Introduction Foodborne botulism is caused by the anaerobic bacterial agent-Clostridium botulinum-that is a gram-positive bacteria (1) and one of the most common life-threatening agents in the United States, Europe and Iran (2-4). In 2011, 140 cases of botulism were reported to the US Centers for Disease Control and Prevention which 14% of cases were due to food-borne botulism (5). Seven types of clostridium named A-G are studied (6) in which A, B, E, and F are the main potent poisoning types in human that produce botulinum neurotoxin (BoNT). These types of clostridium get absorbed in GI after ingestion and may lead to morbidities such as paralysis and mortality, although their toxins are sensitive to heat (4,7). Mostly, foodborne botulism is associated with consuming canned tuna fish, home-preserved or commercial food which contain vegetables (4,8-10). C. botulism releases neurotoxins into the blood and they bind to cells and lead to the impairment of the voluntary motor presynaptic cholinergic receptors and autonomic neuromuscular junctions (11-13). This leads to dizziness, blurred vision, slurred speech, ptosis (14) descending flaccid paralysis and respiratory failure because of the failure of transmission (11-13). All in all, the clinical symptoms can be observed after an incubation period and they are dependent on the serotype and degree of exposure to the toxin (15,16). Therefore, clinical findings are the principal key to the early diagnosis of botulism (2). Case Presentation A 48-year-old Caucasian woman referred to the emergency department complaining about acute dysphonia accompanied with dysarthria which cooccurred with dizziness, progressive symmetric hypotonia in upper and lower limbs, dilated pupils, facial paresthesia and bilateral ptosis. She had no dysphagia, fever, respiratory distress or vertigo. She had a history of consuming local dairy cheese. Based on clinical findings, the patient was admitted with the impression of botulinum intoxication. Botulism anti-toxin was administered. One vial of tetravalent botulism antitoxin was given intravenously as a 1:10 vol/vol dilution in 0.9% sodium chloride TDS. Since the most common cause of mortality is respiratory failure (17), supportive care was prepared and O 2 therapy, cardiac monitoring, pulse oximetry, and rapid sequence intubation equipment were considered and prepared in case of necessity. To rule out other probable causes, a neurology consult was requested. Blood and feces sample were taken and the probable occurrence of botulism was informed to the Health Center. The patient gradually became better. On the fifth day, the patient still had dysphonia and perioral paresthesia. She was hospitalized

Objective: The purpose of this study was to evaluate the effect of atorvastatin administration on amiodarone-induced pulmonary fibrosis in rats. Materials and Methods: Thirty-six male Wistar rats were randomly divided into 4 groups. The control group (CTL) received distilled water (0.3 ml intratracheally on days 0 and 2 and 0.5 ml orally from day 0 for 3 weeks). The atorvastatin group (AT), in addition to intratracheal distilled water, received 1 mg/kg of atorvastatin orally from day 0 for 3 weeks. The amiodarone group (AMI) received 2 intratracheal instillations of amiodarone (6.25 mg/kg in 0.3 ml of water) on days 0 and 2 and 0.5 ml of distilled water (like the CTL). The amiodarone plus atorvastatin group (AMI + AT) received both these drugs (same doses and methods as for the AMI and AT). After 28 days, the rate of lung fibrosis was estimated according to pathological criteria of lung sections and measurements of hydroxyproline in pieces of left lung tissue. Results: The lung hydroxyproline content was higher in the treated groups (CTL: 0.35 ± 0.017, AT: 0.38 ± 0.012, AMI: 0.375 ± 0.018 and AMI + AT: 0.38 ± 0.012 unit/mg protein), but did not reach significance when compared with the CTL (p = 0.56). Amiodarone administration significantly increased the score of pulmonary fibrosis (0.5) in comparison with the AT (0.125) and CTL (0) (p < 0.5). The combination of amiodarone and atorvastatin exacerbated the pulmonary fibrosis (1.5; p < 0.01) compared to the AMI (0.5; p < 0.001), AT (0.125) and CTL (0). Conclusion: In this study, the concomitant administration of amiodarone and atorvastatin increased pulmonary fibrosis in rats.

Objective: Behcet’s disease (BD) is a chronic multisystem inflammatory disease classified as Variable Vessel Vasculitis with unclear etiology. We designed this systematic review and meta-analysis to evaluate vitamin D status in Behcet’s disease patients with this background Methods: We performed this systematic review and meta-analysis according to (PRISMA) guidelines. We included all observational studies in humans published in English, evaluating the association of 25(OH)D concentrations in Behcet’s patients. Two reviewers (HRK and AE) independently searched the databases and screened articles based on their titles and abstracts. A third reviewer resolved all disagreements. We performed analysis using Cochrane Program Review Manager Version 5.3. The protocol for this review was registered on PROSPERO (CRD42020197426). Results: A total of 341 publications were initially identified according to the search strategy. Finally, 12 publications were included in the meta-analysis. We performed this meta-analysis on 1265 participants from different studies with a sample size from 63 to 224 individuals. In studies comparing Active and Inactive subgroups of patients with Behcet’s Disease, we found a significantly lower serum level of vitamin D in patients with Active BD (-0.4; 95%CI: -0.61, -0.25; p<0.00001). We found that the serum level of vitamin D in Behcet’s Disease is significantly higher than Health Controls (0.5; 95%CI: 0.15, 0.50; p=0.00001). Conclusion: We demonstrated that the existing evidence is consistent with the hypothesis that an increased serum level of vitamin D would be associated with substantially lower risk of active Behcet’s disease.

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