Pulmonary eosinophilia

Pulmonary eosinophilia

    * Introduction
    * Signs and symptoms
    * Diagnosis
    * Treatment
Eosinophilic lung diseases are a heterogeneous group characterized by the accumulation of eosinophils in the alveoli, interstitium, or both. Peripheral blood eosinophilia is also common. Known causes of eosinophilia include: infectious especially helminth infections, pneumonitele induced by drugs, systemic disorders such as Churg-Strauss syndrome, allergic bronchopulmonary aspergillosis. Frequently the cause is unknown.
Diagnosis is based on demonstration of opacities on chest radiology and identification in peripheral blood eosinophilia than 450/microL, bronchoscopy lavage fluid or lung tissue biopsy. However, pulmonary eosinophilia may occur in the absence of peripheral eosinophilia. X-ray opacity associated with pulmonary eosinophilia in the blood are sometimes called pulmonary eosinophilic infiltrates. Eosinophils are exquisitely sensitive to corticosteroids and disappear completely in the flow of blood to a few hours after administration of corticosteroids. This rapid disappearance of blood can hide the diagnosis in patients who receive corticosteroids before diagnosis.
The two main eosinophilic lung diseases of unknown etiology are chronic and acute eosinophilic pneumonia. Hypereosinophilic syndrome a systemic disease affecting multiple organs is very dangerous. Chronic eosinophilic pneumonia is a disease of unknown etiology characterized by abnormal accumulation of eosinophils in lung chronic. It really is not chronic, acute or subacute but rather with the evolution of the appellant. The prevalence and incidence is unknown. Etiology is suspected to be an allergic diathesis. Most patients are smokers. Patients often have fulminant disease characterized by cough, fever, progressive dyspnea, wheezing, and night sweats. Pneumonia clinical presentation may suggest a community benefit. Asthma accompanies or precedes the disease in more than 50% of cases. Those with recurrent symptoms may be weight loss.
Patients uniformly respond to systemic corticosteroids, intravenous or oral. The lack of response suggests another diagnosis. Initial treatment is prednisone. Clinical improvement is rapid. Even in 48 hours. Complete resolution of symptoms and radiographic abnormalities occur in 14 days in most patients. Symptoms and radiographic abnormalities are reliable for diagnosis.
Symptomatic or radiographic relapse occurs in 50-80% of cases either after cessation of therapy or more frequently to decrease the dose of corticosteroids. Relapse may occur from months to years after initial episode. Therefore, steroid therapy is continued indefinitely occasionally. Inhaled corticosteroids such as beclomethasone, fluticasone seem to be especially effective in reducing oral corticosteroid dose. Relapse seems to indicate treatment failure, a higher morbidity or adverse prognosis. Patients continue to respond to corticosteroids as the initial episode.
Acute eosinophilic pneumonia is a disease of unknown etiology of character for quick eosinophilic infiltration of the lungs. Compared with acute and chronic form aeasta is not reappear. The incidence and prevalence is unknown. Especially affects patients aged between 20 and 40 years with a male: female of 21:1. The cause is unknown but may be an acute hypersensitivity reaction to an unidentified inhaled antigen in an otherwise healthy person. Cigarette smoking may be involved.
Cause acute disease onset with fever and short as seven days. The symptoms are nonproductive cough, dyspnea, malaise, myalgia, night sweats, and pleuritic chest pain. Diagnosis is suspected in patients with symptoms of acute pneumonia unresponsive to antibiotics and gradually leading to respiratory failure. Most patients get better spontaneously. Many are treated with prednisone. In patients with respiratory failure methylprednisolone are preferred. The prognosis is excellent, response to corticosteroids and full recovery without recurrence is universal.
Pathogenesis and causes: General pathophysiology of eosinophilic diseases: Lung disease associated with tissue or blood eosinophilia is a heterogeneous group of disorders. Were offered different nosologii. Some syndromes are intertwined. Factors ingested or inhaled, including drugs and infectious agents (parasites, fungi, mycobacteria) may trigger an eosinophilic immune response. It can be easy and autolytic that Loeffler's syndrome. Intrinsic pulmonary eosinophilic syndromes are usually idiopathic in nature. They include a diverse group of syndromes and idiopathic autoimmune blood dyscrasias ranging from the vasculitis. This group includes chronic eosinophilic pneumonia, idiopathic hypereosinophilic syndrome, Churg-Strauss syndrome and eosinophilic granuloma.
Eosinophilia and pulmonary infiltrates have been reported in patients with AIDS lymphoma, a variety of inflammatory lung diseases and collagen diseases. Airway inflammation in COPD is mostly neutrophilic, but 20-40% of sputum samples taken from patients showing eosinophilic inflammation associated with high levels of IL-5. Asthma can occur with marked eosinophilia with or without infiltrates. Eosinophilic bronchitis without asthma is characterized by cough for at least two months, a total of more than 3% eosinophils in sputum and airway obstruction without evidence. The average age of patients are affected, and have a history of smoking nonatopici. Acitivarea and eosinophilic infiltration occurs in the superficial layers of tissue. Eosinophilic lung disease pathophysiology: Tissue pathology is largely related to the product release toxic eosinophilic. This product includes major alkaline protein, protein-derived neurotoxin and major cation that injure the respiratory epithelium induces and influences the production of mucus ciliostaza. These injuries can be caused by release of reactive oxygen species. Release of platelet activating factor and leukotrienes contribute to bronchospasm.
Eosinophils are dominant suntin tissue and numbers several hundred folds more abundant than in the mucosal tissue. At the same time the number of eosinophils does not necessarily indicate the involvement of eosinophils in affected tissues expansion. eosinophils are numerous in mucosal epithelial tissues interface with the external environment, such as the respiratory, gastrointestinal. Eosinophils are not present in the lungs healthy people as their presence in tissues and bronchoalveolar lavage fluid identify a disease process. Extrinsic eosinophilic syndromes: Löffler syndrome: pathogenesis is unknown but probably reflects a hypersensitivity response to an antigen ingested or inhaled the food, medications or an infectious agent. Many of the causes sidnromului are believed to be related to infection with Ascaris. DRESS syndrome: drug rash with eosinophilia and systemic symptoms is a short DRESS drug hypersensitivity reaction with severe rash, fever, lymphadenopathy and damage to various tissues such as hepatitis, pneumonia or myositis. Sulfonamides, phenobarbital, sulfasalazine, carbamazepine and phenytoin cause this syndrome. Parasitic infections: parasites that migrate and cross the lungs can cause bronchospasm, dyspnea and pulmonary infiltrates. Embolization microfilariilor or degenerate eggs expose antigens in local immune system leads to granuloma formation. Schistosomiaza: The most common complication is pulmonary hypertension, chronic lung embolization of eggs. Strongiloidosis: patients who are immunocompromised including those who were newly prescribed corticosteroids hiperinfectie syndrome can develop massive release of larvae in the intestine and lung migration. Sepsis and respiratory failure may occur with bacteremia enteritis. Fungal causes: allergic bronchopulmonary aspergillosis is an immune response to antigens aspergilus the airways of individuals with COPD. Inflammatory response leads to airway reactivity, hipersecrietie of mucus, epithelial damage, bronchiectasis, eosinophilic pneumonia with fibrosis and parenchymal damage.