High-Dose Intravenous Methylprednisolone Pulse Therapy as Initial Treatment in Cryptogenic Fibrosing Alveolitis

Gulsvik, Amund; Kjelsberg, Frank; Bergmann, Arild; Frøland, Stig S.; Rootwelt, K; Vale, J R

doi:10.1159/000194935

Cited by 15 publications

(9 citation statements)

References 11 publications

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“…Section 1734 solely to indicate this fact. tion after kidney transplantation (21), bronchial asthma (8), idiopathic pulmonary fibrosis (10), and bronchiolitis obliterans after lung transplantation (28). In experimental studies, MP inhibited the endotoxin-induced lung vascular permeability in sheep (5), ROS-induced increase in microvascular permeability of isolated rat lungs (15), and zymosan-induced pulmonary damage in rabbits (6).…”

mentioning

confidence: 99%

Effect of steroid on hyperoxia-induced ICAM-1 expression in pulmonary endothelial cells

Suzuki¹,

Nishio²,

Takeshita

et al. 2000

American Journal of Physiology-Lung Cellular and Molecular Phys

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Intercellular adhesion molecule-1 (ICAM-1) of the vascular endothelium plays a key role in the development of pulmonary oxygen toxicity. We studied the effect of steroid on hyperoxia-induced ICAM-1 expression using cultured endothelial cells in vitro. Human pulmonary artery endothelial cells (HPAECs) were cultured to confluence, and then the monolayers were exposed to either control (21% O(2)-5% CO(2)) or hyperoxic (90% O(2)-5% CO(2)) conditions with and without a synthetic glucocorticoid, methylprednisolone (MP). MP reduced hyperoxia-induced ICAM-1 and ICAM-1 mRNA expression in a dose-dependent manner. Neutrophil adhesion to hyperoxia-exposed endothelial cells was also inhibited by MP treatment. In addition, MP attenuated hyperoxia-induced H(2)O(2) production in HPAECs as assessed by flow cytometry. An electrophoretic mobility shift assay demonstrated that hyperoxia activated nuclear factor-kappaB (NF-kappaB) but not activator protein-1 (AP-1) and that MP attenuated hyperoxia-induced NF-kappaB activation dose dependently. With Western immunoblot analysis, IkappaB-alpha expression was decreased by hyperoxia and increased by MP treatment. These results suggest that MP downregulates hyperoxia-induced ICAM-1 expression by inhibiting NF-kappaB activation via increased IkappaB-alpha expression.

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confidence: 99%

Effect of steroid on hyperoxia-induced ICAM-1 expression in pulmonary endothelial cells

Suzuki¹,

Nishio²,

Takeshita

et al. 2000

American Journal of Physiology-Lung Cellular and Molecular Phys

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“…For some years MPPT has been used as an alternative treatment in immunoreactive diseases (3,7,10,16,21,25), in which the clinical effects have been shown to last several weeks. Apart from decreased natural killer cell activity (17), the exact modes of action of MPPT are still speculative, and the rationale for such megadoses has been questioned (2).…”

Section: Discussionmentioning

confidence: 99%

“…In controlled studies of methylprednisolone pulse therapy (MPPT), intravenous methyl-prednisolone (MP) Ig has proved effective for months in the treatment of immune-inflammatory disorders such as rheumatoid arthritis (25), lupus nephritis (3), acute allograft rejection after kidney transplantation (16), and idiopathic pulmonary fibrosis (7). Eurthermore, an effect has been suggested in systemic lupus erythematosus (10) and ankylosing spondylitis (21).…”

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confidence: 99%

Methylprednisolone pulse therapy in acute severe asthma

Engel

Dirksen

Frølund

et al. 1990

Allergy

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Methylprednisolone pulse therapy (MPPT) has been shown to possess a long-lasting effect in other immune-inflammatory diseases without the well-known side effects caused by long-term treatment with glucocorticosteroids. In an attempt to reduce the long-term use of oral steroids in asthmatics, we conducted this double-blind, double-dummy study to compare the use of MPPT (1 g of methylprednisolone intravenously) (8 patients) with a short course of oral prednisolone (10 patients) in asthmatics presenting with acute severe asthma. Both treatments were effective in relieving the acute attack of asthma. The MPPT-treated patients did not show a faster resolution than did the orally treated group. No patients needed assisted ventilation, and no deaths occurred. One week after the treatment FEV1 tended to decrease in the methylprednisolone group compared with the oral prednisolone group (P = 0.06). The patients initially receiving MPPT needed supplementary prednisolone earlier and in higher doses than did the patients receiving oral prednisolone as initial treatment. At the end of the 12 weeks' study period, the groups reached identical FEV1. In conclusion, we did not find intravenous methylprednisolone superior to oral prednisolone in the treatment of acute attacks of severe asthma, but methylprednisolone pulse therapy had a shorter duration as regards protection against future asthma attacks.

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“…However, no prospective placebo controlled randomized trial has been performed [Walter et al 2006], their efficacy is unproven [Lynch and McCune, 1997]. With these caveats, the 1999 ATS consensus, recommended treatment daily with 40 to 100 mg of prednisone or prednisolone for 2 to 4 months, with a subsequent gradual taper over the highdose intravenous "pulse" methylprednisolone (1 to 2 g once weekly or biweekly), which has no proven advantage over oral corticosteroids [Gulsvik et al 1986]. …”

Section: Treatment "Classics" Treatment Of Pulmonary Fibrosismentioning

confidence: 99%

Review: New perspectives in the treatment of idiopathic pulmonary fibrosis

Rogliani

Mura

Porretta

et al. 2008

Ther Adv Respir Dis

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Idiopathic pulmonary fibrosis (IPF) is the most frequent idiopathic interstitial pneumonia with a prevalence ranging from 5 to 15 per 100,000 persons, and above 175 per 100,000 in the older population. IPF is a relentlessly progressive fibrotic lung disorder leading to death within a median duration of 3 years. It was hypothesized in the 1970s that pulmonary fibrosis initiates as an "alveolitis" progressing to interstitial fibrosis with connective tissue deposition, derangement of the lung architecture and functional impairment. However, in vitro studies indicated that alveolar/bronchiolar injured epithelial cells can drive the fibrotic process in the absence of macrophages and with minimal inflammation. This, together with the inability of classic immunosuppressive therapy to cure IPF, generated new pathogenesis paradigms and intense research into the role of the lack or the excessive production of anti-fibrotic or profibrotic mediators, oxidant injury, exaggerated coagulation, thus leading to investigate new treatment strategies. Preliminary results of some of such trials have shown significant reductions in lung function decline, disease exacerbation and mortality.

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High-Dose Intravenous Methylprednisolone Pulse Therapy as Initial Treatment in Cryptogenic Fibrosing Alveolitis

Cited by 15 publications

References 11 publications

Effect of steroid on hyperoxia-induced ICAM-1 expression in pulmonary endothelial cells

Effect of steroid on hyperoxia-induced ICAM-1 expression in pulmonary endothelial cells

Methylprednisolone pulse therapy in acute severe asthma

Review: New perspectives in the treatment of idiopathic pulmonary fibrosis

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