Current Issue : April-June
Volume : 2022
Issue Number : 2
Articles : 5 Articles
Immune checkpoint inhibitors (ICIs) are standard treatments for patients with lung cancer.
PD-1/PD-L1 or CTLA4 antibodies are chosen as the first-line therapy, contributing to the longterm
survival and tolerability. Unlike molecular targeting agents, such as gefitinib, lung cancer
patients with a poor performance status (PS) display unsatisfactory clinical improvements after ICI
treatment. Several previous reports also demonstrated that the PS is identified as one of the most
probable prognostic factors for predicting poor outcomes after ICI treatment. However, first-line
pembrolizumab seemed to be effective for lung cancer patients with a PS of 2 if PD-L1 expression
was greater than 50%. Currently, the induction of ICIs in patients with lung cancer with a poor PS is
controversial. These problems are discussed in this review....
Diffuse pulmonary lymphangiomatosis (DPL), an exceptionally rare disease, mainly occurs
in children and young adults of both sexes. Even though DPL is considered to be a benign disease,
its prognosis is relatively poor. Because of its rarity, little guidance on diagnosis and treatment is
available, which makes working with patients with DPL challenging for clinicians. We present here a
case of a young man with DPL in whom treatment with sirolimus and propranolol rapidly achieved
positive radiological and clinical effects....
Background and Objectives: In the intensive care unit (ICU), renal failure and respiratory
failure are two of the most common organ failures in patients with systemic inflammatory response
syndrome (SIRS). These clinical symptoms usually result from sepsis, trauma, hypermetabolism or
shock. If this syndrome is caused by septic shock, the Surviving Sepsis Campaign Bundle suggests
that vasopressin be given to maintain mean arterial pressure (MAP) > 65 mmHg if the patient is
hypotensive after fluid resuscitation. Nevertheless, it is important to note that some studies found
an effect of various mean arterial pressures on organ function; for example, a MAP of less than
75 mmHg was associated with the risk of acute kidney injury (AKI). However, no published study
has evaluated the risk factors of mortality in the subgroup of acute kidney injury with respiratory
failure, and little is known of the impact of general risk factors that may increase the mortality rate.
Materials and Methods: The objective of this study was to determine the risk factors that might directly
affect survival in critically ill patients with multiple organ failure in this subgroup. We retrospectively
constructed a cohort study of patients who were admitted to the ICUs, including medical, surgical,
and neurological, over 24 months (2015.1 to 2016.12) at Chiayi Chang Gung Memorial Hospital. We
only considered patients who met the criteria of acute renal injury according to the Acute Kidney
Injury Network (AKIN) and were undergoing mechanical ventilator support due to acute respiratory
failure at admission. Results: Data showed that the overall ICU and hospital mortality rate was
63.5%. The most common cause of ICU admission in this cohort study was cardiovascular disease
(31.7%) followed by respiratory disease (28.6%). Most patients (73%) suffered sepsis during their
ICU admission and the mean length of hospital stay was 24.32 25.73 days. In general, the factors
independently associated with in-hospital mortality were lactate > 51.8 mg/dL, MAP 77.16 mmHg,
and pH 7.22. The risk of in-patient mortality was analyzed using a multivariable Cox regression
survival model. Adjusting for other covariates, MAP 77.16 mmHg was associated with higher
probability of in-hospital death [OR = 3.06 (1.374–6.853), p = 0.006]. The other independent outcome
predictor of mortality was pH 7.22 [OR = 2.40 (1.122–5.147), p = 0.024]. Kaplan-Meier survival
curves were calculated and the log rank statistic was highly significant.................
Background and Objectives: We studied whether the extent of exertional oxygen desaturation
and emphysema could cause greater mortality in COPD and asthma independent of airflow
obstruction. Materials and Methods: We performed a 5-year longitudinal observational study in COPD
and asthma patients who matched for airflow obstruction severity. All subjects performed a 6-min
walk test (6MWT) and high-resolution computed tomography (HRCT) and followed spirometry
and oxygen saturation (SpO2) during the 6MWT every 3–6 months. Overall survival was recorded.
Cumulative survival curves were performed according to the Kaplan–Meier method and compared
with the log-rank test. Results: The COPD group had higher emphysema scores, higher Dinspiratory
capacities (ICs) and lower SpO2 during the 6MWT, which showed a greater yearly decline in FEV1
(40.6 mL) and forced vital capacity (FVC) (28 mL) than the asthma group (FEV1, 9.6 mL; FVC, 1.2 mL;
p < 0.05). The emphysema-predominant COPD group had an accelerated annual decline in lung
function and worse survival..................
Bronchopulmonary dysplasia and pulmonary hypertension, or BPD-PH, are serious chronic
lung disorders of prematurity, without curative therapies. Hyperoxia, a known causative factor
of BPD-PH, activates adenosine monophosphate-activated protein kinase (AMPK) 1 in neonatal
murine lungs; however, whether this phenomenon potentiates or mitigates lung injury is unclear.
Thus, we hypothesized that (1) endothelial AMPKa1 is necessary to protect neonatal mice against
hyperoxia-induced BPD-PH, and (2) AMPKa1 knockdown decreases angiogenesis in hyperoxiaexposed
neonatal human pulmonary microvascular endothelial cells (HPMECs). We performed
lung morphometric and echocardiographic studies on postnatal day (P) 28 on endothelial AMPKa1-
sufficient and -deficient mice exposed to 21% O2 (normoxia) or 70% O2 (hyperoxia) from P1–P14. We
also performed tubule formation assays on control- or AMPKa1-siRNA transfected HPMECs, exposed
to 21% O2 or 70% O2 for 48 h. Hyperoxia-mediated alveolar and pulmonary vascular simplification,
pulmonary vascular remodeling, and PH were significantly amplified in endothelial AMPKa1-
deficient mice. AMPKa1 siRNA knocked down AMPKa1 expression in HPMECs, and decreased their
ability to form tubules in normoxia and hyperoxia. Furthermore, AMPKa1 knockdown decreased
proliferating cell nuclear antigen expression in hyperoxic conditions. Our results indicate that
AMPKa1 is required to reduce hyperoxia-induced BPD-PH burden in neonatal mice, and promotes
angiogenesis in HPMECs to limit lung injury....
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