Background Pseudomonas aeruginosa is a common cause of community-acquired and nosocomial-acquired pneumonia. The development of resistance of P. aeruginosa to antibiotics is increasing globally due to the overuse of antibiotics. This article examines, retrospectively, the antibiotic resistance in patients with community-acquired versus nosocomial-acquired pneumonia caused by P. aeruginosa or multidrug-resistant (MDR) P. aeruginosa.MethodsData from patients with community-acquired and nosocomial-acquired pneumonia caused by P. aeruginosa and MDR P. aeruginosa were collected from the hospital charts at the HELIOS Clinic, Witten/Herdecke University, Wuppertal, Germany, between January 2004 and August 2014. An antibiogram was created from all study patients with community-acquired and nosocomial-acquired pneumonia caused by P. aeruginosa or MDR P. aeruginosa.ResultsA total of 168 patients with mean age 68.1 ± 12.8 (113 [67.3% males and 55 [32.7%] females) were identified; 91 (54.2%) had community-acquired and 77 (45.8%) had nosocomial-acquired pneumonia caused by P. aeruginosa. Patients with community-acquired versus nosocomial-acquired pneumonia had a mean age of 66.4 ± 13.8 vs. 70.1 ± 11.4 years [59 vs. 54 (64.8% vs. 70.1%) males and 32 vs. 23 (35.2% vs. 29.9%) females]. They included 41 (24.4%) patients with pneumonia due to MDR P. aeruginosa: 27 (65.9%) community-acquired and 14 (34.1%) nosocomial-acquired cases. P. aeruginosa and MDR P. aeruginosa showed a very high resistance to fosfomycin (community-acquired vs. nosocomial-acquired) (81.0% vs. 84.2%; 0 vs. 85.7%). A similar resistance pattern was seen with ciprofloxacin (35.2% vs. 24.0%; 70.4% vs. 61.5%), levofloxacin (34.6% vs. 24.5%; 66.7% vs. 64.3%), ceftazidime (15.9% vs. 30.9; 33.3% vs. 61.5%), piperacillin (24.2% vs. 29.9%; 44.4% vs. 57.1%), imipenem (28.6% vs. 27.3%; 55.6% vs. 50.0%), piperacillin and tazobactam (23.1% vs. 28.6%; 44.4% vs. 50.0%), tobramycin (28.0% vs. 17.2%; 52.0% vs. 27.3%), gentamicin (26.4% vs. 18.2%; 44.4% vs. 21.4%), and meropenem (20.2% vs. 20.3%; 42.3% vs. 50.0%). An elevated resistance of P. aeruginosa and MDR P. aeruginosa was found for cefepime (11.1% vs. 23.3%; 25.9% vs. 50.0%), and amikacin (10.2% vs. 9.1%; 27.3% vs. 9.1%). Neither pathogen was resistant to colistin (P = 0.574).ConclusionWhile P. aeruginosa and MDR P. aeruginosa were resistant to a variety of commonly used antibiotics, they were not resistant to colistin in the few isolates recovered from patients with pneumonia.

BackgroundPatients with angina pectoris or myocardial infarction frequently present without evidence of cardiac-specific heart enzymes by laboratory analysis or specific pathologic electro-cardiogram findings. The current study analyzed the efficacy of the erythrocyte sedimentation rate as an additional potential indicator for coronary heart disease, the aim being to enable quicker identification of patients with angina pectoris or myocardial infarction so that they can be more rapidly treated.MethodsPatients with angina pectoris or myocardial infarction who had undergone a heart catheter examination were included in the study. The diagnosis of acute coronary heart disease was made by the physician who performed coronary angiography. Patients without coronary heart disease were used as a control group. The erythrocyte sedimentation rate was measured in all patients. Patients with angina pectoris or myocardial infarction and an inflammatory or tumor disease were excluded.ResultsThe erythrocyte sedimentation rate was prolonged in 79 (58.09%) of 136 patients; 69 (50.74%) patients (95% confidence interval ±8.4%, 42.34%–59.14%) had coronary heart disease and a prolonged erythrocyte sedimentation rate. The erythrocyte sedimentation rate was prolonged in ten (7.35%) patients (95% confidence interval ±4.39%, 2.96%–11.74%) without coronary heart disease by coronary angiography. The specificity of the erythrocyte sedimentation rate for coronary heart disease was 70.59% and the sensitivity was 67.65%.ConclusionErythrocyte sedimentation rate may be a useful additional diagnostic criterion for coronary heart disease.

IntroductionInflammation has been implicated in the development of atherosclerosis in patients with acute coronary syndrome. C-reactive protein is an established nonspecific prognostic inflammatory biomarker for patients with acute coronary syndrome in the medical literature. This has led to a concerted effort to identify circulating inflammatory biomarkers to facilitate predicting the risk for and diagnosing coronary artery disease in at-risk subjects. The objective of this study was to search after novel inflammatory biomarkers reported as useful for diagnosing coronary artery disease.MethodsThe PubMed database was searched for reports published from January 1, 2000 to June 30, 2012 of novel circulating biomarkers for coronary artery disease in addition to the established biomarker, C-reactive protein. The search terms used were “infarction”, “biomarkers”, and “markers”, and only original articles describing clinical trials that were written in English were included. All published articles were separately examined carefully after novel inflammatory markers for acute coronary syndrome. All irrelevant publications without content pertaining to inflammatory biomarkers for acute coronary syndrome were excluded from this study. Our results reflect all articles concerning biomarkers in humans.ResultsThe PubMed search yielded 4,415 research articles. After further analysis, all relevant published original articles examining 53 biomarkers were included in this review, which identified 46 inflammation biomarkers useful for detecting coronary artery disease.ConclusionThe emergence of diverse novel biomarkers for coronary artery disease has provided insight into the varied pathophysiology of this disease. Inflammatory biomarkers have tremendous potential in aiding the prediction of acute coronary syndrome and recurrent ischemic episodes, and will eventually help improve patient care and management.

Background:Alteplase is used to treat acute ischemic stroke. However, it has several documented adverse effects, including the development of orolingual angioedema (OA). Although, OA is a rare side-effect, it is thought to be life-threatening and is difficult to treat. Until date, little is known about this condition and a better understanding of OA may contribute to improve the morbidity and mortality amongst patients that develop this condition.Materials and Methods:Using the PubMed and Medknow databases, we searched for peer reviewed published articles on OA after alteplase administration in 1950-2012. We gathered demographic data and investigated the relationship between the location of OA, neurological symptoms and the site of cerebral ischemia. In addition, we studied the effects of hypertensive premedication on OA development. We identified 19 published manuscripts that fulfilled our search criteria. These manuscripts reported 41 cases of OA after alteplase administration.Results:We found that this condition is associated with cerebral ischemia (P < 0.012) and that 65.9% (n = 27) of patients who developed OA had a hypertensive drug as a premedication.Conclusions:Although OA is a rare side-effect of alteplase, it can occur depending upon the localization of acute cerebral ischemia.

Cannabis is the most widely smoked illicit substance in the world. It can be smoked alone in its plant form, marijuana, but it can also be mixed with tobacco. The specific effects of smoking cannabis are difficult to assess accurately and to distinguish from the effects of tobacco; however its use may produce severe consequences. Cannabis smoke affects the lungs similarly to tobacco smoke, causing symptoms such as increased cough, sputum, and hyperinflation. It can also cause serious lung diseases with increasing years of use. Cannabis can weaken the immune system, leading to pneumonia. Smoking cannabis has been further linked with symptoms of chronic bronchitis. Heavy use of cannabis on its own can cause airway obstruction. Based on immuno-histopathological and epidemiological evidence, smoking cannabis poses a potential risk for developing lung cancer. At present, however, the association between smoking cannabis and the development of lung cancer is not decisive.

Asthma and chronic obstructive pulmonary disease (COPD) are two of the most common chronic lung diseases worldwide. Distinguishing between these different pulmonary diseases can be difficult in practice because of symptomatic similarities. A definitive diagnosis is essential for correct treatment. This review article presents the different symptoms of these two chronic inflammatory lung diseases following a selective search of the PubMed database for relevant literature published between 1996 and 2012. While cough occurs in both diseases, asthmatics often have a dry cough mainly at night, which is often associated with allergies. In contrast, COPD is usually caused by years of smoking. Paroxysmal dyspnea, which occurs in asthma, is characterized by shortness of breath, while in COPD it occurs during physical exertion in early stages and at rest in later stages of the disease. Asthma often begins in childhood or adolescence, whereas COPD occurs mainly in smokers in later life. It is possible to live with asthma into old age, whereas the life expectancy of patients with COPD is significantly limited. Currently, there is no general curative treatment for either disorder.

Background: Denosumab is a human monoclonal antibody that has been used successfully in the treatment of giant cell tumors of bone. These tumors are rare and, in principle, benign, but they are highly aggressive, locally advanced, osteolytic bone tumors that can metastasize to the lungs. Denosumab is an effective treatment when these tumors cannot be surgically removed or when surgical resection is likely to lead to severe morbidity (eg, loss of limbs or joints). The aim of this systematic review and meta-analysis was to investigate patients with giant cell tumors of bone who experienced tumor progression during treatment with denosumab and to compare them with patients who experienced reduction of their giant cell tumors of bone during treatment with denosumab. Methods: Embase, Cochrane Library, and MEDLINE/PubMed databases were searched for trials submitted by January 7, 2020, that reported the efficacy and safety of denosumab in patients with giant cell tumors of bone. Results: Sixty studies were reviewed, involving a total of 1074 patients who had giant cell tumors of bone and were treated with denosumab. Of the 60 studies, 58% of the patients were from case series studies, 39% from open-label phase II studies, and 3% from case reports. The response rate for denosumab as a treatment for giant cell tumors of bone was 97.5%, with statistical significance ( P < .0001). Pain in the limbs was statistically the most common adverse event for denosumab treatment in case series studies ( P < .0001). No treatment-related deaths occurred in the reviewed studies. Conclusion: Cumulative evidence supports the addition of surgery to optimal medical therapy with denosumab to reduce tumor size, clinical symptoms, and mortality among patients with giant cell tumors of bone.

Chronic kidney disease (CKD) often accompanies obstructive sleep apnea (OSA). A causative connection of the two disease entities is uncertain. However, eliminating OSA improves the prognosis of CKD patients. In the present study we examined a possible relationship between OSA and CKD, and whether there would be a mutual enhancing interaction in the severity of the two diseases. The study was of a retrospective nature and encompassed 382 patients over the period of 1 January 2014-30 June 2015. The OSA diagnosis was supported by a polysomnographic examination in 363 (95.0%) patients. Blood samples were taken for the determination of kidney function indices. The influence on OSA and CKD of comorbidities also was examined. We found a high probability of a simultaneous occurrence of OSA and CKD; with the odds ratio of 3.94 (95% CI 1.5-10.3%; p = 0.005). The 363 patients with OSA were stratified into 73 (20.1%) mild, 98 (27.0%) moderate, and 192 (52.9%) severe OSA cases according to the apnea-hypopnea index. CKD was found in 43 (58.9%) patients with mild OSA, 73 (74.5%) with moderate OSA, and 137 (71.4%) with severe OSA. Most OSA patients also suffered from hypertension and obesity. For comparison, CKD was detected in 7 (36.8%) out of the 19 patients without OSA (p < 0.003). We conclude that CKD develops significantly more often in patients with OSA than in those without it, and CKD frequency increases with the severity of OSA.