Search

Objective: To explore whether antiphospholipid antibodies (aPL) are markers of vascular related damage or merely evidence of toxic related autoimmunity, we investigated the presence of different aPL in patients with toxic oil syndrome (TOS) and compared the profile with patients with eosinophilia myalgia syndrome (EMS)., Methods: Reactivity against cardiolipin, P-serine, P-inositol, and P-choline was investigated by ELISA in the blood of 266 patients with acute and chronic TOS, 25 healthy relatives of TOS patients, and 48 patients with EMS., Results: 32% of TOS and 13% of EMS patients had IgG antibodies against cardiolipin and other polyanions. 20% of both TOS and EMS patients presented IgM antibodies against anionic and zwitterionic phospholipids. 36% of TOS healthy relatives had IgM antibodies against differently charged phospholipids. Among 200 patients with chronic TOS, there was no significant association between antibodies and clinical manifestations., Conclusion: aPL with different specificity are present in a high percentage of patients with TOS and EMS. The significance of these antibodies remains unclear.

Objective: To determine the longterm clinical and functional outcome among a large group of patients with toxic oil syndrome (TOS)., Methods: One hundred individuals with onset in 1981 were randomly selected for followup in 1993 from a national TOS database. Clinical and laboratory data for 1981 were collected by retrospective chart review. Ninety-one survivors were reevaluated in 1993 by direct interview, examination, the Health Assessment Questionnaire (HAQ), and the visual analog scale (VAS) for pain. A semiquantitative Total Clinical Score (TCS) was created to assess relative global outcome in 1993, for comparison with the HAQ, and for developing a predictive model based on disease manifestations at onset., Results: Fifty-eight percent continue to have symptoms consisting predominantly of muscle cramping (60%), fatigue (55%), arthralgias (43%), subjective cognitive impairment (44%), psychiatric disease (27%), and soft tissue tenderness (22.5%). Severe neuromuscular sequelae, sclerodermatous skin disease, or pulmonary hypertension were not detected. The most notable laboratory findings at followup were hypercholesterolemia (55%) and hyperglycemia (14.5%). A good correlation was demonstrated between both the HAQ and the VAS for pain with the TCS. A statistical model indicated that alopecia, Raynaud's phenomenon, and sensory neuropathy were predictive of outcome., Conclusion: TOS is commonly associated with longterm neuromuscular and articular disease. Multiple factors implicated in the adaptation to chronic disease may contribute to this morbidity.

The eosinophilia-myalgia syndrome (EMS) was associated with ingestion of L-tryptophan containing products and was accompanied by altered metabolism of L-tryptophan during the active phase. Many patients with EMS exhibited clinical and histopathological features similar to another epidemic, the toxic oil syndrome (TOS), associated with ingestion of adulterated rapeseed oil. We hypothesized that patients with TOS, like patients with EMS, may have had altered metabolism of L-tryptophan during the acute phase of the illness. Therefore, we quantitated the tryptophan metabolites, L-kynurenine and quinolinic acid, and we measured neopterin, a marker of interferon-gamma (IFN-gamma), in blood obtained during the acute phase of each syndrome. Patients with TOS or EMS had significantly higher L-kynurenine and quinolinic acid than healthy control subjects or rheumatic disease control subjects. Neopterin was also elevated in patients with untreated TOS and EMS, and correlated strongly with L-kynurenine and quinolinic acid. Our data suggest that indoleamine-2,3-dioxygenase (IDO), the rate limiting enzyme of the kynurenine pathway of L-tryptophan metabolism, was activated in both syndromes by cytokines including IFN-gamma, and that perhaps products of tryptophan metabolism played a role in the pathogenesis of EMS and TOS.