of glucocorticoeteroids or combined with cytostatics. <
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