Clinical, radiological, laboratory and bronchoscopic features characterizing each type of bronchogenic carcinoma

Background: To analyse the clinical, radiological, laboratory, and bronchoscopic findings characterizing each type of bronchogenic carcinoma.Methods: A cross-sectional study was conducted on 123 bronchogenic carcinoma patients. They were subjected to history taking, laboratory investigations, computed tomographic scan and fiberoptic bronchoscopy.Results: The mean age of the patients was 56.9±6.7 years, 76.4% were males and 78.9% were smokers. Most of them were symptomatic, adenocarcinoma (ADC) being the highest symptomatic one. Expectoration, fingers clubbing, and fever were common in ADC and small cell lung cancer (SCLC). Dyspnea, haemoptysis, dysphonia, dysphagia, vocal cord paralysis, anorexia and weight loss were common in SCLC and squamous cell carcinoma (SCC). Deep venous thrombosis was common in ADC and SCC. Mass lesion, atelectasis, chest wall invasion and elevated hemidiaphragm were common in SCLC and SCC. Ipsilateral mediastinal lymph nodes enlargement, cavitary lesion, and apical lesion were common in SCC and ADC. Contralateral mediastinal lymph nodes enlargement was common in SCLC. Nodular lesion, consolidation and pleural effusion were common in ADC. Hypercalcemia and hyponatremia were common in SCC. Malignant pleural effusion was common in ADC. Most of the patients had bronchoscopically-visible lesions; SCLC and SCC being the highest visible types. Most of the SCC and SCLC were centrally located, while LCC and ADC were mainly peripherally located. Most of cases were diagnosed via bronchoscopy. More than half of the studied cases were inoperable at presentation, especially SCLC and SCC.Conclusions: The 4 pathological types are distinguished from each other’s by certain clinical, radiological, laboratory and bronchoscopic features

Sonographic Assessment of Diaphragm Thickness and Its Effect on Inspiratory Muscles' Strength in Patients with Chronic Obstructive Pulmonary Disease

Objective: To assess diaphragm thickness and to assess its effect on inspiratory muscles’ strength in patients with chronic obstructive pulmonary disease (COPD). Methods: Case-control study was conducted on 113 male patients with COPD compared to 114 age-matched non-COPD males. Spirometric indices, maximum inspiratory pressure (MIP%), maximum expiratory pressure (MEP%), 6-min walk distance (6MWD), PaO2, PaCO2, and ultrasound measurement of diaphragm thickness were performed for all participants. The studied COPD cases were classified according to the diaphragm muscle thickness into a group with normal diaphragm muscle thickness (thickness end expiration ≥1.8 mm) and a group with diaphragm muscle thinning (thickness end expiration <1.8 mm). Results: Thickening fraction (TF) on right side, spirometric indices, MIP%, MEP%, were significantly lower in patients with COPD than in controls. Patients with diaphragm muscle thinning represented 11.5% of patients with COPD which represent 21.7% of cases with severe-to-very severe COPD. In patients with diaphragm muscle thinning, age, smoking index, and PaCO2 were significantly higher, whereas body mass index (BMI), TF bilaterally, forced expiratory volume (FEV)1%, MIP%, MEP%, 6MWD, and PaO2 were significantly lower than those with normal diaphragm muscle thickness. Additionally, TF and MIP% showed a significant negative correlation with age, smoking index, and PaCO2 and a significant positive correlation with FEV1, PaO2, BMI, and 6MWD. By multiple logistic regression analysis, the most significant factors relevant to the diaphragm muscle thinning were forced vital capacity (FVC)%, smoking index, forced expiratory flow rate at 25-75% of vital capacity (FEF)25%–75%,, and FEV1%. Conclusion: Thinning of the diaphragm was related to COPD severity, smoking index, and older age. Reduced inspiratory muscles’ strength (MIP%) was related to diaphragm thickness (TF), FEV1/FVC ratio, smoking index, and FVC%. Assessment of diaphragm thickness in COPD patients is recommended with early implementation to pulmonary rehabilitation program

Atherosclerosis is Associated Comorbidity in Patients with Chronic Obstructive Pulmonary Disease: Ultrasound Assessment of Carotid Intima Media Thickness

Objective: To assess atherosclerotic comorbidity in chronic obstructive pulmonary disease (COPD) patients and its relationship to COPD severity, hypoxemia, and hypercapnia. Methods: A hospital-based observational case-control study was conducted on 86 male COPD patients, and 86 age-matched healthy subjects (non-COPD group). Carotid intima-media thickness (CIMT) was assessed by Doppler ultrasound; in addition, spirometry and arterial blood gas tests were done. Results: CIMT was significantly increased in the COPD group compared to the non-COPD group (0.84±0.15 vs. 0.63±0.076, p<0.001). When the CIMT value of ≥0.8 mm was defined as a cutoff value for a thickened CIMT complex, 64% of COPD patients versus 8.1% of non-COPD subjects had a thickened CIMT. COPD patients with a thickened CIMT were older and had a higher PaCO2, lower FEV1%, FVC, and FEF25–75% compared to COPD patients with a normal CIMT. Thickened CIMT in COPD patients was significantly associated with hypoxemia (p=0.008, OR=8.2), hypercapnia (p=0.04, OR=6.2), and airflow limitation (p=0.11, OR=2.1). There was no significant difference in CIMT in relation to COPD severity (p=0.83). Conclusion: Atherosclerosis is prevalent in COPD patients, even in the early stages of the disease. Hypoxemia, hypercapnia, and airflow limitation are risk factors of atherosclerosis in COPD patients

Diagnostic Significance of hsa-miR-21-5p, hsa-miR-192-5p, hsa-miR-155-5p, hsa-miR-199a-5p Panel and Ratios in Hepatocellular Carcinoma on Top of Liver Cirrhosis in HCV-Infected Patients

Early hepatocellular carcinoma (HCC) diagnosis is challenging. Moreover, for patients with alpha-fetoprotein (AFP)-negative HCC, this challenge is augmented. MicroRNAs (miRs) profiles may serve as potential HCC molecular markers. We aimed to assess plasma homo sapiens—(hsa)-miR-21-5p, hsa-miR-155-5p, hsa-miR-192-5p, and hsa-miR-199a-5p—expression levels as a panel of biomarkers for HCC in chronic hepatitis C virus (CHCV) patients with liver cirrhosis (LC), especially AFP-negative HCC cases, as a step toward non-protein coding (nc) RNA precision medicine. Subjects and methods: 79 patients enrolled with CHCV infection with LC, subclassified into an LC group without HCC (n = 40) and LC with HCC (n = 39). Real-time quantitative PCR was used to measure plasma hsa-miR-21-5p, hsa-miR-155-5p, hsa-miR-192-5p, and hsa-miR-199a-5p. Results: Plasma hsa-miR-21-5p and hsa-miR-155-5p demonstrated significant upregulation, while hsa-miR-199a-5p demonstrated significant downregulation in the HCC group (n = 39) when compared to the LC group (n = 40). hsa-miR-21-5p expression was positively correlated with serum AFP, insulin, and insulin resistance (r = 0.5, p r = 0.334, p = 0.01, and r = 0.303, p = 0.02, respectively). According to the ROC curves, for differentiating HCC from LC, combining AFP with each of hsa-miR-21-5p, hsa-miR-155-5p, and miR199a-5p improved the diagnostic sensitivity to 87%, 82%, and 84%, respectively, vs. 69% for AFP alone, with acceptable specificities of 77.5%, 77.5%, and 80%, respectively, and AUC = 0.89, 0.85, and 0.90, respectively vs. 0.85 for AFP alone. hsa-miR-21-5p/hsa-miR-199a-5p and hsa-miR-155-5p/hsa-miR-199a-5p ratios discriminated HCC from LC at AUC = 0.76 and 0.71, respectively, with sensitivities = 94% and 92% and specificities = 48% and 53%, respectively. Upregulation of plasma hsa-miR-21-5p was considered as an independent risk factor for HCC development [OR = 1.198(1.063–1.329), p = 0.002]. Conclusions: Combining each of hsa-miR-21-5p, hsa-miR-155-5p, and hsa-miR-199a-5p with AFP made it possible to identify HCC development in the LC patients’ cohort with higher sensitivity than using AFP alone. hsa-miR-21-5p/hsa-miR-199a-5p and hsa-miR-155-5p/hsa-miR-199a-5p ratios are potential HCC molecular markers for AFP-negative HCC patients. hsa-miR-21-5p was linked, clinically and via in silico proof, to insulin metabolism, inflammation, dyslipidemia, and tumorigenesis in the HCC patients’ group as well as for an upregulated independent risk factor for the emergence of HCC from LC in the CHCV patients