Here’s a link to the video story regarding misdiagnosis of penicillin allergy: Your Allergy to Penicillin May Be Non-Existent
Link to print version: Allergy to Penicillin?
An excerpt: Dr. Thanai Pongdee, an allergist at the Mayo Clinic in Jacksonville, Florida and colleagues tested 384 people who said they were allergic to penicillin. Tests showed 94 percent of them were in fact, not allergic.
In a small retrospective single-center study (GC Ives et al. J Pediatr 2016; 178: 275-7), the authors found that small bowel diameter, as measured on calibrated luminal contrast studies was predictive of enteral autonomy.
Measurements of >35 mm of bowel lumen was considered dilated. 29 patients had adequate imaging for the study. Necrotizing enterocolitis was the most common etiology of short bowel syndrome in this study. 16 (55%) of the intestinal failure group achieved enteral autonomy in an average of 1.3 years. 11 (38%) of patients underwent an intestinal lengthening procedure.
Key findings:
My take: Bigger (diameter) is not better.
Related blog posts:
Lighthouse in Rockland
A recent article and editorial (DH Leung et al. Liver Transpl 2016; 22: 1584-92 & editorial by JC Bucuvalas, S Feng 1466-68) provides a better picture of long-term survival for pediatric patients facing the prospect of liver transplantation.
Among patients less than 2 years in the UNOS data sharing registry, there were 994 with biliary atresia (BA) and 221 with other chronic liver disease.
The key data:
Reviewing the article, it is not clear to me if patients removed the waitlist (eg due to sepsis and other causes) are included in this analysis. Thus, the true postlisting mortality may be higher than 20% if all needy individuals are considered.
From the editorial -other aspects:
My take (with help from editorial): To improve outcomes, this means starting with candidate selection and working on each step: traversing wait-list management and optimizing posttransplant care.
Related blog posts:
Mural in Rockland, ME
MI Abdalla et al. Inflamm Bowel Dis 2016; 22: 2658-64. This article reviewed the impact of an ostomy on QOL (quality of life) for Crohn’s disease patients. n=402 with ostomy compared with 4331 CD patients without.
Key findings:
WKM Liew et al. J Pediatr 2016; 178: 227-32. In this study with 16 patients (aged 6-24 years) who received thalidomide, more information on neuropathy is provided. “All subjects with cumulative doses greater than 60 g developed polyneuropathy.” 4 of 5 subjects receiving the drug for >20 months developed neuropathy. Two important points:
V Collij et al. Inflamm Bowel Dis; 2016; 22: 2562-70. “We identified drugs that target the proteins encoded by IBD candidate genes.” Key finding: There were 113 drugs that could potentially be used in IBD treatment, including 14 known IBD drugs, 48 drugs that are/have been tested for IBD, 19 being tested for other inflammatory diseases, and 32 new investigational medications.
from one of the best days all year on board “Bufflehead”
A Amiot et al. Clin Gastroenterol Hepatol November 2016 Volume 14, Issue 11, Pages 1593–1601.
Phase 3 trials have shown the efficacy of vedolizumab, which binds to integrin α4β7, in patients with Crohn’s disease (CD) or ulcerative colitis (UC). We investigated the effectiveness and safety of vedolizumab in patients who failed anti-tumor necrosis factor therapy.
From June through December 2014, there were 173 patients with CD and 121 patients with UC who were included in a multicenter nominative compassionate early access program granted by French regulatory agencies. This program provided patients with access to vedolizumab before it was authorized for marketing. Vedolizumab (300 mg) was administered intravenously at weeks 0, 2, and 6, and then every 8 weeks. Disease activity was assessed using the Harvey–Bradshaw Index for CD and the partial Mayo Clinic score for UC. We report results obtained after the 14-week induction phase.
Among the 294 patients treated with vedolizumab (mean age, 39.5 ± 14.0 y; mean disease duration, 10.8 ± 7.6 y; concomitant steroids, 44% of cases), 276 completed the induction period, however, 18 discontinued vedolizumab because of a lack of response (n = 14), infusion-related reaction (n = 2), or infections (n = 2). At week 14, 31% of patients with CD were in steroid-free clinical remission and 51% had a response; among patients with UC, 36% were in steroid-free clinical remission and 50% had a response. No deaths were reported. Severe adverse events occurred in 24 patients (8.2%), including 15 (5.1%) that led to vedolizumab discontinuation (1 case of pulmonary tuberculosis and 1 rectal adenocarcinoma).
In a cohort of patients with CD or UC who failed previous anti–tumor necrosis factor therapy, approximately one third of patients achieved steroid-free clinical remission after 14 weeks of induction therapy with vedolizumab. This agent had an acceptable safety profile in these patients.
Related Blog Posts:
A retrospective study from Boston has gained attention for suggesting that repeat biopsies may be needed for celiac disease (published online, MM Leonard et al JPGN, doi: 10.1097/MPG.0000000000001460). In my view, this may be a little early for that recommendation for asymptomatic patients with normal serology.
Full Abstract:
Objective: Our objective was to determine the rate of mucosal recovery in pediatric patients with celiac disease on a gluten free diet. We also sought to determine whether IgA tissue transglutaminase (tTG) correlates with mucosal damage at the time of a repeat endoscopy with duodenal biopsy in these patients.
Methods: We performed a retrospective chart review of one-hundred and three pediatric patients, under 21 years of age, with a diagnosis of celiac disease defined as Marsh 3 histology, and who underwent a repeat endoscopy with duodenal biopsy at least twelve months after initiating a gluten free diet.
Results: We found that 19% of pediatric patients treated with a gluten free diet had persistent enteropathy. At the time of the repeat biopsy, tTG was elevated in 43% of cases with persistent enteropathy and 32% of cases in which there was mucosal recovery. Overall the positive predictive value of the autoantibody tissue transglutaminase was 25% and the negative predictive value was 83% in patients on a gluten free diet for a median of 2.4 years.
Conclusions: Nearly one in five children with celiac disease in our population had persistent enteropathy despite maintaining a gluten free diet and IgA tTG was not an accurate marker of mucosal recovery. Neither the presence of symptoms nor positive serology were predictive of a patient’s histology at the time of repeat biopsy. These findings suggest a revisitation of monitoring and management criteria of celiac disease in childhood.
Link to full text: A few other key points:
My take: I think it is premature to recommend routine followup biopsies in asymptomatic patients with normal serology. I think a prospective study will be helpful; the majority of patients in this study who underwent repeat biopsy were symptomatic and 9% were not adherent to their diet. Thus, this may not reflect a typical patient with celiac disease at followup. In addition, it would be helpful with regard to whether persistent histological findings have clinical significance.
Despite these limitations –this is how this article is being reported (from news-medical.net), here’s an excerpt from a recent summary:
Alessio Fasano, MD, director of the MGHfC center and co-senior author of the study, was also surprised by the results, which were based on a retrospective examination of the biopsy and medical records of 103 children with celiac disease treated at MGHfC or BCH. The children had been on the gluten-free diet for at least one year and were determined by dietitians and other hospital health care practitioners to have complied well with the diet. But repeat biopsies found persistent intestinal damage in 19 percent of them. “The number of children who don’t heal on the gluten-free diet was much higher than what I expected,” Fasano says.
From NBC News: Congress Doesn’t Scare Drug Execs Into Lowering Prices
Excerpt:
Congress’s routine of publicly shaming drug company executives over high prices works no better than a placebo: It may make some people feel better, but it doesn’t treat the problem…
But a review by The Associated Press of the list prices of nearly 30 brand-name medications and generic versions targeted by congressional investigators shows most haven’t budged since coming under federal scrutiny, according to figures from Truven Health Analytics.
Related posts:
Despite the flood of articles touting the success and costs of the new hepatitis C virus (HCV) treatments, direct-acting antivirals (DAA), currently hepatitis C remains more dangerous than HIV and it is likely to continue to exert a huge mortality and morbidity for at least three more decades in the United States.
One study and an associated editorial look into this subject further:
In the study, the authors used a validated HCV burden simulation model (HEP-SIM) and noted the following:
“Even in the oral DAA era, 320,000 patients will die, 157,000 will develop hepatocellular carcinoma, and 203,000 will develop decompensated cirrhosis in the next 35 years.”
Part of the problems will be a large number of individuals who remain unaware of their diagnosis (560,000 by year 2020) but other barriers include medication costs.
From the editorial -some pushback on the cost-savings argument:
My take: To bend the HCV curve faster, there will need to be increased HCV screening, increased treatment capacity, and reasonable costs.
Related blog posts:
Acadia Natl Park
There has been a deluge of articles regarding the microbiome; yet, many aspects of microbiome derangements may have limited clinical significance. In addition, in many circumstances, it is not clear if the changes in the microbiome represent the proverbial chicken or the egg. How much of the changes in the microbiome are a consequence rather than a cause of a clinical problem?
One fascinating article (A Caminero et al. Gastroenterol 2016; 151: 670-83) looks at the role of the microflora with regard to gluten breakdown and immunogenicity. Thanks to Ben Gold who prompted me to take a 2nd look at this study.
In this study, the authors took bacteria isolated from the small intestines of Celiac disease (CD) patients or controls and colonized germ-free mice. Subsequently, “after gluten gavage, gliadin amount and proteolytic activities were measured” and characterized.
Key findings:
The others selected P aeruginosa from CD patients as it was not present in controls, though most strains were in fact within the phylum Firmicutes. Lactobacillus spp was chosen from the healthy subjects “because it constitutes a core resident group in the human small intestine that is involved in gluten metabolism in vitro and is altered in CD patients.”
Overall, the study provides some evidence that changes in microbiome could trigger intestinal inflammation. Thus, since autoimmunity and celiac disease have an environmental trigger, this study implicates changes in the microflora as a risk factor for developing celiac disease in the susceptible host (see Figure 7 in the source article).
My take (from authors): This study identified “both pathogenic and protective microbe-gluten-host interactions that may modulate autoimmune risk in HLA-DQ2 susceptible persons.”
Acadia Natl Park
gutsandgrowth 