Diagnosis and management of interstitial pneumonitis associated with interferon therapy for chronic hepatitis C.

Interstitial pneumonitis (IP) is an uncommon pulmonary complication associated with interferon (IFN) therapy for chronic hepatitis C virus (HCV) infection. Pneumonitis can occur at any stage of HCV treatment, ranging from 2 to 48 wk, usually in the first 12 wk. Its most common symptoms are dyspnoea, dry cough, fever, fatigue, arthralgia or myalgia, and anorexia, which are reversible in most cases after cessation of IFN therapy with a mean subsequent recovery time of 7.5 wk. Bronchoalveolar lavage in combination with chest high resolution computed tomography has a high diagnostic value. Prompt discontinuation of medication is the cornerstone, and corticosteroid therapy may not be essential for patients with mild-moderate pulmonary functional impairment. The severity of pulmonary injury is associated with the rapid development of IP. We suggest that methylprednisolone pulse therapy followed by low dose prednisolone for a short term is necessary to minimize the risk of fatal pulmonary damage if signs of significant pulmonary toxicity occur in earlier stage. Clinicians should be aware of the potential pulmonary complication related to the drug, so that an early and opportune diagnosis can be made.

[Clinical features of interstitial pneumonitis due to interferon alpha therapy for chronic hepatitis C].

OBJECTIVE: To analyze the clinical features of interstitial pneumonitis (IP) associated with interferon therapy for chronic hepatitis C. METHODS: We report the first case of IP in China resulting from pegylated interferon alpha-2a in combination with ribavirin for treatment of hepatitis C viral infection. A statistical analysis of the related literatures documenting such IP cases was performed using SPSS 11.5 software. RESULTS: Of the 22 patients reported to develop IP after interferon therapy alone or in combination with ribavirin, 83%, 72% and 56% of the patients had the symptoms of dyspnoea, dry cough and fever, respectively. Twenty of these cases presented with restrictive pulmonary functional impairment and/or hypoxemia, and diffuse infiltration on chest radiography and/or CT. Complications were documented in 71% of the cases within 12 weeks of the treatment. The majority (85%) of the patients had favorable prognoses with an average recovery time of 7.5 weeks. Compared with the patients with mild and moderate pulmonary function impairment, 8 patients with severe pulmonary functional impairment had early onset of IP during the interferon therapy (6.6 vs 14.1 weeks, P<0.05), and a higher rate of corticosteroid treatment (75% vs 54%, P>0.05). CONCLUSION: IP is a rare pulmonary complication associated with IFN therapy, and patients with chronic hepatitis C should be followed up closely in the first 12 weeks of interferon therapy. Prompt discontinuation of medication is mandatory in the presence of IP, and corticosteroid therapy may not be essential for patients with mild or moderate pulmonary functional impairment under close monitoring. The severity of pulmonary damage is associated with the time of complication occurrence, and corticosteroids are required when obvious pulmonary toxicity occurs in early stage of the treatment (within 6 weeks) to reduce the pulmonary damage.

[Expression of E-cadherin, beta-catenin and cyclin D1 in epidermal skin lesions of patients with active psoriasis vulgaris].

OBJECTIVE: To examine the expressions of E-cadherin, beta-catenin and cyclin D1 in the skin lesions of patients with psoriasis vulgaris, and understand their possible roles in keratinocyte hyperproliferation in these patients. METHODS: Immunohistochemistry was performed to detect the expressions of E-cadherin, beta-catenin and cyclin D1 in the normal skin tissues and psoriatic lesions. RESULTS: In normal skin tissues, positive staining for E-cadherin and beta-catenin was detected in all layers of the normal epidermis at the sites of cell-cell junctions, and downregulation of E-cadherin and beta-catenin expression was found in the granular layer and basal layer of the psoriatic lesions. Cyclin D1 overexpression was observed mainly in the basal layer of the lesions, which was correlated to abnormal expression of beta-catenin. CONCLUSION: Downregulation of E-cadherin and beta-catenin expression and cyclin D1 overexpression in psoriatic skin are probably involved in keratinocyte hyperproliferation in psoriasis vulgaris.

[A novel retinoid CD437 induces apoptosis of human epidermoid carcinoma A431 cells].

OBJECTIVE: To investigate the effect of a novel retinoid CD437 and all-trans retinoic acid (ATRA) in inducing cell apoptosis and inhibiting the proliferation of human epidermoid carcinoma A431 cells and normal human epidermal keratinocytes. METHODS: MTT assay was used to determine the inhibitory effects of CD437 and ATRA on the growth of A431 cells and normal human epidermal keratinocytes, and the cell morphological changes were observed microscopically. Flow cytometry was used to investigate the effect of CD437 and ATRA on the cell cycle and apoptosis. RESULTS: CD437 was more effective than ATRA in inhibiting the proliferation of A431 cells and normal human epidermal keratinocytes. CD437 increased the percentage of sub-G1 populations in A431 cells and induced G1 arrest in normal human epidermal keratinocytes. ATRA appeared to be relatively ineffective for inducing apoptosis in A431 cells as compared to CD437. CD437 did not duce obvious apoptosis in normal human epidermal keratinocytes. CONCLUSION: CD437 is more effective than ATRA in inhibiting the proliferation and inducing apoptosis in A431 cells and shows selective apoptosis-inducing effect against malignant keratinocytes, suggesting its potential in the prevention or treatment of cutaneous carcinoma.

[Expression of E-cadherin and beta-catenin in Bowen's disease and squamous cell carcinoma].

OBJECTIVE: To investigate the involvement of E-cadherin-catenin adhesion system in Bowen's disease (BD) and cutaneous squamous cell carcinoma (SCC). METHODS: Fifteen normal skin, 28 BD and 18 SCC specimens were stained with monoclonal antibodies against E-cadherin and beta-catenin. Evaluation of the staining results was performed with semi-quantification of the pattern and intensity of staining, percentage of positive cells, and cytoplasmic staining. RESULT: Normal skins strongly expressed membranous E-cadherin and beta-catenin, but their expression was remarkably reduced in BD and SCC. Abnormal staining of beta-catenin was observed in the cytoplasm or cell nuclei of BD and SCC. CONCLUSION: Abnormal expression of the E-cadherin/catenin complex is common in SCC and BD.