Diagnostic Evaluation of Patients Presenting to Primary Care with Rectal Bleeding

Background

Rectal bleeding is a common, frequently benign problem that can also be an early sign of colorectal cancer. Diagnostic evaluation for rectal bleeding is complex, and clinical practice may deviate from available guidelines.

Objective

To assess the degree to which primary care physicians document risk factors for colorectal cancer among patients with rectal bleeding and order colonoscopies when indicated, and the likelihood of physicians ordering and patients receiving recommended colonoscopies based on demographic characteristics, visit patterns, and clinical presentations.

Design

Cross-sectional study using explicit chart abstraction methods.

Participants

Three hundred adults, 40–80 years of age, presenting with rectal bleeding to 15 academically affiliated primary care practices between 2012 and 2016.

Main Measures

1) The frequency at which colorectal cancer risk factors were documented in patients’ charts, 2) the frequency at which physicians ordered colonoscopies and patients received them, and 3) the odds of ordering and patients receiving recommended colonoscopies based on patient demographic characteristics, visit patterns, and clinical presentations.

Key Results

Risk factors for colorectal cancer were documented between 9% and 66% of the time. Most patients (89%) with rectal bleeding needed a colonoscopy according to a clinical guideline. Physicians placed colonoscopy orders for 74% of these patients, and 56% completed the colonoscopy within a year (36% within 60 days). The odds of physicians ordering recommended colonoscopies were significantly higher in patients aged 50–64 years of age than in those aged 40–50 years (OR?=?2.23, 95% CI: 1.04, 4.80), and for patients whose most recent colonoscopy was 5 or more years ago (OR?=?4.04, 95% CI: 1.50, 10.83). The odds of physicians ordering and patients receiving recommended colonoscopies were significantly lower for each primary care visit unrelated to rectal bleeding (OR?=?0.85, 95% CI: 0.75, 0.96).

Conclusions

Diagnostic evaluation of patients presenting to primary care with rectal bleeding may be suboptimal because of inadequate risk factor assessment and prioritization of patients’ other concurrent medical problems.

     

Molecular Analysis of Codon 548 in the rpoB Gene Involved in Mycobacterium tuberculosis Resistance to Rifampin

Most Mycobacterium tuberculosis rifampin-resistant strains have been associated with mutations in an 81-bp rifampin resistance-determining region (RRDR) in the gene rpoB. However, if this region alone were targeted, rifampin-resistant strains with mutations outside the RRDR would not be detected. In this study, among 51 rifampin-resistant clinical isolates analyzed by sequencing 1,681-bp-long DNA fragments containing the RRDR, 47 isolates contained mutations within the RRDR, three isolates contained mutations both within and outside the RRDR, and only one isolate had a single missense mutation (Arg548His) located outside the RRDR. A drug susceptibility test of recombinant Mycobacterium smegmatis and M. tuberculosis isolates carrying mutated rpoB (Arg548His) showed an increased MIC for rifampin compared to that of the control strains. Modeling of the Arg548His mutant RpoB-DNA complex revealed that the His548 side chain formed a more stable hydrogen bond structure than did Arg548, reducing the flexibility of the rifampin-resistant cluster II region of RpoB, suggesting that the RpoB Arg548His mutant does not effectively interact with rifampin and results in bacterial resistance to the drug. This is the first report on the relationship between the mutation in codon 548 of RpoB and rifampin resistance in tuberculosis. The novel mutational profile of the rpoB gene described here will contribute to the comprehensive understanding of rifampin resistance patterns and to the development of a useful tool for simple and rapid drug susceptibility tests.     

Angiotensin II type 1a receptor signals are involved in the progression of heart failure in MLP-deficient mice.

BACKGROUND: Angiotensin II (AT) is implicated in the development of cardiac remodeling, which leads to heart failure, and pharmacological inhibition of the AT type 1 (AT1) receptor has improved mortality and morbidity in patients of heart failure. The aim of this study was to elucidate the role of the AT1 receptor in disease progression in muscle LIM protein (MLP)-deficient mice, which are susceptible to heart failure because of defective function of mechanosensors in cardiomyocytes. METHOD AND RESULTS: Hearts from MLP knockout (MLPKO) mice and MLP-AT1a receptor double knockout (DKO) mice were analyzed. MLPKO hearts showed marked chamber dilatation with cardiac fibrosis and reactivation of the fetal gene program. All of these changes were significantly milder in the DKO hearts. Impaired left ventricular (LV) contractility and filling were alleviated in DKO hearts. However, the impaired relaxation and downregulated expression of sarcoplasmic reticulum calcium-ATPase 2 were unchanged in DKO hearts. CONCLUSIONS: The AT1a receptor is involved in progression of LV remodeling and deterioration of cardiac function in the hearts of MLPKO mice. These results suggest that blockade of the receptor is effective in preventing progression of heart failure in dilated cardiomyopathy.     

Rotationplasty for limb salvage in the treatment of malignant tumors: a report of two cases

Limb salvage is now more common than amputation after radical excision to treat malignant tumors. In a skeletally immature patient who has malignant tumors in a lower extremity, rotationplasty offers a more reliable and durable option than other limb salvage procedures. It is an excellent method of resolving the problem of unequal leg lengths, and preserves best limb function with few complications. Here, we present our experience with rotationplasty for limb salvage in the treatment of malignant tumors, with good functional results seen in follow-up examination 11 years after surgery.     

Rosiglitazone improves insulin sensitivity and glucose tolerance in subjects with impaired glucose tolerance

OBJECTIVE: This study was designed to evaluate the effects of rosiglitazone (ROS) on insulin sensitivity, beta-cell function, and glycaemic response to glucose challenge and meal in subjects with impaired glucose tolerance (IGT). METHODS: Thirty patients with IGT (ages between 30 and 75 years and BMI (body mass index) < or = 27 kg/m2) were randomly assigned to receive either placebo (n = 15) or ROS (4 mg/day) (n = 15). All participants underwent a 75-g oral glucose tolerance test (OGTT), meal test, and frequently sampled intravenous glucose tolerance test (FSIGT) before and after the 12-week treatment. RESULTS: After 12 weeks of ROS treatment, there were significant increases in total cholesterol (TC) (4.25 +/- 0.22 vs 4.80 +/- 0.17 mmol/l, P < 0.001), high-density lipoprotein cholesterol (HDL-C) (1.25 +/- 0.07 vs 1.43 +/- 0.06 mmol/l, P < 0.05), and low-density lipoprotein cholesterol (LDL-C) (2.70 +/- 0.15 vs 3.37 +/- 0.17 mmol/l, P < 0.05) without changes in triglyceride concentration, TC/HDL-C and LDL-C/HDL-C ratio. Although the acute insulin response (AIR) to intravenous glucose and disposition index (measured as the ability of pancreatic beta-cell compensation in the presence of insulin resistance) remained unchanged, the insulin sensitivity (SI) and glucose effectiveness (SG) were remarkably elevated (0.38 +/- 0.06 vs 0.54 +/- 0.09 x 10(-5) min(-1)/pmol, P < 0.05; 0.017 +/- 0.002 vs 0.021 +/- 0.001 min(-1), P < 0.05, respectively) in the ROS group. The glucose, insulin, and c-peptide areas under curve (AUC) in response to OGTT and the glucose and insulin AUC during meal were significantly ameliorated in the ROS group. Five out of 15 (33%) and two out of 15 (13%) subjects treated with ROS and placebo, respectively, reversed to normal response during OGTT (P < 0.05). CONCLUSION: Rosiglitazone treatment significantly improved insulin resistance and reduced postchallenge glucose and insulin concentrations in patients with impaired glucose tolerance without remarkable effects on beta-cell secretory function.