Bronchoalveolar lavage fluid findings in patients with chronic hepatitis C virus infection.

Abstract

Background -Hepatitis C virus (HCV) infection has recently been incriminated as an aetiological agent in idiopathic pulmonary fibrosis. This study was performed to determine the cellularity and lymphocyte phenotypes ofbronchoalveolar lavage (BAL) fluid in patients with chronic hepatitis C. Methods -BAL fluid and lavage lymphocyte subsets from 13 patients (10 men) with active chronic hepatitis C, diagnosed by sustained elevated serum glutamic pyruvic transaminase and typical histological findings in the liver, were analysed. Lavage findings in these patients were compared with those from 13 healthy volunteers (eight men) as controls. To elucidate whether HCV infection is related to the pathogenesis ofIPF, we investigated the cellularity and lymphocyte phenotypes of bronchoalveolar lavage (BAL) fluid, and performed pulmonary function tests in patients with chronic hepatitis C. Methods SUBJECTSThirteen patients (10 men) of median age 57 years (range 31-64) with chronic hepatitis C proven by the typical histological findings observed within the previous six months and the presence of sustained elevated serum levels of glutamic pyruvic transaminase (GPT) for at least six months were studied. All patients were positive for antibody to HCV in serum and negative for hepatitis B surface antigen. They were treated with interferon after this study. The following patients were excluded from the study: those who had received a course of antiviral or immunosuppresive therapy which may lead to alveolitis within six months; those who had a positive titre for autoantibodies to collagen diseases; those who exhibited leucopenia (<3000/ml) and thrombopenia (<80 000/ml). None of the patients had a familial history of IPF and none had pulmonary fibrosis as determined from symptoms, physical signs, and radiographic findings. Thirteen healthy volunteers (eight men) of median age 49 years (range 24-67) acted as controls.Subjects in both groups were defined as smokers if they currently smoked cigarettes and ex-smokers if they had not smoked within the preceding six months. This study was performed according to the criteria of the Helsinki Declaration and free and informed consent was obtained from all patients and normal volunteers.BRONCHOALVEOLAR LAVAGE (BAL) Subcutaneous injections of atropine (0 5 mg) and pethidine hydrochloride (0 5 mg/kg) were given. The oral pharynx and upper airway was anaesthetised with 2% lignocaine (lidocaine).

Hypoxia-Induced Pulmonary Vascular Remodeling

“…In patients with high-altitude pulmonary edema (HAPE), increased numbers of neutrophils and macrophages, in bronchoalveolar lavage fluid, as compared with healthy individuals, have been observed. 185,186 In addition, increased levels of tumor necrosis factor (TNF)-␣, IL-1-␤, IL-6, and IL-8 have been noted, levels that quickly reversed to normal following return to normoxic conditions. 186 Chronic hypoxic exposure results in the robust and persistent appearance of mononuclear cells in the PA adventitia and media of both weanling rats and neonatal calves.…”

Bronchoalveolar lavage fluid analysis in individuals with chronic hepatitis C

“…This discrepancy may depend upon geographical differences or differences in the false positive rate of anti-HCV testing as a result of different testing procedures used by different investigators. Several investigators have shown that signi®cantly difference in cell counts as well as increased levels of lymphocytes and eosinophils are present in the bronchoalveolar lavage¯uid of individuals with HCV-induced chronic active hepatitis [Kubo et al, 1996;Yamaguchi et al, 1997]. These previous data suggest but do not prove that HCV infection may be a putative cause of idiopathic pulmonary ®brosis.…”

Study of Cough Reflex Sensitivity in a Group of Egyptian Patients with Chronic Hepatitis C Virus Infection

“…Some studies showed an increase in eosinophil number in the lungs of these patients [17] and eosinophils are well known to produce powerful inflammatory mediators [18] that could be provoked by viral infections [19]. It is also possible that these cells may have a role.…”