Israel Medical Association Journal

Background: Hyperplastic polyps (HPs) of the colon are the most common colorectal polyps. Metabolic syndrome components such as obesity and hyperlipidemia are considered the most common etiological factors for HPs as well contributing to the pathogenesis of fatty liver disease. Objectives: To determine the possible association between biopsy-proven steatohepatitis and hyperplastic colonic polyps. 

Methods: This retrospective cohort observational study conducted at the Holy Family Hospital in Nazareth, Israel, included subjects who underwent screening colonoscopy over a 2 year period. Data were extracted from the patient charts and included demographics, anthropometric measurements, vital signs, underlying diseases, medical therapy, laboratory data, and results of the liver biopsy. The colonoscopy report and pathological report of each extracted polyp were also evaluated.

Results: A total of 223 patients were included in the study: 123 patients with biopsy-proven non-alcoholic steatohepatitis (NASH) and 100 patients without NASH who served as the control. Fourteen colonic adenomas (11% of patients) were found in the NASH group vs. 16 (16%) in the control group (P = 0.9); 28 HPs were found in the NASH group (22.7%) vs. 8 in the control group (8%) (P < 0.05). The multivariate analysis, after adjusting for, age, C-reactive protein and smoking, showed that the presence of NASH (OR 1.69, 95%CI 1.36–1.98, P < 0.01) was associated with increased risk for HP. 

Conclusions: Our study found an association between biopsy-proven steatohepatitis and the burden of hyperplastic polyp.

 

Background: Legg-Calvé-Perthes disease (LCPD) is an idiopathic hip osteonecrosis prevalent in children < age 15 years. The etiology remains incompletely understood, partly because of multiple potential environmental risk factors and partly because of lack of genetic markers. It has been hypothesized that hyperactivity may induce mechanical stress and/or vascular damage at a fragile joint. 

Objectives: To assess children with LCPD for markers of attention deficit hyperactivity disorder (ADHD) relative to their unaffected comparably aged siblings to exclude the contribution of hyperactive behavior versus environmental and/or genetic factors in LCPD. 

Methods: All children followed in the Pediatric Orthopedic Clinic, and their comparably aged siblings, were recruited. ADHD was assessed using the TOVA computerized test and DSM-IV criteria. Quality of life and sleep disorders as ancillary tests were assessed using the Child Health Questionnaire (Parent Form 50), Pediatric Outcomes Data Collection Instrument, and Pediatric Daytime Sleepiness Scale.

Results: Sixteen children with LCPD (age 9.1 ± 3.3, 75% males) were compared with their closest-aged siblings (age 9.3 ± 2.6, 30% males). Mean TOVA scores of children with LCPD (-3.79 ± 2.6) and of their non-LCPD siblings (-3.6 ± 4.04) were lower relative to the general population (0 ± 1.8, P < 0.0001). Both group means were in the ADHD range (≤ -1.8) implying that 73% of this LCPD cohort and 53% of their non-LCPD siblings performed in the ADHD range, relative to 3.6% incidence expected in the general population (P < 0.0001). Other test results were similar in both groups. 

Conclusions: Our findings in a small cohort of children with LCPD and their comparably aged siblings do not support an association between LCPD and ADHD. ADHD markers were equally high in the LCPD children and siblings. 

 

Autoimmune diseases constitute a diverse group of disorders characterized by cellular and humoral responses against self. The humoral autoimmune responses are directed against various cellular and extracellular components. These responses are highly specific for each autoimmune disease and result in the production of autoantibodies that characterize certain disease entities, representing a valuable tool for the diagnosis of autoimmune diseases. Furthermore, certain autoantibodies are helpful in the prognosis of disease development, progression and severity, as well as in the classification of patients with distinct disease subtypes. Today, the value of autoantibodies in the follow-up of patients is limited, but preliminary data suggest that they may be useful in predicting response to treatment. 

Background: Both cigarette smoking and chronic kidney disease (CKD) are linked to cardiovascular morbidity and development of atherosclerosis. However, the relationship between cigarette smoking and renal function is not clearly understood. 

Objectives: To investigate the relationship between cigarette smoking and renal function, and determine whether the intensity of cigarette smoking influences renal function.

Methods: We conducted a retrospective analysis of subjects attending the screening center at the Rabin Medical Center. Subjects were classified as smokers, non-smokers and past smokers. Renal function was evaluated by means of the CKD-EPI equation for estimating glomerular filtration rate (eGFR). Multivariate and gender-based analyses were performed.

Results: The study population comprised 24,081 participants, of whom 3958 (17%) were classified current smokers, and 20,123 non-smokers of whom 4523 were classified as past smokers. Current smokers presented a higher eGFR compared to the non-smoking group (100.8 vs. 98.7, P < 0.001) as well as higher rates of proteinuria (15.3% vs. 9.3%, P < 0.001). The difference in eGFR between smokers and non-smokers was more significant in males than in females. Past smokers had the lowest eGFR of all groups, this difference remained significant after age adjustments (P = 0.005). 

Conclusions: Cigarette smoking is associated with higher eGFR compared to non-smoking. This difference was more pronounced in males than females, implying a gender-based difference. The higher prevalence of proteinuria in smokers suggests a mechanism of hyperfiltration, which might result in future progressive renal damage.

 

Background: Only a minority of patients with essential tremor (ET) and Parkinson’s disease (PD) undergo deep brain stimulation (DBS) surgery. Data on patient selection factors are useful.

Objectives: To compare the clinical characteristics of ET and PD patients who underwent DBS surgery with those of patients who had not undergone surgery.

Methods: We abstracted data from the electronic medical records of 121 PD and 34 ET patients who underwent DBS surgery at Columbia University Medical Center during the period 2009–2014. We compared this group with 100 randomly selected PD and 100 randomly selected ET patients at the Center who had not undergone DBS surgery. 

Results: Among other differences, age of onset in PD patients who had undergone surgery was younger than in those who did not: 14.9% vs. 3.0% with onset before age 40 (P = 0.003). They had also tried nearly double the number of medications (3.9 ± 1.7 vs. 2.3 ± 1.5, P < 0.001). Interestingly, there was no difference in the proportion of patients with tremor (81.0% vs. 88.0%, P = 0.16). Medical co-morbidities (heart and lungs) were less common in the PD patients who underwent DBS surgery. In the ET group, tremor causing impairment in activities of daily living occurred in all surgical patients compared to 73.0% of non-surgical patients (P < 0.001). The former had tried nearly double the number of medications compared to the latter (3.2 ± 1.7 vs. 1.3 ± 1.3, P < 0.001).

Conclusions: These data add to our understanding of the numerous clinical factors associated with patient referral to DBS surgery. 

 

Background: Chronic kidney disease (CKD) is often accompanied by impairment of cardiac function that may lead to major cardiac events. Erythropoietin (EPO), a kidney-produced protein, was shown to be beneficial to heart function. It was suggested that reduced EPO secretion in CKD may play a role in the initiation of heart damage. 

Objectives: To investigate molecular changes in the EPO/erythropoietin receptor (EPO-R) axis in rat cardiomyocytes using a rat model for CKD.

Methods: We established a rat model for CKD by kidney resection. Cardiac tissue sections were stained with Masson’s trichrome to assess interstitial fibrosis indicating cardiac damage. To evaluate changes in the EPO/EPO-R signaling cascade in the myocardium we measured cardiac EPO and EPO-R as well as the phosphorylation levels of STAT-5, a downstream element in this cascade.

Results: At 11 weeks after resection, animals presented severe renal failure reflected by reduced creatinine clearance, elevated blood urea nitrogen and presence of anemia. Histological analysis revealed enhanced fibrosis in cardiac sections of CKD animals compared to the sham controls. Parallel to these changes, we found that although cardiac EPO levels were similar in both groups, the expression of EPO-R and the activated form of its downstream protein STAT-5 were significantly lower in CKD animals.

Conclusions: CKD results in molecular changes in the EPO/EPO-R axis. These changes may play a role in early cardiac damage observed in the cardiorenal syndrome.