Pulmonary infection by Mycoplasma hominis (M hominis) in lung transplant (LTx) recipients is an uncommon yet potentially severe complication. Bronchial dehiscence in the context of M hominis infection has not been previously reported. In this report, we discuss a case of donor‐derived M hominis infection in a LTx recipient with bilateral bronchial anastomoses dehiscence and stenosis. The infection was managed using a multidisciplinary approach: repeat surgical revision of the necrotic anastomosis; targeted antibiotic therapy with the combination of oral and inhaled fluoroquinolones, and oral doxycycline and continuous ventilatory support. Response to therapy was monitored through repeat bronchoscopy and serial quantitative PCR assays for M hominis in bronchoalveolar lavage and aspiration. The rare nature of M hominis infection after LTx, its difficult detection in conventional cultures and innate resistance to beta‐lactams make diagnosis and timely treatment of this organism challenging. We recommend that transplant centers have a low threshold for screening for Mycoplasma infection, particularly in patients with unsatisfactory postoperative course and little response to broad‐spectrum antimicrobial and antifungal coverage. Monitoring with PCR may help to adapt the duration of antibiotic therapy.

Background The Mauriac syndrome was described in 1930 as a peculiar combination of poorly controlled diabetes mellitus type 1, stunted growth and glycogenic hepatopathy. More recently, lactic acidosis was recognized as an additional feature, often induced by insulin treatment. Case presentation A 17-year old girl known for diabetes type 1A and Mauriac syndrome was admitted to the emergency room with hyperglycemia of > 41 mmol/l without ketoacidosis. Under a standard insulin regimen, hyperglycemia was rapidly corrected but marked hyperlactatemia occurred. Conclusions The mechanism of impaired glucose utilization and lactate elevation independent of ketoacidosis in Mauriac syndrome is intriguing. The rarity of Mauriac syndrome and its resemblance to glycogen storage diseases suggest the presence of a specific metabolic or genetic predisposition that remains to be identified.

Background.Recent evidence identified exposure to particulate matter of size ≤2.5 µm (PM2.5) as a risk factor for high prevalence of small airway dysfunction (SAD). We assessed the prevalence of SAD in a European region with low air pollution levels.Methods.SAD was defined as a maximum mid-expiratory flow (MMEF) <65% of predicted value (PV) or MMEF<lower limit of normal (LLN) measured by spirometry in the Swiss PneumoLaus cohort. We performed bivariate and multivariable analysis with MMEF criteria, age, gender, body mass index (BMI), respiratory symptoms, and smoking status. Mean PM2.5values were obtained from a Swiss national database.Results.Among 3351 participants (97.6% Caucasian, 55.8% female sex, mean age 62.7 years), we observed MMEF <65% PV in 425 (12.7%) and MMEF<LLN in 167 (5.0%) individuals. None of the participants had both MMEF<LLN and ≥65% PV. MMEF <65% PV and MMEF<LLN were significantly associated with age, smoking status, cough, sputum, dyspnoea, whereas a positive association with MMEF <65% PV was observed for individuals aged >65 years only. In an area where ambient PM2.5concentration was <15 µg·m−3during the observation period (2010 and 2020), ≥72% of participants with SAD were ever smokers.Conclusions.The observed low prevalence of SAD of 5.0–12.7% depending on criteria employed may be related to lower PM2.5exposure. Smoking was the main factor associated with SAD in an area with low PM2.5exposure. Employing a MMEF threshold <65% PV carries a risk of SAD overdiagnosis in the elderly individuals.

No abstract

No abstract

No abstract

No abstract

No abstract