Fatal Pulmonary Intra-Alveolar Fibrosis after Paraquat Ingestion

Copland, G. M.; Kolín, A; Shulman, Harry

doi:10.1056/nejm197408082910607

Cited by 90 publications

(14 citation statements)

References 8 publications

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“…Three of these also smoked marijuana regularly. Alveolar hemorrhage has been associated with toxic contamination of marijuana with paraquat, however this exposure is associated with a histologic pattern of diffuse alveolar damage rather than capillaritis (32). No other history of drug exposure was found with the exception of one patient with amphetamine use in addition to marijuana.…”

Section: Discussionmentioning

confidence: 98%

Diffuse alveolar hemorrhage with underlying isolated, pauciimmune pulmonary capillaritis.

Jennings¹,

King²,

Tuder³

et al. 1997

Am J Respir Crit Care Med

117

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Diffuse alveolar hemorrhage (DAH) resulting from pulmonary capillaritis typically accompanies the systemic vasculitides and collagen vascular diseases. Isolated pulmonary capillaritis and DAH without systemic disease occurs in patients with antineutrophil cytoplasmic antibodies. However, isolated pulmonary capillaritis and DAH is not described for patients without clinical or serologic evidence for an underlying systemic disease. To describe such patients, we undertook a retrospective chart review of 29 patients with DAH and biopsy-proven pulmonary capillaritis from seven Denver hospitals. Eight (28%) were diagnosed with isolated pulmonary capillaritis without clinical, serologic, or histologic evidence of an associated illness. Their median age was 30 yr. No association with occupational or drug exposures was identified. All had lower respiratory tract symptoms; seven had upper respiratory tract symptoms. None demonstrated systemic disease or evidence of glomerulonephritis. All were antineutrophil cytoplasmic antibody negative. Other serologies were not significant where measured. Direct immunofluorescence studies of lung tissue were negative in five. Six presented with acute respiratory failure, four requiring mechanical ventilation. One died during initial hospitalization; seven survived. Median follow-up is 43 mo (7 to 73 mo). Five remain in remission. Two experienced multiple recurrences of DAH but without development of systemic disease while on therapy. Herein we characterize DAH and isolated pulmonary capillaritis in the absence of clinical, serologic, or histologic evidence indicating an accompanying systemic illness. The prognosis for this group appears favorable.

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Section: Discussionmentioning

confidence: 98%

Diffuse alveolar hemorrhage with underlying isolated, pauciimmune pulmonary capillaritis.

Jennings¹,

King²,

Tuder³

et al. 1997

Am J Respir Crit Care Med

117

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“…18 The survivor of the early phase usually dies from irreversible respiratory failure resulting from an obliterative fibrosing alveolitis. 20 These pulmonary alterations occur following fibroblast proliferation and augmented collagen synthesis. 3,4 In recent years, some pieces of evidence have accumulated to identify the role of the production of reactive oxygen species, in conjunction with paraquat metabolism, in mediating toxicity of this xenobiotic.…”

Section: Discussionmentioning

confidence: 99%

Captopril inhibits the pulmonary toxicity of paraquat in rats

Candan

Alagözlü

2001

Hum Exp Toxicol

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Paraquat (PQ) is a herbicide that is very toxic to all living organisms. It generates free radicals and leads to acute or chronic lung injury. Free radicals are often associated with fibrogenesis, which occurs in various disease states. The purpose of this study was to determine whether captopril prevents paraquat toxicity in lung tissue. Paraquat alone increased the level of lipid peroxidation (LPO) and the activity of superoxide dismutase (SOD) after 4, 12, 24 and 72 h of administration. Also, the level of hydroxyproline showed an increase after 24 h of paraquat administration. However, paraquat also decreased the level of glutathione (GSH) and the activity of glutathione peroxidase (GSH-Px). Captopril (50 mg/kg i.p.) and paraquat were simultaneously injected (40 mg/kg i.p.), and the captopril injection 1 h after paraquat ameliorated the biochemical toxicity induced by paraquat. This was evidenced by a significant reduction in LPO and balancing the endogenous anti-oxidant capacity by normalizing the activities of SOD and GSH-Px and the GSH content in the lung tissue. Moreover, captopril injection prevented the increase of hydroxypro-line content as an index of lung fibrosis. From these results, the beneficial effects of captopril on paraquat toxicity appear to be through enhancement of the endogenous anti-oxidant system preventing the lung fibrosis.

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“…These patients had a histopathological pattern including hyaline membranes and mural incorporation of intra-alveolar fibrosis, suggesting the organising stage of diffuse alveolar damage rather than typical organising pneumonia [306,308]. Paraquat ingestion usually results in diffuse alveolar damage, but hyaline membranes were not present in a fatal case with intra-alveolar fibrosis [310]. Organising pneumonia has been Amiodarone [90,230,[233][234][235][236][237][238][239][240] Amphotericin B [241] Bleomycin [18,[242][243][244][245][246][247][248][249][250][251][252] Busulfan [230,253,254] Busulfan and cyclophosphamide [230] Carbamazepine [255,256]; in association with carbamazepine induced lupus [257] Cephalosporin (cefradin) [258] Chlorambucil [259] Doxorubicin Possible recall after radiation to the breast [260] Fluvastatin [261] Gold salts [262,263] Hexamethonium [264] Interferon-a [264,265] Interferon-a2b, pegylated interferon a2b …”

Section: Fungimentioning

confidence: 91%

Cryptogenic organising pneumonia

Jf¹

2006

Eur Respir J

485

466

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Organising pneumonia is defined histopathologically by intra-alveolar buds of granulation tissue, consisting of intermixed myofibroblasts and connective tissue. Although nonspecific, this histopathological pattern, together with characteristic clinical and imaging features, defines cryptogenic organising pneumonia when no cause or peculiar underlying context is found. Rapid clinical and imaging improvement is obtained with corticosteroid treatment, but relapses are common after stopping treatment.

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Fatal Pulmonary Intra-Alveolar Fibrosis after Paraquat Ingestion

Cited by 90 publications

References 8 publications

Diffuse alveolar hemorrhage with underlying isolated, pauciimmune pulmonary capillaritis.

Diffuse alveolar hemorrhage with underlying isolated, pauciimmune pulmonary capillaritis.

Captopril inhibits the pulmonary toxicity of paraquat in rats

Cryptogenic organising pneumonia

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