Is there any evidence for a viral cause in achalasia?

Background:Achalasia, as an incurable disease is defined by the lack of normal esophageal peristalsis and loss of lower esophageal sphincter relaxation due to impaired myenteric neural plexus. The exact cause of myenteric neural cells degeneration in achalasia is still unknown. One hypothesis is that certain neurotropic viruses and autoimmune factors cause the inflammatory response in myenteric network, which consequently destroy neural cells. This study was designed to find the evidence of viral causes of achalasia

Methods: In this case-control study, 52 patients with achalasia and 50 controls referred to Shariati Hospital, were evaluated for the genome of neurotropic viruses, HPV, and adenovirus by polymerase chain reaction [PCR] and reverse transcription [RT] PCR techniques

Results:Genome assessment of neurotropic DNA viruses turned out negative in the patients, however, the genome of HSV-1 [Herpes simplex virus] was found in tissues of six controls. No neurotropic RNA viruses were observed in the tissue samples and whole blood of both the patients and controls.Among non-neurotropic viruses, adenovirus genome was positive in tissues of two out of 52 patients and three out of 50 controls. In addition, one out of 52 patients and two out of 50 controls were positive for HPV infection in tissues

Conclusion: We could not detect any significant relationship between achalasia and HPV, adenovirus, and neurotropic viruses in the cases. Nevertheless, it does not exclude the hypothesis of either an alternate viral species or resolved viral infection as the etiology of achalasia

Assessment of pneumatic balloon dilation in patients with symptomatic relapse after failed Heller myotomy: a single center experience

Background: Although Heller myotomy is one of the most effective treatments for achalasia, it may be associated with early or late symptom relapse in some patients. Therefore, additional treatment is required to achieve better control of symptoms. Aim: To evaluate the safety and efficacy of pneumatic balloon dilation [PBD] in patients with symptom relapse after Heller myotomy

Methods: Thirty six post-myotomy patients were evaluated from 1993 to 2013. Six patients were excluded from the analysis because of comorbid diseases or epiphrenic diverticula. Thirty patients were treated with PBD. Primary outcome was defined as a decrease in symptom score to 4 or less and a reduction greater than 80% from the baseline in the volume of barium in timed barium esophagogram in 6 weeks. Achalasia symptom score [ASS] was assessed at 1.5, 3, 6, and 12 months after treatment and then every six months in all patients and PBD was repeated in case of symptom relapse [ASS>4]

Results: The mean age of the patients was 45.5 +/- 13.9 years [range: 21-73]. Primary outcome was observed in 25 patients [83%]. The mean ASS of the patients dropped from 7.8 before treatment to 1.3 +/- 2.0 at 1.5 months after treatment [p=0.0001]. The mean volume and height of barium decreased from 43.1 +/- 33.4 and 7.1 +/- 4.7 to 6.0 +/- 17.1 and 1.1 +/- 2.2, respectively [p=0.003, p=0.003]. The mean duration of follow-up was 11.8 +/- 6.3 years. At the end of the study, 21 patients [70%] reported sustained good response. No major complications such as perforation or gross bleeding were seen

Conclusion: PBD is an effective and safe treatment option for achalasia in patients with symptom relapse after Heller myotomy

Oral omeprazole in patients undergoing combination endoscopic therapy for bleeding peptic ulcers A: prospective double-blind randomized study

Endoscopic therapies can decrease the morbidity of patients with high risk peptic ulcer. The aim of this study was to evaluate the beneficial effects of oral omeprazole therapy in patients with bleeding peptic ulcer who received combined endoscopic treatment [epinephrine injection and Argon Plasma Coagulation]. Eighty six patients with bleeding from gastric, duodenal or stomal ulcers and endoscopic stigmata of recent bleeding were enrolled in our study. All patients received injection of epinephrine [1:10,000] and also their ulcers were treated with Argon Plasma Coagulator. The patients then randomly assigned to receive oral omeprazole [40 mg every 12 hours] or placebo. Five [11.6%] of 43 patients in the placebo group had rebleeding; but no rebleeding was detected among 43 patients in omeprazole group [p= 0.05]. One patient in the Placebo group underwent surgery for control of his rebleeding; but none of the patients in omeprazole group needed surgery. One patient in the placebo group and none of the patients in the omeprazole group died. The average hospital stay was 5 days in the omeprazole group and 5.8 days in the placebo group. Addition of oral omeprazole to combined endoscopic therapy significantly reduces recurrent bleeding rates