The reports which suggested the relation between viral hepatitis and pulmonary diseases have recently increased in number. Furthermore, recent studies of an immune response to CD8+ T lymphocytes and inflammatory cytokines are currently encouraging the presence of a connection between chronic HCV infection and pathogenesis of ILDs [6, 7].
ILDs were not detected in group [A] patients
Sixty-two percent of patients showed unremarkable CT results while 32% showed pleural effusion. El-Badrawy et al. [13] performed this study on different groups of patients including those with low or moderate viremia and also did not depict ILD among them.
ILDs were depicted in 27% of group [B] patients
All of them showed non-fibrotic pattern with predominant attenuation and nodular rather than reticular changes. Cellular type of NSIP and sub-acute type hypersensitivity pneumonitis were the most common types, accounting for 37% and 29.6%, respectively; the former presented by sub-pleural GGOs while the latter showed mixed GGO and air trapping (head cheese) with or without centrilobular ground-glass nodules. COP was found in 11% of patients, and all of them presented shortly after immunotherapy; Atol sign was characteristic. CEP and nodal sarcoidosis were both found in 7.4% of patients; the latter showed a positive recent history of immunotherapy. LIP and alveolar protreinosis were depicted only in 3.7% of patients each; the latter showed characteristic (crazy-paving pattern).
Segna et al. [14]. simply stated that HCV patients showed a high incidence for the development of ILD and El-Badrawy et al. [13] also declared the presence of ILD and variable idiopathic interstitial pneumonias (IIPs) among those patients with high viremia.
Similar to our findings, Hodnett et al. [15] stated that sub-pleural ground-glass attenuation was classic for cellular type of NSIP, while “Atol sign” was described for COP and “crazy-paving pattern” was described for alveolar proteinosis. Also, Lynch et al. [16] similarly clarified that “head cheese” pattern in HP was attributed to obliterative bronchiolitis.
Fibrotic ILD was found in 50% of group [C] patients which had high viremia in PCR and restrictive PFT. They presented with predominant reticular changes and fibrosis sequel including traction bronchiectasis/bronchiolectasis and honeycombing with architectural distortion. Fibrosing type of NSIP and UIP/IPF were the main detected types accounting for 38% and 34%, respectively; the latter showed characteristic honeycombing. Chronic HP was also found in 20% of involved patients with background of head cheese pattern and fibrosis. Post-management parenchymal fibrosing type of sarcoidosis was found only in 8% of them.
Our results agreed with findings of Hodnett et al. [15] as traction bronchiectasis and bronchiolectasis with sub-pleural ground-glass attenuation were characteristic in fibrosing NSIP, while characteristic honeycombing predominated UIP patients. Also, they agreed with findings of Abehsera et al. [17] as fibrosing sarcoidosis typically affects upper and middle lung zones with parenchymal distortion and peri-lymphatic nodules.
Our results match that of Saleh et al. [18], Hassan et al. [19], and Rabea et al. [20]; they all correlate the incidence of IPF in HCV patients to their hypoxemia level in ABG and more restrictive pattern of pulmonary functions. El Badrawy et al. [13] also correlate it to the degree of viral activity using PCR viremia level.
Among patients in group [B] and group [C] together, 38.5% of patients showed ILD. Based on the calculated chi-square critical value (CV), p values, and prevalence rates, a mild hypothetical connection between non-fibrotic ILD and high HCV viremia was statistically confirmed. A moderate hypothetical connection between fibrotic ILD and high HCV viremia associated with restrictive pulmonary functions was statistically confirmed. A mild to moderate hypothetical connection between ILD and active viral hepatitis depicted by high HCV viremia was statistically confirmed regardless of the result of the pulmonary function tests.
The most important merit of this research and used techniques were the following: (1) proved relation not only between HCV and ILD but also between blood viremia and predominant pattern of ILD using PCR, PFT, and HRCT; (2) characterization of predominant ILD pattern using HRCT which could replace lung biopsy and save patients from its hazards; (3) semi-quantitative method for assessment of degree lung fibrosis help in disease characterization and patient outcome determination.
The study was mildly limited by the overlap of the pulmonary function parameters rendering some results equivocal hence DLCO was mainly used.