Preoperative steroid therapy inhibits cytokine production in the lung parenchyma in asthmatic patients.
OBJECTIVE
During or after surgery, asthma attacks due to airway hyperresponsiveness (AHR) are likely to occur in patients with bronchial asthma. Preoperative administration of corticosteroid for prevention of perioperative asthma attacks is useful. We examined the mechanism of prevention of perioperative asthma attacks by the preoperative administration of corticosteroid in vitro.


METHODS
Five patients with asthma were treated with 20 mg of prednisolone orally for 2 preoperative days and 80 mg of methylprednisolone IV immediately before and after surgery. In another five patients without asthma, no steroids were administered. A noncarcinomatous part of the resected tissue from each patient with lung cancer was passively sensitized with the serum of an atopic patient. In the patients without asthma, the tissue was treated with or without dexamethasone, and then mite antigen was added.


METHODS
The culture supernatant and lung tissue were recovered, and the supernatant was assayed for histamine, leukotriene E(4) (LTE(4)), interleukin (IL)-5, and tumor necrosis factor (TNF)-alpha. Degranulation of mast cells was measured by tryptase staining of the lung tissue, and the expression of messenger RNA (mRNA) of IL-5 and TNF-alpha was determined by the reverse transcriptase-polymerase chain reaction method.


RESULTS
While preoperative administration of corticosteroid did not suppress the release of histamine and LTE(4) from the lungs of asthmatic patients, it completely suppressed IL-5 and TNF-alpha production at the mRNA level. The same results were obtained in lung tissues of nonasthmatic patients treated in vitro with dexamethasone.


CONCLUSIONS
Our results suggest that corticosteroid treatment reduces AHR and prevents perioperative attacks of asthma primarily by suppressing the production of inflammatory cytokines.
Mitsuta
K
K
Second Department of Internal Medicine, Nagasaki University School of Medicine, Nagasaki, Japan.
Shimoda
T
T
Fukushima
C
C
Obase
Y
Y
Ayabe
H
H
Matsuse
H
H
Kohno
S
S
D000284:Administration, Oral; D000328:Adult; D000368:Aged; D001249:Asthma / Q000517:prevention & control*; D016535:Bronchial Hyperreactivity / Q000517:prevention & control*; D016207:Cytokines / Q000037:antagonists & inhibitors* / Q000235:genetics; D005260:Female; D015870:Gene Expression / Q000187:drug effects; D006636:Histamine Release / Q000187:drug effects; D006801:Humans; D007262:Infusions, Intravenous; D015848:Interleukin-5 / Q000037:antagonists & inhibitors / Q000235:genetics; D007431:Intraoperative Complications / Q000517:prevention & control*; D017999:Leukotriene E4 / Q000378:metabolism; D008168:Lung / Q000187:drug effects / Q000276:immunology / Q000473:pathology; D008175:Lung Neoplasms / Q000473:pathology / Q000601:surgery*; D008297:Male; D008775:Methylprednisolone / Q000008:administration & dosage* / Q000009:adverse effects; D008875:Middle Aged; D011013:Pneumonectomy; D011239:Prednisolone / Q000008:administration & dosage* / Q000009:adverse effects; D011292:Premedication; D011656:Pulmonary Emphysema / Q000473:pathology / Q000601:surgery*; D012333:RNA, Messenger / Q000187:drug effects / Q000235:genetics; D014409:Tumor Necrosis Factor-alpha / Q000037:antagonists & inhibitors / Q000235:genetics
D016207:Cytokines; D015848:Interleukin-5; D012333:RNA, Messenger; D014409:Tumor Necrosis Factor-alpha; D017999:Leukotriene E4; D011239:Prednisolone; D008775:Methylprednisolone