A Large Case-series of Successful Treatment of Patients Exposed to Mold and Mycotoxin.

PURPOSE: The goal of this study was to present the results of treatment of 100 chemically sensitive and chronically mold-exposed patients, who continued to be disabled even after decontamination of their houses or work places or they were physically removed from their sources of mold. METHODS: Molds were identified, serum anti-mold immunoglobulin G antibodies were measured, patients were skin-tested, immunologic abnormalities were recorded, and objective neurologic tests were performed in a subset of patients. FINDINGS: Patient sensitivities and exposures were confirmed by measuring serum immunoglobulin G anti-mold antibodies, intradermal skin testing, and trichothecene toxin breakdown products in the urine. Patients were positive (44%-98%) for individual molds. Abnormalities in T and B cells were found in >80% of patients. Respiratory signs were present in 64% of all patients, and physical signs and symptoms of neurologic dysfunction were present in 70%. Objective autonomic nervous system test results were abnormal in almost 100% of patients tested. Objective neuropsychological evaluations were conducted in 46 of the patients who exhibited symptoms of neurologic impairment and showed typical abnormalities in short-term memory, executive function/judgment, concentration, and hand/eye coordination. Patients (N = 100) with documented mold exposure were divided into 3 groups: (1) those who improved easily, with mold avoidance and antigen injections; (2) those who improved after desensitization to their mold antigens plus additional mycotoxin antigens; and (3) those who had their regular mold antigens, additional mycotoxin antigens, along with regimens that included sauna, oxygen therapy, and nutrients. Approximately 85% of all patients cleared completely; 14% had partial improvement, and 1% remained unchanged. IMPLICATIONS: Exposure to molds has been increasingly recognized as a major reason for patients presenting with multiple organ symptoms that could not otherwise be explained. Early diagnosis and appropriate treatment could be very successful.

Molecularly imprinted polymer as sorbent in micro-solid phase extraction of ochratoxin A in coffee, grape juice and urine.

A simple, environmental friendly and selective sample preparation technique employing porous membrane protected micro-solid phase extraction (µ-SPE) loaded with molecularly imprinted polymer (MIP) for the determination of ochratoxin A (OTA) is described. After the extraction, the analyte was desorbed using ultrasonication and was analyzed using high performance liquid chromatography. Under the optimized conditions, the detection limits of OTA for coffee, grape juice and urine were 0.06 ng g(-1), 0.02 and 0.02 ng mL(-1), respectively while the quantification limits were 0.19 ng g(-1), 0.06 and 0.08 ng mL(-1), respectively. The recoveries of OTA from coffee spiked at 1, 25 and 50 ng g(-1), grape juice and urine samples at 1, 25 and 50 ng mL(-1) ranged from 90.6 to 101.5%. The proposed method was applied to thirty-eight samples of coffee, grape juice and urine and the presence of OTA was found in eighteen samples. The levels found, however, were all below the legal limits.

Alkalinization of urinary pH accelerates renal excretion of ochratoxin A in pigs.

The mycotoxin ochratoxin A (OA) is a cause of endemic nephropathy in farm animals and humans. Reabsorption of OA along the nephron results from nonionic diffusion and by carrier-mediated mechanisms, indicating that urine alkalinization may help to accelerate OA excretion and thus reduce its toxicity. The aim of the present study was to investigate the effect of a dietary sodium bicarbonate supplementation as a means of increasing urinary pH on the systemic availability and excretion of OA in pigs. Dietary supplementation of 2% sodium bicarbonate significantly increased urinary pH (5.7 +/- 0.2 to 8.3 +/- 0.1) and daily urine volume (1108 +/- 276 to 2479 +/- 912 mL). The systemic availability of OA and its dechloro-analog, Ochratoxin B (OB), calculated as the area under the curve (AUC) was reduced to 75 and 68%, respectively, of the control group (P < 0.05). This effect was due mainly to an accelerated elimination of OA and OB in the urine. The faster renal elimination may be due to reduced reabsorption of the ochratoxins by nonionic diffusion, and other H(+)-dependent mechanisms. Thus, urinary alkalinization may be an efficient means to partially reduce the toxic effects of OA in pigs.

Therapy of cytotoxic mushroom intoxication.

Poisoning by cytotoxic mushrooms (Amanita phalloides and related species) is associated with severe morbidity and a high mortality rate. Due to the difficulty of performing controlled studies and to the poor knowledge of the pharmacodynamics of toxins in human poisoning, there is considerable debate about appropriate treatment, particularly the feasibility and the efficacy of detoxification. Because circulating amatoxins can be detected in the serum of poisoned patients as long as 30 h after ingestion, a detoxification treatment should ideally increase the rate of toxin elimination in order to minimize the toxic exposure of highly susceptible cells, such as hepatocytes. We found forced diuresis to be the most effective procedure for toxin removal. Other techniques, such as plasmapheresis and peritoneal dialysis, proved much less useful for this purpose. The administration of cathartics, adsorbent agents, and gastroduodenal lavage, are indicated for preventing further absorption of toxins from the gut. An important part of therapy is early and vigorous volume replacement, to correct the severe hypovolemia which results from massive fluid loss during the cholera-like phase of intoxication. Use of this therapeutic approach in 53 patients with amatoxin poisoning resulted in a high survival rate and a low incidence of severe liver injury.