Serum lactate dehydrogenase and its isoenzymes as predictors of clinical outcomes in acute exacerbation of chronic obstructive pulmonary disease: a retrospective analysis of a hospitalized cohort.

We aimed to test the association between serum lactate dehydrogenase (LDH) and its isoenzymes and treatment outcomes during hospitalization for acute exacerbation of chronic obstructive pulmonary disease (AECOPD). Thirty-eight AECOPD patients were recruited from a tertiary hospital from December 2017 to June 2018. Serum LDH and LDH isoenzymes were measured on venous blood collected at admission. Treatment outcomes included duration of hospital stay, initiation of non-invasive (NIV) or mechanical ventilation, initiation of antipseudomonal antibiotics, change in empirical antibiotic treatment, need for intravenous corticosteroids or methylxanthines, and percentage of change in C-reactive protein from admission to the third day. Multivariate linear and binary logistic regression analyses were used to test the study's objectives. We found that, after adjusting for age, gender, comorbidities, COPD severity, level of hypoxemia, and inflammation markers, each 10 U/L increase in serum LDH was associated with prolongation of the hospital stay by 0.25 (0.03, 0.46) days, 42% higher odds (odds ratio [OR] 1.42 [1.00, 2.03]) for need of NIV, and 25% higher odds (OR 1.25 [1.04, 1.49]) for initiation of antipseudomonal treatment. LDH1 and LDH2 were the LDH isoenzymes that mainly drove these relationships. LDH release in the context of an AECOPD could originate from lung, muscle, or heart tissue damage due to airway inflammation, respiratory muscle recruitment, and myocardial stress. Myocardial injury and aerobic adaptation in respiratory muscles may explain the predominance of LDH1 and LDH2 isoenzymes in these associations.

Lactate dehydrogenase isoenzymes in patients with acute exacerbation of chronic obstructive pulmonary disease: An exploratory cross-sectional study.

We aimed to evaluate differences in serum lactate dehydrogenase (LDH) isoenzymes between patients hospitalized for acute exacerbation of chronic obstructive pulmonary disease (AECOPD) and other lower respiratory tract infections (LRTIs). Based on self-reported COPD diagnosis, 71 participants were divided into AECOPD (n = 38, 29 males, mean age 70.5 years) and LRTI (n = 33, 12 males, mean age 70.4 years) groups. Information on demographics, comorbidities, and COPD severity markers, as well as arterial blood gases and laboratory data were collected, while serum LDH electrophoresis was performed to examine the LDH isoenzymes. Adjusting for sex, age, comorbidities, degree of hypoxemia, inflammation markers, muscle and myocardial enzymes, and total serum LDH, the mean differences (95 % confidence intervals) in the ratios of serum LDH isoenzymes to total serum LDH between groups (LDHxAECOPD - LDHxLRTI) were statistically significant for LDH1 [4.9 (1.4 to 8.3)], LDH2 [3.0 (0.1 to 5.8)], LDH3 [-4.3 (-6.3 to -2.3)], and LDH4 [-3.2 (-4.9 to -1.5)]. A sum of LDH3 and LDH4 ratios below 29 % had the highest discriminative ability to classify a subject in the AECOPD group (AUC 0.841, sensitivity 76 %, specificity 87 %). Aerobic metabolic adaptive mechanisms in respiratory muscles during AECOPD could explain the above differences.

Unilateral pulmonary hypoplasia in an adult patient.

Pulmonary hypoplasia (PH) is a developmental anomaly of the lung parenchyma, characterized by a decrease in the number and size of airways, alveoli and vessels. We present a case of a 31-year-old patient with a history of chronic productive cough and frequent respiratory infections, who was referred for investigation of abnormal chest x-ray. The combination of chest computed tomography (CT) and bronchoscopy set the diagnosis of left pulmonary hypoplasia and the patient was treated surgically with a left pneumonectomy. PH is usually diagnosed immediately after birth, causing severe respiratory failure with high mortality. The less severe, unilateral forms can possibly survive by causing compensatory hyperinflation of the other lung and remain undiagnosed until adulthood, presenting either asymptomatic or with symptoms of chronic bronchitis and recurrent respiratory infections. Chest CT is considered the imaging technique of choice for the diagnosis and for the differential diagnosis from other congenital or acquired conditions. The treatment is usually conservative, although surgical resection is indicated in cases of severe cystic changes and intense symptomatology.