Outcomes of oesophageal self-dilation for patients with refractory benign oesophageal strictures.

BACKGROUND: Current management of refractory benign oesophageal strictures with endoscopic dilations and stenting leads to resolution of dysphagia in only 30% of patients. Oesophageal self-dilation may be an alternative. AIM: To evaluate the efficacy and safety of oesophageal self-dilation at a tertiary referral centre. METHODS: We conducted a retrospective review of patients with refractory benign oesophageal strictures who participated in oesophageal self-dilation at Mayo Clinic (Rochester, MN, USA) between 2003 and 2017. Clinical data including stricture characteristics, Dakkak and Bennett Dysphagia Score, number and dates of endoscopies, and complications were collected. A two-tailed paired Student's t test was used to compare the measures of efficacy, with differences considered significant at a 5% probability level. RESULTS: We identified 52 patients with refractory strictures treated with self-dilation. The median number of endoscopic interventions was reduced from 9.5 (range 5-30) to 0 (range 0-3) within 12 months before and after self-dilation, respectively (P < 0.0001). A median intervention-free interval of 417 days (IQR 256-756 days) was observed. The mean dysphagia score at baseline was 2.5 (95% CI 2.2-2.8) and 0.33 (95% CI 0.11-0.53) after self-dilation. 23 of 27 (85%) patients who received enteral nutrition prior to self-dilation had their feeding tubes removed. CONCLUSIONS: Oesophageal self-dilation is an effective way of maintaining oesophageal patency in refractory benign oesophageal strictures, with safety comparable to current standard of care. Prospective studies are needed to further validate the role of self-dilation in treatment of refractory benign oesophageal strictures.

The influence of porphyrogenic drugs on the glyoxalase enzymes.

A variety of drugs, known to induce acute attacks in porphyric patients has been found to inhibit the glyoxalase pathway. Glyoxalase I is competitively inhibited by sulphadimidine, oxytetracycline, chloramphenicol, etc. Allylisopropyl acetamide (AIA) seems to inhibit glyoxalase II. This inhibition could play a contributing role in the overproduction of porphyrins in porphyria and thus help explain the mechanism of induction of porphyric attacks. The results indicate, that the Heme pathway and the glyoxalase cycle are closely connected.

Compartmentalization of pyridoxal-5'-phosphate during the acute phase of myocardial infarction.

Vitamin B6 nutritional status is assessed by measuring the plasma concentration of one of its vitamers, pyridoxal-phosphate (PLP). Several conditions, e.g., myocardial infarction (MI), can disturb the dynamic equilibrium between the different vitamers resulting in transiently low plasma PLP levels. An important question is whether these low plasma PLP levels observed during MI represent a transient state of deficiency and what the possible clinical consequences of such a fall in plasma PLP could be. Since the main metabolic function of PLP is to act as an intracellular coenzyme, it was decided to monitor the changes not only of PLP but also of PL (transport form of vitamin B6) in both the plasma and red blood cells (RBCs) in patients with myocardial infarctions (MI): 16 patients with proven MI were investigated measuring the aforementioned parameters at regular intervals. It was found that the approximately 40% fall in plasma PLP levels was accompanied by an equivalent increase in RBC PLP levels. Subsequently plasma PLP concentrations returned to normal but RBC PLP values were maintained at the newly elevated steady state (without any vitamin supplementation). Since membranes are impermeable to PLP, the only way in which PLP could have been redistributed to the intracellular compartment was through hydrolysis to PL and rephosphorylation once inside the RBCs. This compartmentalization could be an important adaptive response since it has been shown that PLP reduces O2 affinity of deoxygenated hemoglobin, thereby facilitating O2 delivery to the tissues.(ABSTRACT TRUNCATED AT 250 WORDS)