Allergic fungal rhinosinusitis (AFRS) is the most common form of fungal sinus disease. Its recurrence rate is high despite numerous strategies to prevent it. We conducted a study to assess the eff ect of systemic and topical antifungal agents-both separately and in combination-in preventing recurrence of AFRS following functional endoscopic sinus surgery (FESS). Our initial study population was made up of 50 adults who were diagnosed with AFRS by clinical, radiologic, histopathologic, and laboratory workup and who subsequently underwent FESS. Postoperatively, these patients were randomized into 5 diff erent treatment groups matched for sex, age, and socioeconomic status. Four of the groups received a diff erent antifungal regimen in addition to convenient medical treatment (CMT), while a fi ft h group served as a control. Th e antifungal regimens included oral itraconazole (group A), fl uconazole nasal spray (group B), combined oral itraconazole and nasal fl uconazole (group C), and irrigation with a fl uconazole solution through the nasal fossa (group D); the group of 10 controls (group E) received CMT only. A total of 41 patients were available for follow-up (9 mo maximum). Recurrence rates in the 5 groups were 66.7, 10.0, 14.3, 28.6, and 75.0%, respectively. Based on our fi ndings, we conclude that treatment with topical fl uconazole as either a nasal spray or an irrigation solution can signifi cantly reduce the rate of recurrence of AFRS aft er FESS.

Serum adiponectin was increased in β-thalassaemia major as were pro-inflammatory markers (CRP and IL-6). Its level is directly associated with ferritin and IL-6 levels.

The triggering receptor expressed on myeloid cells-1 (TREM-1) is a member of the immunoglobulin superfamily. TREM-1 has been implicated as an amplifier of inflammation. Soluble TREM-1 (sTREM-1) was investigated in different clinical conditions, but not in hemodialysis (HD) patients. We aimed to investigate sTREM-1 as a marker of inflammation in HD patients. We investigated 40 CKD patients undergoing chronic HD treatment and 15 controls. Routine laboratory investigations in addition to CRP measured by immunoturbidimetry, TNF- α, and sTREM-1 measured by ELISA were assayed in post-hemodialysis patients' blood samples and in controls' blood samples. CRP, TNF-α, and sTREM-1 levels were significantly higher in HD patients than in controls (p < 0.001 for all). sTREM-1 was positively correlated with CRP and TNF-α (r = +0.50, p < 0.001 and r = +0.53, p < 0.001 respectively). It was negatively correlated with hemoglobin concentration (r = -0.69, p < 0.001). Hemoglobin concentration was the significant predictor of sTREM-1 level (p < 0.001). In conclusion, sTREM-1 level is significantly increased in HD patients as are other pro-inflammatory markers.

No abstract

Molecular pathology of chronic obstructive pulmonary disease (COPD) is still being investigated to discover relationships with disease pathogenesis. Evidence of plasminogen activator inhibitor-1 (PAI-1) overexpression in the sputum and the blood of COPD patients is growing. We aimed to investigate the potential relation between PAI-1 promoter 4G/5G insertion/deletion polymorphism and COPD development. In a case-control study, we genotyped 117 COPD patients and 160 control subjects for PAI-1 promoter 4G/5G polymorphism by an allele-specific polymerase chain reaction analysis. All subjects were male smokers. In the co-dominant model, there was a significant difference in the distribution of 5G/5G, 4G/5G and 4G/4G genotypes between COPD patients and controls (p = 0.002). In the recessive model, carriers of 4G/4G genotype were significantly higher in COPD patients than controls (p = 0.01). Carriers of 4G/4G genotype were at higher risk to develop COPD than those carrying 5G/5G or 4G/5G genotypes (crude odds ratio (OR) = 2.10, 95% confidence interval (CI) = 1.19-3.73, adjusted OR = 2.5, 95% CI = 1.22-3.99). In conclusion, PAI-1 4G/5G genetic variations are associated with COPD development in males.

Association between variable agent-induced hepatocellular carcinoma (HCC) and both PAI-1 4G/5G polymorphism and plasminogen activator inhibitor (PAI-1) levels compared to healthy controls have been reported in earlier studies. We aimed to assess serum PAI-1 and PAI-1 4G/5G polymorphism in hepatitis C virus (HCV)-induced HCC, HCV-induced liver cirrhosis, and viral infection-free apparently healthy control subjects. Forty nine HCC, 52 cirrhosis, and 105 controls were genotyped for PAI-1 4G/5G using an allele-specific polymerase chain reaction analysis. In addition, for 31 HCC, 24 cirrhosis, and 28 controls, serum PAI-1 level was measured by enzyme-linked immunosorbent assay (ELISA). There was no significant difference in PAI-1 4G/5G genotype distribution between cirrhosis and controls (p = 0.33, p = 0.15, and p = 0.38 for the codominant, dominant, and recessive models, respectively) or between HCC and cirrhosis (p = 0.5, p = 0.24, and p = 0.69 for the codominant, dominant, and recessive models, respectively). Serum PAI-1 was significantly higher in cirrhosis than controls and significantly lower in HCC than cirrhosis (p < 0.001 for both). Serum PAI-1 did not differ significantly among the three PAI-1 4G/5G genotypes in controls, cirrhosis, and HCC (p = 0.29, p = 0.28, and p = 0.73 respectively). We documented higher serum PAI-1 in HCV-induced HCC than viral infection-free controls, but interestingly, lower than HCV-induced liver cirrhosis patients. This was not genotype related. Further studies will be needed to clearly elucidate the underlying mechanism.

Aim:  To evaluate the value of peripheral blood mammaglobin (MG) gene expression for diagnosis and prediction of metastasis in breast cancer patients. Methods:  MG expression was detected by nested reverse‐transcription polymerase chain reaction in the peripheral blood of 46 females (32 breast cancer, 12 benign breast lesions, 2 no breast abnormalities). In total 28 breast cancer patients were followed up through a period of 34 months for the development of metastasis. Results:  MG expression was detected in 16/32 (50%) breast cancer patients but not in patients with benign lesions or healthy participants. Five patients had metastasis at diagnosis. During the 34 months of follow up, five more MG‐positive patients showed metastatic lesions and none of the MG negative patients who were followed up developed metastasis. Conclusion:  The study suggests blood MG expression is a specific molecular marker for detection of occult mammary carcinoma cells of patients with operable breast cancer. It might be of value as a predictor of subsequent metastasis. Large‐scale studies and longer follow‐up periods are needed.

MNS16A genetic variations are associated with DLBCL susceptibility.