Remission of refractory esophageal lichen planus induced by tofacitinib.

As of now, there exists no established therapy for ELP. Retinoids, which are standard in treating cutaneous LP, do not exhibit positive effects in ELP. While topical glucocorticosteroids often yield favorable responses in esophageal inflammation, some cases prove recalcitrant or refractory. In such instances, various immunosuppressive therapies have been attempted with variable success.This report details a severe case of ELP that showed resistance to prednisolone, acitretin, alitretinoin, adalimumab, tacrolimus, hydroxychloroquine plus mycophenolate mofetil, and cyclophosphamide. The initiation of the JAK inhibitor tofacitinib induced an impressive clinical, endoscopic, and histological remission. This positive response to a JAK inhibitor is discussed in the context of our evolving understanding of the immune-mediated pathogenesis of this disease.

Drug-induced esophageal injuries with an atypical presentation mimicking acute coronary syndrome.

BACKGROUND: Pill-induced esophageal injury may cause severe complications if not diagnosed in a timely fashion. The condition is under-recognized and under-reported, and some patients present with atypical clinical or endoscopic features mimicking other common conditions. If the diagnosis is missed the patient will continue to take the offending drug, potentially worsening the illness. We present a case in which acute coronary syndrome was the initial working diagnosis leading to a delay in diagnosis of doxycycline-induced esophageal injury. The patient developed multiple esophageal ulcers and hemorrhage. CASE PRESENTATION: A 50-year-old male driver with a history of hypertension and dyslipidemia was brought to the emergency department with complaints of severe retrosternal chest pain, vomiting, diaphoresis and syncope. On initial evaluation, acute coronary syndrome was considered due to the clinical presentation and history of cardiovascular risk factors. Electrocardiogram and serum troponins were normal. On the second day of his admission, the patient developed odynophagia and bloody vomitus. Esophagogastroduodenoscopy revealed extensive esophageal ulcerations with hemorrhage. The patient was taking Doxycycline capsules for an acute febrile illness. Doxycycline is the oral medication most commonly reported to cause esophageal injury. Doxycycline was discontinued, and the patient was treated with intravenous omeprazole and oral antacid suspension. The patient improved, was discharged after 6 days of hospitalization, and reported resolution of all symptoms at an outpatient follow-up visit 3 weeks later. CONCLUSION: Medication-induced esophageal injury can present with atypical symptoms mimicking acute coronary syndrome. This condition should be included in the initial differential diagnosis of patients presenting with acute chest pain, especially those taking oral medications known to cause esophageal injury.

Opioid-Induced Esophageal Dysfunction: Differential Effects of Type and Dose.

OBJECTIVE: Data regarding opioid effects on esophageal function are limited. We previously demonstrated an association between chronic opioid use and esophageal motor dysfunction characterized by esophagogastric junction outflow obstruction, distal esophageal spasm, achalasia type III, and possibly Jackhammer esophagus. Our aim was to characterize the influence of different opioids and doses on esophageal dysfunction. METHODS: Retrospective review of 225 patients prescribed oxycodone, hydrocodone, or tramadol for >3 months, who completed high-resolution manometry from 2012 to 2017. Demographic and manometric data were extracted from a prospectively maintained motility database. Frequency of opioid-induced esophageal dysfunction (OIED, defined as distal esophageal spasm, esophagogastric junction outflow obstruction, achalasia type III, or Jackhammer esophagus on high-resolution manometry, was compared among different opioids. The total 24-hour opioid doses for oxycodone, hydrocodone, and tramadol were converted to a morphine equivalent for dose effect analysis. RESULTS: OIED was present in 24% (55 of 225) of opioid users. OIED was significantly more prevalent with oxycodone or hydrocodone use compared with tramadol (31% vs 28% vs 12%, P = 0.0162), and for oxycodone alone vs oxycodone with acetaminophen (43% vs 21%, P = 0.0482). There was no difference in OIED for patients taking hydrocodone alone vs hydrocodone with acetaminophen. Patients with OIED were taking a higher median 24-hour opioid dose than those without OIED (45 vs 30 mg, P = 0.058). DISCUSSION: OIED is more prevalent in patients taking oxycodone or hydrocodone compared with tramadol. There is greater likelihood of OIED developing with higher doses. Reducing the opioid dose or changing to tramadol may reduce OIED in opioid users.

Oesophageal ulcer due to a herbal remedy.

Herbal-induced oesophageal lesions are rare. We report the case of an 85-year-old male who presented with cough and odynophagia. An upper endoscopy showed white deposit under the proximal oesophageal sphincter. Biopsy of the lesion revealed an oesophageal ulcer with adherent plant material and ruled-out candidiasis. At this point, the patient divulged self-preparation of an herbal remedy consisting of Aloe Vera pulp, whisky, honey, ginger and turmeric. Aloe Vera, ginger and turmeric are commonly used to sooth some gastroenterological symptoms in Complementary and Alternative Medicine. Incorrect extraction of Aloe Vera pulp and adding honey to it transformed the recipe into a sticky paste that may have injured the oesophageal mucosa. Follow-up showed that the cough and odynophagia subsided after discontinuing this herbal remedy.

Hepatocyte Growth Factor Facilitates Esophageal Mucosal Repair and Inhibits the Submucosal Fibrosis in a Rat Model of Esophageal Ulcer.

BACKGROUND/AIMS: Esophageal mucosal damage often causes scar tissue, leading to refractory stricture. The aim of this study was to clarify the effect of hepatocyte growth factor (HGF) on esophageal mucosal repair and fibrosis leading to stricture in a rat model of esophageal ulcer. METHODS: Esophageal ulcers were induced in rats by topical exposure of the lower esophageal serosa to acetic acid, followed by intraperitoneal administration of HGF (200 µg/day) using an osmotic pump for 7 days. The effect of HGF on esophageal mucosal injury was investigated macroscopically and microscopically. The effect of HGF on epithelial cell proliferation and the expression of genes closely associated with the development of fibrosis were also examined. RESULTS: The administration of HGF for 7 days led to a significant reduction in the ulcerative area and enhanced the proliferation of esophageal epithelial cells. HGF treatment significantly decreased the fibrosis, and subsequently attenuated not only the foreshortening but also the narrowing of the esophagus. The expression levels of tissue inhibitor of metalloproteinase (TIMP)-1, -2, and matrix metalloproteinase (MMP)-2, -9 were significantly decreased among rats treated with HGF. CONCLUSION: HGF facilitates the repair of esophageal mucosal injury and may also ameliorate the esophageal fibrosis, possibly through enhanced re-epithelization.

The effect of platelet-rich plasma on motility changes in experimental caustic esophageal burn.

BACKGROUND: Besides stricture formation, diminished esophageal motility after caustic esophageal burns also plays a role in the deterioration of the clinical course. In this study, we aimed to investigate the effect of caustic burn on the esophageal contractions and the effect of platelet-rich plasma (PRP) on these changes. METHODS: Twenty-one Wistar albino rats were divided into three groups [Sham operation (n = 8), caustic esophageal burn with NaOH (n = 6), PRP treatment after caustic burn (n = 7)]. After 3 weeks, esophagectomy was performed and contractions and EFS responses were evaluated in the organ bath. RESULTS: KCl- and acetylcholine-induced responses were reduced in the Burn group, but increased in Sham and PRP groups (p < 0.05). EFS responses were higher in Burn group compared to the other groups. Response with L-arginine was increased in Burn group, but decreased in PRP group. There was more decrease in the contraction in Sham and PRP groups compared to the Burn group after SNP (sodium nitroprusside) incubation (p < 0.05). L-NAME (Nω-Nitro-L-arginine methyl ester) did not change the EFS responses in the Burn group, but EFS responses were decreased significantly in Sham and PRP groups (p < 0.05). EFS responses were decreased in all groups, but more in the Sham and PRP groups after Y-27632 (Rho-kinase inhibitor) incubation (p < 0.05). CONCLUSIONS: For the first time, we demonstrated that both cholinergic and non-adrenergic non-cholinergic mechanisms are responsible for the altered motility in corrosive esophageal injury. Our results suggest that PRP treatment may be helpful in regulating the esophageal motility and decreasing altered contractions in corrosive burns. This effect may also contribute to the reduction of stricture formation, especially by reducing inappropriate contractions of the esophageal wall during the post-burn healing phase.

Intramural hematoma of the esophagus after thrombolysis for ischemic stroke.

Intramural dissecting hematoma is an unusual esophageal condition with a threatening presentation but excellent prognosis when managed conservatively.We report the case of an 88-year-old woman who developed an intramural hematoma of the esophagus after intravenous thrombolysis for an acute ischemic stroke. Before thrombolysis, nasogastric intubation was attempted unsuccessfully. She was kept on nil by mouth, intravenous hydration, proton pump inhibitor, antiemetics,and an antibiotic initiated 2 days before for periodontal disease. The esophageal hematoma regressed, and she resumed oral diet asymptomatically.To our knowledge, this is the first report of this type of lesion after thrombolysis for an ischemic stroke. A brief discussion and literature review are presented.

[Two cases of dabigatran-induced esophageal ulcer indicating the usefulness of drug administration guidance].

Here we report two cases of dabigatran-induced esophageal ulcer. Case 1 was a 67-year-old man who presented with heartburn that developed a month after dabigatran administration. Case 2 was an 81-year-old woman who presented with epigastralgia that developed within a few days of dabigatran administration. Endoscopic findings were similar in both cases, including shallow esophageal ulcers covered with a thin whitish membrane. The patients were advised to consume the drug with plenty of water during meals and to remain in a sitting position for 30 min after consumption. This method successfully decreased their symptoms and ulcers, indicating that drug administration guidance is extremely effective in managing dabigatran-induced esophageal injury.

[Results of emergency management of esophageal lesions related to caustic ingestion in children in the emergency department of the General Reference Hospital of Niamey (Niger)]. / Résultats de la prise en charge médico-chirurgicale en urgence des lésions œsophagiennes liées aux ingestions de produits caustiques chez l'enfant dans le service des urgences de l'Hôpital général de référence de Niamey (Niger).

Introduction: Caustic ingestion in children is a public health problem; it is mainly due to domestic accidents due to improper packaging and storage of caustic products. It is a medical and surgical emergency whose management is multidisciplinary. The lesions caused by the accidental ingestion of caustics can affect the functional and vital prognosis in 10% of cases. Methodology: A retrospective, descriptive study from January 2020 to December 2022 (2 years), carried out in the emergency department of the General Reference Hospital of Niamey (Niger). The study included patients less than 15 years old admitted for ingesting a caustic product. Results: Our study included 17 patients. The average age was 5 years, with age extremes of 2 to 11 years. We noted a male predominance with a sex ratio (M/F) of 2.4. Ingestion of caustic products was accidental in all cases. The caustic product was caustic soda in 59%. The average quantity of product ingested was 5 ml (2 ml to 20 ml). The average consultation time was 3 days (3 hours to 15 days). Clinically, dysphagia was the most functional sign, represented by 13 cases, or 76%. Regarding general signs, 3 patients (18%) were admitted with fever; blood pressure was normal in 15 patients (88%); and 2 patients (18%) were admitted in a state of shock. The respiratory rate was normal in 14 patients (82%). Four patients (24%) were admitted in a state of deterioration in the general condition associated with severe malnutrition and dehydration. On physical examination, 2 patients (12%) presented with abdominal defense at the epigastric level. Examination of the ENT sphere revealed benign buccopharyngeal ulcerations in 2 patients (12%). Esogastroduodenal fibroscopy was performed in 4 patients (24%). The caustic lesions observed in the esophagus were: Zargar stage I at 25%, stage Ila at 50%, and stage Illb at 25%. In the stomach, the lesions were Zargar stage I in 75% of cases and stage III in 25% of cases. An injected thoracic-abdominopelvic computed tomography (CT) was performed in 3 patients (18%). It revealed a lack of enhancement of the esophageal wall compatible with esophageal necrosis in one patient. An esophagogastroduodenal transit was performed in 8 patients (47%) admitted more than 72 hours after ingestion of the caustic. They showed esophageal stenoses longer than 3 cm in 3 patients, multiple esophageal stenoses in 2 patients, a single esophageal stenosis in 2 patients, and a single antropyloric stenosis in 1 patient. Therapeutically, all patients benefited from antiemetics to avoid vomiting and proton pump inhibitors. Intravenous antibiotic prophylaxis with third-generation cephalosporin was administered to 12 patients (71%). Corticosteroid therapy based on IV prednisolone at a dose of 1 g/1.73 m2 per day was used to limit or prevent stenoses in 9 patients (53%). Parenteral nutrition was administered to 7 patients (41%). Endoscopic dilations were performed in 2 patients (12%). Emergency surgical treatment was performed in 7 patients (41%): 3 patients underwent transitional feeding gastrostomies; in 3 others, esophagoplasties by colon transplant were performed, and 1 patient was treated by stripping of the esophagus associated with total gastrectomy. The postoperative course was marked by a leak of esocolic anastomosis in one patient for whom conservative treatment was performed with good progress. The average length of hospital stay was 5 days (1-32 days). Conclusion: Accidental caustic ingestions can have serious consequences. Preventing these accidents relies on raising public awareness of the dangers associated with improper storage of these products.

Acute therapy with intravenous omeprazole on caustic esophageal injury: a prospective case series.

The ingestion of caustic substances may result in significant esophageal injury. There is no standard treatment protocol for esophageal injury and most patients are treated with a proton pump inhibitor or H2 antagonist. However, there is no clinical study evaluating the efficacy of omeprazole for caustic esophageal injury. A prospective study of 13 adult patients (>18 years of age) who were admitted to our hospital for caustic ingestion between May 2010 and June 2010 was conducted. Mucosal damage was graded using a modified endoscopic classification described by Zargar et al. Patients were treated with a proton pump inhibitor and maintained without oral intake until their condition was considered stable. Patients received omeprazole 80 mg in bolus IV, followed by continuous infusion of 8 mg/hour for 72 hours. A control endoscopy was performed 72 hours after admission. There was significant difference regarding endoscopic healing between the before and after omeprazole infusion (P = 0.004). There was no hospital mortality at the follow-up. Omeprazole may effectively be used in the acute phase treatment of caustic esophagus injuries.

[Peculiarities of occupational esophagogastroduodenal pathology in personnel serving at CW disposal and storage facilities].

In a process of medical care and supervision on staff and military personnel, eliminating the chemical weapons, it was revealed that they are more susceptible to esophagogastroduodenal pathology in comparison with the control group. Moreover, the given pathology has an asymptomatic disease course but associated with high contamination of Helicobacter pylori. Marked inflammation changes, atrophic and fibrosis manifestation and microcirculation dysfunction have been confirmed by histological analysis of gastric mucosa. We supposed that the complex of occupational health risk factors, including possible subliminal toxic influence of eliminated CW components determines this pathological dysfunction. Negative influence of shift work and irregular nutrition rhythm are not excluded. The findings of this research are dictating the necessary of revision of military medical expertise principles and the development of the more effective treatment and prophylactic methods.