دکتر علی موحد

Chronic rhinosinusitis (CRS) is a high prevalent disease throughout the world. The aim of this study was to investigate the epidemiological and clinical characteristics of the CRS patients.

A total of 241 CRS patients aged 15-70 years were recruited. The prevalence of allergic diseases and its association with CRS, disease severity, and quality of life (QoL) were assessed using GA2LEN and SNOT-22 questionnaires, respectively. Patients' clinical diagnoses and allergic comorbidities were evaluated using paranasal sinus computed tomography (CT), nasal endoscopy, and paraclinical tests (smell identification test, fractional exhaled nitric oxide (FeNO), skin prick test (SPT), pulmonary function test (PFT)).

The mean (±SD) age of all participants was 40.1±11.1 years, with a gender distribution of 56% male and 44% female. Nasal polyps (NP) were diagnosed in 42.4% of patients. The total mean SNOT-22 scores and the mean scores of the nasal symptoms category were significantly higher in CRS patients with NP (CRSwNP) compared to CRS without NP (CRSsNP) (OR = 2.3, 95%CI = 9.6–0.55, P = 0.028). Furthermore, there was a significant association between CRSwNP and persistent allergic rhinitis comorbidity (P = 0.006). Finally, a significant association was found between CRSwNP and severe SPT reactivity to Dermatophagoides farina and date palm pollen (P = 0.04 and P < 0.001, respectively).

This study suggests that higher SNOT-22 scores may impact QoL in CRSwNP patients. Additionally, a significant association was found between CRS and respiratory allergic diseases.

Familial hypercholesterolemia (FH) is the most common genetic disease in the world and an autosomal dominant disease characterized by increased plasma cholesterol and low-density lipoprotein (LDL) concentrations. The clinical diagnosis of the disease is based on family history, the findings of medical examinations, and the measurement of cholesterol levels. The most important cause of FH is the mutation in one of the LDL-R, APOB, and PSCK9 genes. About 90% of mutations occur in the LDL-R gene, which accounts for a total of 2,000 different mutations. Different types of mutations have been observed on different exons of the LDL-R gene, but most of the mutations have been reported on Exon 4. The aim of this study was to sequence and analyze Exon 4 in patients with familial hypercholesterolemia in Bushehr province in Iran.

In this study, 32 patients were selected based on global criteria for diagnosing the disease, and a portion of LDL-R containing complete sequence of exon 4 was amplified using LDLRE4F1/ LDLRE4R1 Primers and blood genomic DNA as a template. PCR products were sequenced and compared with reference sequence to find probable muta tions.

The results of sequencing and comparison with the reference sequence showed that no mutation was found in the exon 4 LDL-R gene. Therefore, this exon did not play a role in FH in the population under study.

Therefore, the cause of FH may be due to the mutations in other areas of the LDL-R gene or other genes, such as APOB and PSCK9.

Iranian Naja oxiana (the Elapidae family) known as cobra snake inhabits in the northwestern part of Iran. This study aimed to evaluate the edematogenic potency of the crude venom with intraplantar injection into mice. Additionally, the inhibitory effects of three different drugs (i.e., promethazine, dexamethasone, and piroxicam) on paw edema were examined. Moreover, the gelatinase activity of this venom was assessed using the zymography method. Paw edema was induced by the intraplantar injection of different concentrations of the venom (0.5-5 μg dissolved in 50 μl of normal saline) into the mice (six in each group). It was estimated through the measurement of the increase in the paw thickness (%) with a digital caliper. The paws were pretreated and the rate of changes was measured after the venom injection. Pathological findings in the treated paws were evaluated with hematoxylin and eosin staining. Paw thickness reached its maximum amount within 5 min and resolved after 1 h. This venom had no gelatinase activity using the zymography method ruling out its role in edema. It caused non-hemorrhagic diffuse edema with the infiltration of inflammatory cells (i.e., leukocytes and lymphocytes) in the dermis. Intraperitoneal pretreatment with drugs significantly inhibited the venom-induced (1 μg/paw) edema; however, all the mice died unexpectedly a day after piroxicam injection. This in vitro and in vivo preliminary study demonstrated for the first time that N. oxiana venom-induced non-hemorrhagic edema in a short time. Dexamethasone (phospholipase A2 inhibitor; 1 mg/kg) and promethazine (H1 inhibitor; 5 mg/kg) decreased the venom-induced edema (p <0.001). It is suggested to carry out further studies to identify different mediators in venom-induced edema formation.