Tension pneumoperitoneum after intussusception pneumoreduction

Intussusception is the most common cause of intestinal obstruction in infancy. Presentation, diagnostic workup, and treatment are well understood and noncontroversial. Complications of bowel perforation are also well documented. We discuss a case of tension pneumoperitoneum after intestinal perforation during intussusception pneumoreduction in a 5-month-old child and review initial presentation, diagnosis, and management of this disease. It is important to recognize this rare complication of pneumoreduction and promptly treat the ensuing tension pneumoperitoneum.     

Inducible microsomal prostaglandin E synthase is overexpressed in colorectal adenomas and cancer.

Recently, an inducible microsomal human prostaglandin E synthase (mPGES) was identified. This enzyme converts the cyclooxygenase (COX) product prostaglandin (PG) H(2) to PGE(2), an eicosanoid that has been linked to carcinogenesis. Increased amounts of PGE(2) have been observed in many tumor types including colorectal adenomas and cancers. To further elucidate the mechanism responsible for increased levels of PGE(2) in colorectal tumors, we determined the amounts of mPGES and COX-2 in 18 paired samples (tumor and adjacent normal) of colorectal cancer. With immunoblot analysis, mPGES was overexpressed in 83% of colorectal cancers. COX-2 was also commonly up-regulated in these tumors; marked differences in the extent of up-regulation of mPGES and COX-2 were observed in individual tumors. Immunohistochemistry revealed increased mPGES immunoreactivity in neoplastic cells in both colorectal adenomas and cancers compared with adjacent normal colonic epithelium. Cell culture was used to investigate the regulation of mPGES and COX-2. Chenodeoxycholate markedly induced COX-2 but not mPGES in colorectal cancer cells. Tumor necrosis factor-alpha induced both mPGES and COX-2, but the time course and magnitude of induction differed. As reported previously for COX-2, overexpressing Ras caused a several-fold increase in mPGES promoter activity. Taken together, our results suggest that overexpression of mPGES in addition to COX-2 contributes to increased amounts of PGE(2) in colorectal adenomas and cancer. The mechanisms controlling the expression of these two enzymes are not identical.     

The epidemiology of varicose veins: the Framingham Study

The epidemiology of varicose veins was examined in 3,822 adults in the Framingham Study. Findings indicate that the incidence of varicose veins is higher among women than men, with no clear age differences. Compared to women without varicose veins, women with varicose veins were more often obese (p less than .01), had lower levels of physical activity (p less than .001) and higher systolic blood pressure (p less than .001), and were older at menopause (p less than .001). Women who reported spending eight or more hours in an average day in sedentary activities (sitting or standing) also had a significantly higher incidence of varicose veins than those who spent four or fewer hours a day in such activities (p less than .05). For men, varicose veins coexisted with lower levels of physical activity (p less than .05) and higher smoking rates (p less than .05). While men and women with varicose veins had a higher incidence of atherosclerotic cardiovascular disease than those without varicose veins, only the excess risk of coronary heart disease in women was statistically significant (p less than .05). However, this finding was not significant after controlling for body mass and systolic blood pressure. These results suggest that increased physical activity and weight control may help prevent varicose veins among adults at high risk, and reduce the overall risk of atherosclerotic cardiovascular disease as well.     

Epidermal growth factor-induced cyclooxygenase-2 expression is mediated through phosphatidylinositol-3 kinase, not mitogen-activated protein/extracellular signal-regulated kinase kinase, in recurrent respiratory papillomas.

PURPOSE: Recurrent respiratory papillomas, caused by human papillomaviruses, are premalignant tumors that overexpress the epidermal growth factor receptor (EGFR). The goals of this study were as follows: (a) to evaluate the expression of cyclooxygenase-2 (COX-2) in papillomas, (b) to investigate the role of EGFR signaling in COX-2 expression, and (c) to determine whether COX-2 activity is important for the growth of papilloma cells. EXPERIMENTAL DESIGN: Immunohistochemistry, Western blotting, and real-time PCR were used to determine levels of COX-2 in papilloma and normal laryngeal tissue. Explant cultures of both normal laryngeal and papilloma cells were used to define the signaling pathways that regulate COX-2 expression and investigate the potential of targeting COX-2 as a strategy to suppress papilloma growth. RESULTS: COX-2 levels were markedly increased in papillomas. In vitro studies suggested that overexpression in papillomas reflected activation of EGFR-->phosphatidylinositol 3-kinase signaling. Treatment with prostaglandin E2 (PGE2) induced COX-2, whereas celecoxib, a selective COX-2 inhibitor, suppressed levels of COX-2, suggesting a positive feedback loop. Moreover, treatment with PGE2 stimulated papilloma cell growth, whereas celecoxib suppressed proliferation and induced apoptosis. CONCLUSIONS: Overexpression of COX-2 in papillomas seems to be a consequence of enhanced EGFR-->phosphatidylinositol 3-kinase signaling. We propose a positive feedback loop for COX-2 expression, with induction of COX-2 resulting in enhanced PGE2 synthesis and further expression of COX-2 that contributes to the growth of papillomas in vivo. These data strengthen the rationale for evaluating whether nonsteroidal anti-inflammatory drugs, prototypic COX inhibitors, will be useful in the management of respiratory papillomas.     

Population implications of electrocardiographic left ventricular hypertrophy

Left ventricular (LV) hypertrophy on the electrocardiogram is an ominous harbinger of cardiovascular disease in the general population markedly increasing the risk of coronary heart disease, cardiac failure, stroke and peripheral arterial disease. This contribution to risk exceeds that of the often accompanying hypertension. Once overt coronary disease occurs, electrocardiographic LV hypertrophy also further escalates risk of cardiovascular morbidity and mortality. The risk associated with electrocardiographic LV hypertrophy is particularly great when repolarization abnormality is present. Electrocardiographic LV hypertrophy and silent electrocardiographic myocardial infarction are similar in evolution and prognosis. LV hypertrophy is an important predictor of risk of cardiac failure; the electrocardiographic manifestation of LV hypertrophy predisposes to cardiac failure more than x-ray cardiac enlargement. Electrocardiographic LV hypertrophy heralds the onset of serious cardiovascular disease and premature mortality despite lack of associated symptoms. The serious prognosis of this abnormality warrants vigorous preventive management. More prospective data are needed comparing the prognosis of echocardiographic anatomical hypertrophy with that diagnosed by electrocardiography.     

Eosinophilic Ascites Due to Hyperinfection with Strongyloides stercoralis

We report the case of a patient with cryptogenic cirrhosis, new onset ascites, and hyperinfection with Strongyloides stercoralis who had significant eosinophilia of the peritoneal fluid. The eosinophilia resolved with treatment of the S. stercoralis infection, and did not recur during two subsequent episodes of ascites and spontaneous bacterial peritonitis. Eosinophilic ascites is rare in parasitic infection, but it has been described in a variety of disorders which are discussed.     

Response to influenza vaccination in community and in nursing home residing elderly: relation to clinical factors

Intramuscular (IM) influenza vaccines are about 50% effective in preventing respiratory illness among the elderly. The aim of this study was to identify factors associated with immune response to influenza vaccination among nursing home and community-residing elderly. 114 nursing home (NHE) and 62 community residing elderly (CE) were vaccinated with a commercial IM vaccine. Serum antibodies were evaluated by HIA, and the impact of subjects' clinical characteristics on seroconversion was determined. Factors that were associated with low seroconversion among NHE, included: type II diabetes [for B/Harbin: p=0.044, OR 0.12, (CI: 0.015-0.94)], and antibody titer prior to vaccination A/(H1N1): p=0.03, OR 2.38, (CI: 1.09-5.22); A/(H3N2): p=0.015, OR 2.68 (CI: 1.22-5.92), B/Harbin: p=0.057, OR 4.46 (CI: 0.96-20.85)]. Factors that were associated with lower seroconversion CE elderly, included older age [A/(H1N1): p=0.008, OR 0.846, (CI 0.75-0.96), B/Harbin: p=0.016, OR 0.812, (CI:0.69-0.96)], and antibody titer prior to vaccination A/(H1N1): p=0.029, OR 4.08, (CI: 1.16-14.37); A/(H3N2): p<0.0001, OR 11.495 (CI: 3.18-41.55)]. There was no significant difference in seroconversion between nursing home residing elderly and community elderly. We conclude that Type-II diabetes and antibody titer>1:40 prior to vaccination are associated with reduced response to the influenza vaccination in nursing home elderly.     

The effect of HIV and HPV coinfection on cervical COX-2 expression and systemic prostaglandin E2 levels

Human immunodeficiency virus (HIV-1) infection causes chronic inflammation. COX-2-derived prostaglandin E(2) (PGE(2)) has been linked to both inflammation and carcinogenesis. We hypothesized that HIV-1 could induce COX-2 in cervical tissue and increase systemic PGE(2) levels and that these alterations could play a role in AIDS-related cervical cancer. Levels of cervical COX-2 mRNA and urinary PGE-M, a biomarker of systemic PGE(2) levels, were determined in 17 HIV-negative women with a negative cervical human papilloma virus (HPV) test, 18 HIV-infected women with a negative HPV test, and 13 HIV-infected women with cervical HPV and high-grade squamous intraepithelial lesions on cytology. Cervical COX-2 levels were significantly associated with HIV and HPV status (P = 0.006 and 0.002, respectively). Median levels of urinary PGE-M were increased in HIV-infected compared with uninfected women (11.2 vs. 6.8 ng/mg creatinine, P = 0.02). Among HIV-infected women, urinary PGE-M levels were positively correlated with plasma HIV-1 RNA levels (P = 0.003). Finally, levels of cervical COX-2 correlated with urinary PGE-M levels (P = 0.005). This study shows that HIV-1 infection is associated with increased cervical COX-2 and elevated systemic PGE(2) levels. Drugs that inhibit the synthesis of PGE(2) may prove useful in reducing the risk of cervical cancer or systemic inflammation in HIV-infected women.