Coinfection of Invasive Pulmonary Aspergillosis and Pneumocystis Jiroveci Pneumonia in a Non-HIV Patient

Invasive pulmonary aspergillosis (IPA) and pneumocystis jiroveci pneumonia (PCP) are life-threatening opportunistic infections that occur in immunocompromised hosts. Early diagnosis and treatment of these opportunistic infections is essential to the survival of immunocompromised patients. We report a 60-year-old man undergoing short-term steroid therapy after surgical resection of a brain tumor infected with combined invasive pulmonary aspergillosis and pneumocystis jiroveci pneumonia diagnosed by bronchoscopy with bronchoalveolar lavage. Our case demonstrated that short-term systemic steroid therapy in non-HIV patients with underlying chronic lung conditions and malignancies was a risk factor for IPA and PCP, and for a combination of these infections

Serum markers in interstitial pneumonia with and without Pneumocystis jirovecii colonization: a prospective study

<p>Abstract</p> <p>Background</p> <p>In patients with chronic respiratory disease, <it>Pneumocystis jirovecii (P. jirovecii) </it>colonization is observed, and may influence disease progression and systemic inflammation. <it>Pneumocystis </it>pneumonia causes interstitial changes, so making a diagnosis of PCP in patients who have interstitial pneumonia (IP) with <it>P. jirovecii </it>colonization is sometimes difficult based on radiography.</p> <p>Methods</p> <p>This study investigated the prevalence of <it>P. jirovecii </it>colonization in IP patients and assessed pulmonary injury due to <it>P. jirovecii </it>colonization by measurement of serum markers (KL-6, SP-A, SP-D, and (1→3) β-D-glucan (β-D-glucan)) and the peripheral lymphocyte counts, prospectively. A total of 75 patients with idiopathic pulmonary fibrosis (n = 29), collagen vascular-related interstitial pneumonia (n = 19), chronic bronchitis or pneumonia (n = 20), and <it>Pneumocystis </it>pneumonia (n = 7) were enrolled in this prospective study. <it>P. jirovecii </it>DNA was detected in sputum samples, while serum markers and the lymphocyte count were measured in the peripheral blood.</p> <p>Results</p> <p>IP patients (idiopathic pulmonary fibrosis and collagen vascular-related IP) who received oral corticosteroids had a high prevalence of <it>P. jirovecii </it>colonization (23.3%). In IP patients, oral corticosteroid therapy was a significant risk factor for <it>P. jirovecii </it>colonization (<it>P </it>< 0.05). Serum markers did not show differences between IP patients with and without <it>P. jirovecii </it>colonization. The β-D-glucan level and lymphocyte count differed between patients with <it>Pneumocystis </it>pneumonia or <it>P. jirovecii </it>colonization.</p> <p>Conclusion</p> <p>Serum levels of KL-6, SP-A, SP-D, and β-D-glucan were not useful for detecting <it>P. jirovecii </it>colonization in IP patients. However, the serum β-D-glucan level and lymphocyte count were useful for distinguishing <it>P. jirovecii </it>colonization from <it>pneumocystis </it>pneumonia in IP patients.</p

Targeting Oncogenic KRAS in Non-Small-Cell Lung Cancer

Recent advances in molecular biology and the resultant identification of driver oncogenes have achieved major progress in precision medicine for non-small-cell lung cancer (NSCLC). v-Ki-ras2 Kirsten rat sarcoma viral oncogene (KRAS) is the most common driver in NSCLC, and targeting KRAS is considerably important. The recent discovery of covalent KRAS G12C inhibitors offers hope for improving the prognosis of NSCLC patients, but the development of combination therapies corresponding to tumor characteristics is still required given the vast heterogeneity of KRAS-mutated NSCLC. In this review, we summarize the current understanding of KRAS mutations regarding the involvement of malignant transformation and describe the preclinical and clinical evidence for targeting KRAS-mutated NSCLC. We also discuss the mechanisms of resistance to KRAS G12C inhibitors and possible combination treatment strategies to overcome this drug resistance

THE PROTECTIVE EFFECT OF PROPRANOLOL ON ISCHEMIC MYOCARDIUM: AN ELECTRON MICROSCOPIC STUDY

The protective effect of propranolol on ischemic myocardium was studied experimentally and clinically by electron microscope. In an animal experiment, ischemic changes were produced in the posterior papillary muscle of the rabbit following 3, 15, and 30 minutes of occlusion of the circumflex coronary artery. Propranolol (0.25 mg/kg) was injected into the left atrial cavity before occlusion of the artery. The posterior papillary muscle was excised and examined by electron microscope. In clinical experience, propranolol (20 µg/kg) was given intravenously to 6 patients who underwent open heart surgery. Transmural left ventricular myocardial biopsy was performed after the anoxic cardiac arrest and the material, particularly the subendocardium, was examined by electron microscope. It was shown that propranolol was effective, both in the experiment and in the clinical experience, in preserving ischemic myocardium. The possible mechanisms through which propranolol might act were considered to be (1) indirect effect of altered oxygen supply vs. demand, effected by reducing heart rate and reducing cardiac output due to the drug’s function as a beta blocker, (2) direct cellular effect, i.e., reducing myocardial substrate metabolism along with stabilization of cellular structure, and (3) increase collateral circulation to the subendocardium