Plasma omentin levels in drug-free patients with schizophrenia.

AIMS: We aimed to investigate plasma omentin concentrations in non-obese, drug-free patients with schizophrenia in comparison with healthy volunteers. METHOD: Thirty-two patients with schizophrenia and 33 control subjects were recruited. Plasma omentin levels were determined by enzyme-linked immunosorbent assay. RESULTS: Plasma levels of omentin (ng/ml) were found to be markedly lower in patients with schizophrenia (median = 7.7, 25th percentile = 6.3, 75th percentile = 604.9) than in controls (median = 486, 25th percentile = 326, 75th percentile = 794.2, p < 0.01). No significant difference was found between drug-free (n = 23) and drug-naive (n = 9) patients with respect to plasma omentin levels. Omentin concentrations correlated negatively with severity of illness, suggesting that patients with more severe pathology had lower fasting levels of omentin (n = 32; r = -0.387; p = 0.029). CONCLUSION: The present results suggest that plasma omentin levels are decreased in physically healthy, non-obese, antipsychotic-free patients with schizophrenia when compared with physically and mentally healthy individuals. To our knowledge, this is the first study that demonstrated the association between omentin and schizophrenia.

Carboxyatractyloside poisoning in humans.

OBJECTIVE: Cocklebur (Xanthium strumarium) is an herbaceous annual plant with worldwide distribution. The seeds contain the glycoside carboxyatractyloside, which is highly toxic to animals. We describe nine cases of carboxyatractyloside poisoning in humans which, to our knowledge, has not previously been reported. The clinical, laboratory and histopathological findings and our therapeutic approach are also discussed. SUBJECTS AND METHODS: The patients presented with acute onset abdominal pain, nausea and vomiting, drowsiness, palpitations, sweating and dyspnoea. Three of them developed convulsions followed by loss of consciousness and death. RESULTS: Laboratory findings showed raised liver enzymes, indicating severe hepatocellular damage. BUN and creatinine levels were raised, especially in the fatal cases who also displayed findings of consumption coagulopathy. CPK-MB values indicative of myocardial injury were also raised, especially in the fatal cases. Three of the patients died within 48 hours of ingesting carboxyatractyloside. Post-mortem histopathology of the liver confirmed centrilobular hepatic necrosis and renal proximal tubular necrosis, secondary changes owing to increased permeability and microvascular haemorrhage in the cerebrum and cerebellum, and leucocytic infiltrates in the muscles and various organs including pancreas, lungs and myocardium. CONCLUSIONS: Carboxyatractyloside poisoning causes multiple organ dysfunction and can be fatal. Coagulation abnormalities, hyponatraemia, marked hypoglycaemia, icterus and hepatic and renal failure are signs of a poor prognosis. No antidote is available and supportive therapy is the mainstay of treatment.