ARCHIVES OF IRANIAN MEDICINE
Year:2012 | Volume:15 | Issue:11|Papers Count:16

A recent review and systematic analysis revealed that over two million new cancer cases were attributable to various infections in 2008. Helicobacter pylori (H. pylori) is expectedly the leading infection accounting for as many as 650,000 new cases annually of non-cardia gastric cancer worldwide.1 After the discovery of H. pylori by Warren and Marshall in 1982, accumulating evidence has unmasked a string of associations between the infection and gastric cancer. Now, the central role of H. pylori infection in the pathogenesis of gastric cancer, including both the intestinal and diffuse histological subtypes, is not to be ignored. Although gastric cancer is the outcome of a multi-factorial pathway, the crucial role of an infectious agent involved in its pathogenesis makes it potentially preventable through eradication therapy that utilizes effective antibiotics.

BACKGROUND: Regression of precancerous lesions after H. pylori eradication remains controversial. This study evaluates the change and topography in first degree relatives (FDR) of gastric cancer (GC) patients following H. pylori eradication.METHODS: Participants underwent endoscopy with antrum and corpus histological examinations. Subjects with pangastritis were randomly allocated to placebo or eradication therapy and followed over 41/2 years.RESULTS: Among 989 evaluated FDR, we excluded 468 patients as follows: 108 had macroscopic lesions, 243 had no evidence of any H. pylori infection, and 117 were excluded for other reasons. The remaining subjects (n=521) were allocated to therapy (group A, n=261) or placebo (group B, n=260) groups. Interim analysis of 403 subjects (201 placebo, 202 therapy) showed regression of atrophy (60 out of 97 in the antrum and 37 out of 104 in the corpus) in H.pylori-eradicated versus regression of atrophy (57 out of 184 in the antrum and 23 out of 173 in the corpus) in non-H.pylori-eradicated cases over 21/2 years (P<0.0001). No regression of intestinal metaplasia (IM) occurred in the antrum and corpus of treated subjects over 41/2 years. However, progression of IM occurred in the antrum in 17 out of 90 patients in the non-H. pylori-eradicated versus 4 out of 68 H. pylori-eradicated subjects after 41/2 years (P<0.05).CONCLUSION: Eradication of H. pylori is associated with regression of gastric atrophy but not IM, even in its early stages. Gastric atrophy and IM in the antrum have shown more rapid progression in cases not treated for H. pylori infection (over 41/2 years follow-up) compared to H. pylori-eradicated cases.

BACKGROUND: Pseudomonas aeruginosa is the most important bacterium isolated from burn wounds, and its resistance to imipenem due to metallo-beta-lactamases is increasing. This study was designed to detect vim1, vim2, ipm1 and ipm2 metallo-beta-lactamases genes between Pseudomonas aeruginosa isolates isolated from Shahid Motahari Burns Hospital, Iran.METHODS: To that end, we isolated 483 nonduplicate consecutive isolates of P. aeruginosa from burn infections; and after biochemical confirmation, we examined the imipenem susceptibility via the Kirby-Bauer method. All the imipenem-resistant and imipenem-intermediate isolates were screened for vim1, vim2, ipm1 and ipm2 genes through the PCR method.RESULTS: From the 483 isolates, 272 (56%) and 63 (13%) isolates had resistant and intermediate zones in their imipenem antibiogram pattern, respectively. Fifty-four (16.1%), 7 (2.1%), 22 (6.6%), and 11 (3.3%) of the resistant and intermediate isolates had vim1, vim2, ipm1 and ipm2 genes in their PCR results, respectively.CONCLUSION: MBL-mediated imipenem resistance in P. aeruginosa is a cause for concern in the treatment of infective burn patients. The rate of imipenem resistance due to MBL was increased dramatically and newer versions of MBL families were detected for the first time. These results suggest that an effective method should be provided to fight MBL production in clinical isolates.

BACKGROUND: Paracetamol overdose causes severe hepatotoxicity that leads to liver failure in both humans and experimental animals. The present study investigates the protective effect of honey against paracetamol-induced hepatotoxicity in Wistar albino rats. We have used silymarin as a standard reference hepatoprotective drug.METHODS: Hepatoprotective activity was assessed by measuring biochemical parameters such as the liver function enzymes, serum alanine aminotransferase (ALT) and serum aspartate aminotransferase (AST). Equally, comparative effects of honey on oxidative stress biomarkers such as malondialdyhyde (MDA), reduced glutathione (GSH) and glutathione peroxidase (GPx) were also evaluated in the rat liver homogenates. We estimated the effect of honey on serum levels and hepatic content of interleukin-1beta (IL-1b) because the initial event in paracetamol-induced hepatotoxicity has been shown to be a toxic-metabolic injury that leads to hepatocyte death, activation of the innate immune response and upregulation of inflammatory cytokines.RESULTS: Paracetamol caused marked liver damage as noted by significant increased activities of serum AST and ALT as well as the level of Il-1b. Paracetamol also resulted in a significant decrease in liver GSH content and GPx activity which paralleled an increase in Il-1β and MDA levels. Pretreatment with honey and silymarin prior to the administration of paracetamol significantly prevented the increase in the serum levels of hepatic enzyme markers, and reduced both oxidative stress and inflammatory cytokines. Histopathological evaluation of the livers also revealed that honey reduced the incidence of paracetamol-induced liver lesions.CONCLUSION: Honey can be used as an effective hepatoprotective agent against paracetamol-induced liver damage.

BACKGROUND: This study assesses the accuracy of energy intake (EI) reporting and its relation to anthropometric characteristics and sociodemographic factors. In addition, we attempt to identify foods for which under- or over-reporting is more prevalent.METHODS: EI was assessed for 187 women using a semi-quantitative 168-item food frequency questionnaire (FFQ). Resting metabolic rate (RMR) was measured with an indirect calorimeter. We calculated the EI/RMR ratio to assess the accuracy of EI reporting. This study defined under-reporters as those with an EI/RMR of ≤ 1.34 and over-reporters as those with an EI/RMR of ≥2.4. We measured anthropometric characteristics and collected sociodemographic information. The chi-square test, ANOVA and multiple linear regressions were used for statistical analyses.RESULTS: Among participants, the under-reporting rate was 35.5% and the over-reporting rate was 7.5%. The EI/RMR ratio was significantly higher for younger women compared to older women (P<0.04). Under-reporters had higher weight, waist circumference (WC), body mass index (BMI) and resting metabolism compared to accurate reporters (P<0.05). Resting metabolism was significantly lower among over-reporters than accurate reporters. After adjusting for energy, the consumption of fish, high-fat dairy products, hydrogenated oil, sweets and coffee was lower, whereas consumption of unsaturated oils, tea, salt and yellow vegetables was higher among under-reporters compared to accurate reporters.CONCLUSION: Under-reporting of EI is more frequent than over-reporting among Iranian women. Among various factors that may affect the accuracy of EI reporting, age and anthropometric characteristics might have a significant effect.

BACKGROUND: Visfatin, a novel adiopocytokine, has been proven to be a proinflammatory mediator involved in the process of atherosclerosis. Visfatin has been shown to play a role in plaque destabilization as it is found abundantly in foam cell macrophages within unstable atherosclerotic plaques. The present study is designed to investigate the potential association between serum vistafin levels and the risk of acute myocardial infarction (AMI).METHODS: There were 72 patients (mean age: 61.57±11.40 years) as cases who presented with first-time AMI that were assessed 8 hours after the incident. The control group consisted of 83 healthy volunteers (mean age: 60.30±8.32 years). Plasma visfatin levels were measured using enzyme immunoassay in both groups. Biochemical parameters were analyzed. Blood pressure, body mass index (BMI), waist circumference, diabetes, and hypertension were recorded.RESULTS: Serum visfatin levels were significantly higher in patients with AMI (12.77±8.06 ng/ml) compared to controls (6.57±2.96 ng/ml, P≤0.001). We found that a visfatin level >7.244 ng/ml (log visfatin > 0.86) had a sensitivity of 70% and a specificity of 75% for predicting AMI.CONCLUSION: We have detected high levels of visfatin in patients with AMI. It can be concluded that proinflammatory cytokines such as visfatin may play a role in the development of atherosclerosis as well as destabilization of the atherosclerotic plaque.

BACKGROUND: Device closure of an isolated secundum type atrial septal defect (ASD) has been used as an alternative method for open surgical closure with comparable success and lower morbidity. In this study we evaluated the procedural success and mid-term follow-up results of percutaneous closure of secundum ASD with an AmplatzerTM Septal Occluder (ASO) device or a Figula ASD occluder device.METHODS: From June 2001 to January 2009, 74 consecutive patients were scheduled for percutaneous device closure in two centers in Tehran, Iran. All patients had a stretched defect diameter of 30mm or less. After using a sizing balloon to measure the stop-flow diameter, device implantation was performed under the guidance of a trans-esophageal echocardiography (TEE).The size was generally 1-2 mm larger than the stretched diameter. Patients were followed for an average of 11±4 months.RESULTS: The median stretched diameter of the defect was 20.7±4.8 mm (range: 8-30 mm).A total of 73 devices were used in this study. Device closure was successful in 72 (97.2%) out of 74 patients. Repositioning of the device was required in one patient. Major complications (including significant residual shunt and device embolization) occurred in 3 (4%) patients. There was no procedure-related mortality in our patients. Mild-to-moderate residual shunt was detectable in 10 (13.7%) patients immediately following the procedure and in 5 (6.7%) patients 24 hours after the procedure. None had residual flow across the device at the end of the follow-up period.CONCLUSION: Device closure of ASD has a safety profile comparable to open surgical repair and can effectively close the defect with excellent procedural and mid-term results.

BACKGROUND: Cancer is the fifth leading cause of death worldwide. There are considerable efforts to identify naturally occurring substances for use as new drugs in cancer therapy. Some components of animal venoms have been identified that possess substantial anticancer properties. In our previous studies, the cytotoxic effects of ICD-85 (venom-derived peptides) have been reported on HL-60 and MDA-MB231 cell lines. This has prompted us to investigate the comparative cytotoxic effects of ICD-85 on the HeLa cell line and normal lamb kidney (LK) cells.METHODS: Cells were exposed to various concentrations (8´10-4 to 5.6´10 mg/ml) of ICD-85 at various incubation times (24, 48 and 72 hours). Cell viability was measured by the MTT assay. A morphological study was also carried out using an inverted microscope. Caspase-8 activity was assayed by the Caspase-8 Colorimetric Assay Kit in HeLa cells that were exposed to ICD-85 for 48 hours.RESULTS: Data analysis showed that ICD-85 has a dose-dependent cytotoxic effect on HeLa cells with an inhibitory concentration 50% (IC50) of 26.62±2.13 mg/ml at 24 hours, 27.33±2.35 mg/ml at 48 hours, and 28.13±2.52 mg/ml at 72 hours. Results also indicated that the cytotoxic effect of ICD-85, at 48 and 72 hours incubation times did not show significant alteration compared to 24 hours of exposure. Interestingly, the minimum concentration of ICD-85 which showed a cytotoxic effect on LK cells was found to be 3500-fold less than the minimum concentration that showed a cytotoxic effect on the HeLa cancer cells. While morphological analysis revealed a significant difference that included the characteristic rounding of dying cells by treatment with ICD-85 compared with untreated HeLa cells, this difference was not observed in normal cells. ICD-85 increased caspase-8 activity in HeLa cells after 48 hours of exposure.

BACKGROUND: Nocturnal enuresis is divided into monosymptomatic nocturnal enuresis (MNE) and non-monosymptomatic nocturnal enuresis (NMNE). This study reviews clinical and ultrasonography (US) findings in enuretic children, and compares the organic and functional pathologies of the lower urinary tract (LUT) in children with MNE to those who have NMNE.METHODS: We enrolled 111 neurologically normal children with chief complaints of enuresis in this study. Participants included 60 boys and 51 girls, aged 5-17 years. There were 43 (38.8%) patients diagnosed with MNE and 68 (61.2) % with NMNE. Urine analysis, urine culture and kidney-bladder US were performed for patients. Some patients underwent a voiding cystoureterography (VCUG), urodynamic study (UDS), or both.RESULTS: Patients were divided into three groups: i) MNE, ii) NMNE without daytime incontinence (NMNE -daytime incontinence), and iii) NMNE plus daytime incontinence (NMNE + daytime incontinence). Constipation (P=0.011), encopresis (P=0.003) and urge incontinence (P = 0.001) were significantly more frequent in patients with NMNE +daytime incontinence. Bladder wall thickness (BWT) was the most common US finding. One patient with MNE and 9 with NMNE+ daytime incontinence had vesicoureteral reflux (VUR; P=0.016). Posterior urethral valve (PUV) was reported in one patient with NMNE. Evidence of bladder dysfunction was noted in about half of the patients who underwent UDS, with a higher prevalence in cases that had NMNE +daytime incontinence (P=0.297). Bowel symptoms and VUR were significantly more prevalent in cases with NMNE + daytime incontinence.CONCLUSION: We recommend VCUG in enuretic children who have daytime incontinence. In addition our study has revealed that symptoms suggestive of an overactive bladder (OAB) are not good indicators for bladder dysfunction.

BACKGROUND: This study investigates the expression of CD82/KAI1 and epithelial-cadherin (E-cad) in non-small cell lung cancer (NSCLC).METHODS: Tissues of resected primary NSCLC and normal lung tissue were investigated. Protein expression was detected with immunohistochemical staining. mRNA expression levels of CD82/KAI1 and E-cad were determined by semiquantitative reverse transcriptase polymerase chain reaction (RT-PCR) after mRNA extraction.RESULTS: The expression of CD82/KAI1 and E-cad was significantly lower in NSCLC compared to normal lung tissue (P<0.01). CD82/KAI1 and E-cad mRNA and protein expression were found to be in close relationship with the grade of differentiation, lymph node metastasis and pathologic tumor-node-metastasis (pTNM) stages, and survival in NSCLC (P<0.01), but no relationship was observed with gender, diameter, type, histological type and age (P>0.05). Expression of mRNA CD82/KAI1 and E-cad were consistent with their proteins (P<0.01), and there was a significant relationship between expression of CD82/KAI1 and E-cad. The survival rate of the CD82/KAI1-positive and CD82/KAI1-negative groups was significantly different (P<0.01). In addition, the survival rate was significantly different between the E-cad-positive and E-cad-negative groups. pTNM stages and positive expression of CD82/KAI1 and E-cad were independent prognostic factors of NSCLC (P<0.05).CONCLUSION: Lower expression of CD82/KAI1 and E-cad was found in NSCLC compared to normal lung tissue. Decreased expression of CD82/KAI1 and E-cad was closely related to cellular differentiation, pTNM stages, invasion and metastasis.

Esophageal cancer (EC) is the 8th most common cancer and the 6th most frequent cause of cancer mortality worldwide. Esophageal squamous cell carcinoma (ESCC) is the most common type of EC. Exposure to polycyclic aromatic hydrocarbons (PAHs) has been suggested as a risk factor for developing ESCC. In this paper we will review different aspects of the relationship between PAH exposure and ESCC. PAHs are a group of compounds that are formed by incomplete combustion of organic matter. Studies in humans have shown an association between PAH exposure and development of ESCC in many populations. The results of a recent case-control study in a high risk population in northeastern Iran showed a dramatic dose-response relationship between PAH content in non-tumor esophageal tissue (the target tissue for esophageal carcinogenesis) and ESCC case status, consistent with a causal role for PAH exposure in the pathogenesis of ESCC. Identifying the main sources of exposure to PAHs may be the first and most important step in designing appropriate PAH-reduction interventions for controlling ESCC, especially in high risk areas. Coal smoke and drinking mate have been suggested as important modifiable sources of PAH exposure in China and Brazil, respectively. But the primary source of exposure to PAHs in other high risk areas for ESCC, such as northeastern Iran, has not yet been identified. Thus, environmental studies to determining important sources of PAH exposure should be considered as a high priority in future research projects in these areas.

Brucellosis is the most common worldwide zoonotic infection of which psychosis is a rare feature of this disease. Brucellar psychosis should be considered in a patient with unexplained, nonspecific psychological complaints. Its timely diagnosis relies on special attention to the epidemiologic profile of the patient for a possible exposure to the brucella species. This article has presented three cases of brucellar psychosis initially misdiagnosed because the risk factors which made them at risk for the disease were ignored.

We present the case of an 82-year-old man diagnosed with rectosigmoid cancer and liver metastasis who survived for 19 years following treatment. At the age of 64, the patient twice experienced mucus excretion for which he underwent a colonoscopy that resulted in a diagnosis of rectosigmoid cancer the patient underwent surgery for resection of the tumor and liver metastasis. Histopathology was notable for a diagnosis of rectal adenocarcinoma that infiltrated the entire thickness of the wall, with metastasis to the liver and no lymph node involvement. Post-operative chemotherapy was administered for about four months. The patient remained asymptomatic for 19 years which at that time he presented with liver metastasis, ascites and renal failure.

Microthrombi formation and hemolytic anemia are signs of hemolytic-uremic syndrome (HUS) that result from platelet consumption and red blood cell (RBC) destruction due to vascular damage. HUS manifests as a triad of signs: micro-angiopathic hemolytic anemia, thrombocytopenia, and uremia. Prenatal asphyxia (PA) also leads to renal insufficiency and vascular damage. There is an overlap between the clinical presentation of PA and neonatal atypical HUS. We have reported the case of a neonate with a primary diagnosis of PA and clinical presentation of acute renal failure (ARF), anemia (Hb=10 g/dl) and thrombocytopenia (Plt = 80000). His APGAR scores were 1 (1 minute), 3 (5 minutes), and 7 (10 minutes). A peripheral blood smear (PBS) was performed, which contained schistocytes (32%) with helmet and burr cells. The neonate's cord blood gas values were: pH of 7.07, HCO3=11mmol/L, and CO2 = 57mmHg. The first two days of life, he was anuric with elevated BUN and Cr (2.1mg/dL) levels. Complement (C3) was within normal limits at 0.65 g/L (0.89-1.87 g/L), however C4 was below the lower limit of normal at 0.14 g/L (0.16-0.38 g/L). We ruled out other causes of PA such as maternal illness, placenta abnormalities and infections (TORCH). We hypothesized that atypical neonatal HUS can progress to PA because of the presence of severe anemia and microthrombi formation.

A 46-year-old woman, presented to our Breast Clinic in the Surgery Department with complaints of a lump in the upper, central portion of her right breast (between the 12-and 1-o’clock position), cutaneous fistula and nipple retraction of two years duration. She complained of no other symptoms and on physical examination she appeared healthy, except for the right breast mass.

Dr. Ali Mohammad Handjani, a distinguished Professor of Cardiology at Shiraz University of Medical Sciences passed away in Shiraz, Iran on July 20, 2012. He was a great medical teacher and superb clinician who devoted most of his fruitful life to medical education and patient care.