ABSTRACT
A 37-year-old woman was admitted to our hospital because of acute respiratory distress. Two weeks previously, amoxapine (75 mg/day) had been administered for the first time. Ten days later she developed a high fever, severe hypoxaemia and pulmonary infiltrates on chest CT, including patchy areas of ground-glass opacity, thickening of the interlobular septae and bronchial walls and pleural effusions. BAL showed a predominance of neutrophils, lymphocytes and erythrocytes but not eosinophils. Amoxapine was stopped, resulting in complete resolution of the pulmonary infiltrates. When the patient was re-exposed to amoxapine (52.5 mg total dose), high fever, reduced SaO(2) and pulmonary infiltrates reappeared. We concluded that acute respiratory distress may be associated with amoxapine treatment.
Subject(s)
Amoxapine/adverse effects , Antidepressive Agents, Second-Generation/adverse effects , Respiratory Distress Syndrome/chemically induced , Adult , Female , Humans , Respiratory Distress Syndrome/diagnosis , Respiratory Distress Syndrome/therapyABSTRACT
BACKGROUND: ADAM (a disintegrin and metalloprotease) family members, characterized by a metalloprotease and a disintegrin domain, are membrane-anchored glycoproteins involved in proteolysis and cell adhesion. ADAM8 might have an important role in allergic inflammation. It can cleave a variety of substrates and is a sheddase for VCAM-1 and CD23, the low-affinity IgE receptors. METHODS: To evaluate the contribution of ADAM8 to the pathogenesis of eosinophilic pneumonia (EP), we measured the concentrations of soluble ADAM8 (sADAM8) and its substrates, soluble VCAM-1 (sVCAM-1) and soluble CD23 (sCD23), in bronchoalveolar lavage fluid from patients with smoking-induced acute eosinophilic pneumonia (AEP), chronic idiopathic eosinophilic pneumonia (CEP), and drug-induced eosinophilic pneumonia (drug-EP). RESULTS: The sADAM8 and sVCAM-1 concentrations were increased in AEP and CEP. The sCD23 concentration was elevated in AEP. In AEP, but not CEP, the sADAM8 concentration significantly correlated with those of both sVCAM and sCD23. CONCLUSION: The pathogenesis of AEP, CEP, and drug-EP was distinct with regard to ADAM8. Our results are the first to associate ADAM8 with eosinophilic responses and lung inflammation in humans.
Subject(s)
ADAM Proteins/immunology , Bronchoalveolar Lavage Fluid/immunology , Membrane Proteins/immunology , Pulmonary Eosinophilia/immunology , Adolescent , Adult , CD3 Complex/immunology , Female , Humans , Male , Middle Aged , Solubility , Vascular Cell Adhesion Molecule-1/immunologyABSTRACT
Recent studies have strengthened the concept that bronchial asthma and allergic rhinitis are manifestations of an inflammatory process within a continuous airway. This study was performed to compare clinical findings in asthma with or without rhinitis in Japan. Nasal symptoms were present in 99.6% of asthma patients. The prevalence of allergic rhinitis in patients with asthma was 52.4%. Bronchial asthma attacks in one third of patients with rhinitis were coincident with worsening of nasal symptoms. In adults (> 16 years of age), rhinitis frequently preceded asthma, whereas asthma preceded rhinitis in children (< 16 years of age). The frequency of rhinitis in asthma decreases with increasing age. This study demonstrated a clear link between upper and lower airway disorders in Japan.
Subject(s)
Asthma/complications , Rhinitis, Allergic, Perennial/complications , Rhinitis, Allergic, Seasonal/complications , Asthma/epidemiology , Female , Humans , Japan , Male , Middle Aged , Prevalence , Rhinitis, Allergic, Perennial/epidemiology , Rhinitis, Allergic, Seasonal/epidemiology , Surveys and QuestionnairesABSTRACT
Thymus- and activation-regulated chemokine (TARC/CCL17) is a lymphocyte-directed CC chemokine, which plays a role in the recruitment of CC chemokine receptor-4 positive T helper 2 (Th2) cells. In this study, we measured concentrations of TARC and Th2 cell-derived cytokines in bronchoalveolar lavage (BAL) fluid, as well as TARC concentrations in serum from patients with eosinophilic pneumonia and other interstitial lung diseases. TARC was significantly elevated in BAL fluids from patients with eosinophilic pneumonia (median, 240 pg/ml), whereas TARC was undetectable (< 7 pg/ml) in most cases of hypersensitivity pneumonitis, sarcoidosis, and idiopathic pulmonary fibrosis, as well as in healthy control subjects. Also, when present, quantities were less than 20 pg/ml. Elevated concentrations of interleukin (IL)-4, IL-5, and IL-13 were also detected in BAL fluid from patients with eosinophilic pneumonia. Interestingly, TARC concentrations in BAL fluids were closely correlated with the concentrations of IL-5 and IL-13. A serial examination showed that elevated TARC in BAL fluid rapidly fell to below detectable limits preceding decreases in IL-5 concentration and eosinophil percentage. Our results, in concordance with previous studies, demonstrate the potential activity of TARC for recruiting Th2 cells to the lungs and suggest a significant role for TARC in the pathogenesis of eosinophilic pneumonia.
