No abstract available.
Drug Therapy* ; Respiratory Distress Syndrome, Adult*

Adult ; Humans ; Respiratory Distress Syndrome, Adult ; drug therapy

Acute Lung Injury ; drug therapy ; therapy ; Fluid Therapy ; Glucocorticoids ; therapeutic use ; Humans ; Inflammation ; drug therapy ; therapy ; Respiratory Distress Syndrome, Adult ; drug therapy ; therapy

Drug Therapy, Combination ; Drugs, Chinese Herbal ; therapeutic use ; Humans ; Medicine, Chinese Traditional ; Phytotherapy ; Respiratory Distress Syndrome, Adult ; prevention & control ; Severe Acute Respiratory Syndrome ; complications ; therapy

Glucocorticoids ; adverse effects ; therapeutic use ; Humans ; Respiratory Distress Syndrome, Adult ; drug therapy ; immunology ; metabolism ; Systemic Inflammatory Response Syndrome ; drug therapy ; immunology ; metabolism

Although Mycoplasma pneumonia is frequently observed in immunocompromized patient if, rarely results in acute respiratory distress syndrome (ARDS). The cold agglutinin is positive in 33-76% of patients with M. pneumonia infection. We experienced a case of ARDS due to mycoplasma pneumonia associated with cold agglutinin disease in primary CNS lymphoma. He was a 60-year old primary CNS lymphoma patient with mycoplasma pneumonia and cold agglutinin disease who rapidly progressed to ARDS after 1 cycle of chemotherapy. He completely recovered with roxithromycin, levofloxacin, and ventilator supports. After recovery 2nd cycle of combination chemotherapy and brain radiation therapy was given and, CNS lymphoma is in complete remission until now.
Anemia, Hemolytic, Autoimmune* ; Brain ; Drug Therapy ; Drug Therapy, Combination ; Humans ; Levofloxacin ; Lymphoma* ; Middle Aged ; Mycoplasma* ; Pneumonia ; Pneumonia, Mycoplasma* ; Respiratory Distress Syndrome, Adult* ; Roxithromycin ; Ventilators, Mechanical

Although Mycoplasma pneumonia is frequently observed in immunocompromized patient if, rarely results in acute respiratory distress syndrome (ARDS). The cold agglutinin is positive in 33-76% of patients with M. pneumonia infection. We experienced a case of ARDS due to mycoplasma pneumonia associated with cold agglutinin disease in primary CNS lymphoma. He was a 60-year old primary CNS lymphoma patient with mycoplasma pneumonia and cold agglutinin disease who rapidly progressed to ARDS after 1 cycle of chemotherapy. He completely recovered with roxithromycin, levofloxacin, and ventilator supports. After recovery 2nd cycle of combination chemotherapy and brain radiation therapy was given and, CNS lymphoma is in complete remission until now.
Anemia, Hemolytic, Autoimmune* ; Brain ; Drug Therapy ; Drug Therapy, Combination ; Humans ; Levofloxacin ; Lymphoma* ; Middle Aged ; Mycoplasma* ; Pneumonia ; Pneumonia, Mycoplasma* ; Respiratory Distress Syndrome, Adult* ; Roxithromycin ; Ventilators, Mechanical

OBJECTIVEAlveolar type II (AT II) cells play a crucial role in the maintenance of pulmonary surfactant homeostasis and pulmonary immunity. The effects of dexamethasone (Dex) on the ultrastructure of AT II cells after acute lung injury remain unknown. This study focused on the ultrastructural changes caused by acute lung injury and on the effects of Dex administration on these ultrastructural changes in young rats.

METHODSSeventy-two 21-day-old Sprague-Dawley rats were randomly divided into control, acute lung injury and Dex-treated groups. Rats in the lung injury group were intraperitoneally injected with 4 mg/kg lipopolysaccharide (LPS) in order to induce acute lung injury, while the control rats were injected with the same amount of normal saline (NS). The Dex-treated group was injected first with LPS followed 1 hr later by Dex (5 mg/kg) injection. Eight rats in each group were sacrificed 24, 48 and 72 hrs after LPS or NS injection. Lung samples were obtained from the lower parts of left lungs and fixed with 2.5% glutaraldehyde for transmission electron microscope examination.

RESULTSMicrovilli of AT II cells disappeared and the number of lamellar bodies (LBs) increased in the lung injury group 24 hrs after LPS injection. The ring-like arrangement of LBs around nuclei was present until 48 hrs after LPS injection. By 48 hrs after LPS injection, giant LBs with vacuole-like abnormalities appeared. The shape of nuclei became irregular and the border of the nuclei became blurred. By 72 hrs after LPS injection, the number of LBs was obviously reduced; nucleoli disappeared; and karyolysis occurred in some of the nuclei. In contrast, in the Dex-treated group, LBs crowded on one side of AT II cells and exocytosis appeared on the same side by 24 hrs after LPS injection. By 48 hrs, the number of LBs was reduced. The number of mitochondria increased, and some of them became swollen and enlarged. However, by 72 hrs, the number of LBs increased and the ring-like arrangement of LBs around the nucleus again appeared.

CONCLUSIONSUltrastructural changes of AT II cells following lung injury induced by LPS were time-dependent in young rats. Dex may ameliorate AT II cell injury and promote functional restoration of AT II cells in LPS-induced acute lung injury.

Animals ; Dexamethasone ; pharmacology ; therapeutic use ; Lipopolysaccharides ; toxicity ; Pulmonary Alveoli ; drug effects ; ultrastructure ; Rats ; Rats, Sprague-Dawley ; Respiratory Distress Syndrome, Adult ; chemically induced ; drug therapy ; pathology

ObjectiveExposure to halogens, such as chlorine or bromine, results in environmental and occupational hazard to the lung and other organs. Chlorine is highly toxic by inhalation, leading to dyspnea, hypoxemia, airway obstruction, pneumonitis, pulmonary edema, and acute respiratory distress syndrome (ARDS). Although bromine is less reactive and oxidative than chlorine, inhalation also results in bronchospasm, airway hyperresponsiveness, ARDS, and even death. Both halogens have been shown to damage the systemic circulation and result in cardiac injury as well. There is no specific antidote for these injuries since the mechanisms are largely unknown.

Data SourcesThis review was based on articles published in PubMed databases up to January, 2018, with the following keywords: "chlorine," "bromine," "lung injury," and "ARDS."

Study SelectionThe original articles and reviews including the topics were the primary references.

ResultsBased on animal studies, it is found that inhaled chlorine will form chlorine-derived oxidative products that mediate postexposure toxicity; thus, potential treatments will target the oxidative stress and inflammation induced by chlorine. Antioxidants, cAMP-elevating agents, anti-inflammatory agents, nitric oxide-modulating agents, and high-molecular-weight hyaluronan have shown promising effects in treating acute chlorine injury. Elevated free heme level is involved in acute lung injury caused by bromine inhalation. Hemopexin, a heme-scavenging protein, when administered postexposure, decreases lung injury and improves survival.

ConclusionsAt present, there is an urgent need for additional research to develop specific therapies that target the basic mechanisms by which halogens damage the lungs and systemic organs.

Acute Lung Injury ; chemically induced ; Animals ; Chlorine ; toxicity ; Halogens ; toxicity ; Humans ; Lung ; drug effects ; pathology ; Respiratory Distress Syndrome, Adult ; drug therapy

Antithymocyte globulin (ATG) has long been used for immune-induction and anti-rejection treatments for solid organ transplantations. To date, few cases of ATG-induced acute respiratory distress syndrome (ARDS) have been published. Here, we present a case of ARDS caused by a single low-dose of ATG in a renal transplant recipient and the subsequent treatments administered. Although the patient suffered from ARDS and delayed graft function, he was successfully treated. We emphasize that the presence of such complications should be considered when unexplained respiratory distress occurs. Early use of corticosteroids, adjustment of immunosuppressive regimens, and conservative fluid management, as well as empiric antimicrobial therapies, may be effective strategies for the treatment of ARDS caused by ATG.
Adrenal Cortex Hormones ; therapeutic use ; Adult ; Antilymphocyte Serum ; adverse effects ; Humans ; Kidney Transplantation ; Male ; Respiratory Distress Syndrome, Adult ; chemically induced ; drug therapy