Martin Escribano P, Fernandez Sanchez Alarcos J M, Dominguez-Lozano M J, Diaz de Atauri J, Barbosa-Ayucar C, Cantalapiedra J A, Lopez Encuentra A
Bull Eur Physiopathol Respir. 1984 Jul-Aug;20(4):307-12.
The toxic oil syndrome is a new multisystemic disease, caused by ingestion of adulterated olive oil; this oil had a part of rapeseed oil, which was denatured with aniline for industrial use, and then re-refined. It is estimated that 20,000 people were more or less affected, the mortality being 1.7%. There is no clear pathogenetic mechanism, but the most probable is the generation of free radicals, caused by anilides. The clinical picture began with fever, acute interstitial pneumonia, pruritus, exanthems, myalgias and eosinophilia. The main pathological findings were generalized endothelial lesions, septal oedema, mild inflammatory mononuclear infiltrates and hydropic degeneration of type I and II pneumocytes with desquamation of type I. The pneumonic syndrome had a favourable evolution, except in 5% of the patients who went into acute respiratory distress and suffered an important mortality. In 10% of the patients, a moderate hypoxaemia remained with normal chest film; in these cases, a transbronchial biopsy showed more severe endothelial lesions and, in some of these patients, it was possible to find clinical signs of pulmonary hypertension, which was moderate and did not improve with oxygen or vasoactive agents. The neurological symptomatology was progressive, leading to very severe muscular atrophy and, in some cases, to alveolar hypoventilation. The neuromyopathy, as the other clinical manifestations, improved slowly during the following months. A year after the onset, a pulmonary restriction with a low transfer factor of CO remained, and some patients had residual neuromyopathy and severe scleroderma-like lesions of the skin. (ABSTRACT TRUNCATED AT 250 WORDS)
中毒性油综合征是一种新型多系统疾病,由摄入掺假橄榄油所致;这种橄榄油含有一部分菜籽油,该菜籽油用苯胺进行工业变性处理后再精炼而成。据估计,约20000人或多或少受到影响,死亡率为1.7%。目前尚无明确的发病机制,但最可能的原因是苯胺类化合物导致自由基生成。临床表现以发热、急性间质性肺炎、瘙痒、皮疹、肌痛和嗜酸性粒细胞增多症起病。主要病理表现为全身性内皮损伤、间质水肿、轻度单核细胞炎性浸润以及I型和II型肺细胞的水样变性伴I型肺细胞剥脱。除5%进展为急性呼吸窘迫且死亡率高的患者外,肺部综合征预后良好。10%的患者胸片正常但存在中度低氧血症;在这些病例中,经支气管活检显示内皮损伤更严重,部分患者可出现中度肺动脉高压的临床体征,吸氧或使用血管活性药物均无法改善。神经症状呈进行性发展,导致严重肌肉萎缩,部分病例出现肺泡通气不足。与其他临床表现一样,神经肌肉病变在接下来的几个月中缓慢改善。发病一年后,仍存在肺功能受限及一氧化碳弥散量降低,部分患者有残留的神经肌肉病变和严重的皮肤硬皮病样病变。(摘要截选至250词)