Prevalence and Costs of Esophageal Strictures in the United States.

BACKGROUND & AIMS: Esophageal strictures are a leading cause of dysphagia, but data regarding the epidemiology of esophageal strictures are limited. This study aimed to investigate the prevalence, health care utilization, and financial burden of esophageal strictures in the United States. METHODS: We performed a retrospective cohort study using 2 large national insurance claims databases (MarketScan and Medicare). Using International Classification of Diseases-9 and -10 diagnostic codes, annual prevalence was calculated for both cohorts overall, and stratified by age and sex strata. Most common diagnostic and procedural codes associated with esophageal strictures were extracted and analyzed to estimate health care utilization. Direct annual medical costs of esophageal strictures were calculated. RESULTS: The annual prevalence of esophageal strictures in MarketScan in 2021 was 203.14 cases/100,000 people, whereas the annual prevalence in Medicare cohort in 2017 was 1123.47 cases/100,000. Although rates were relatively stable over time, esophageal stricture prevalence increased with advancing age. No prevalence differences were noticed between males and females. Gastroesophageal reflux disease/erosive esophagitis was the top diagnostic code associated with esophageal strictures, although an increase in the proportion of eosinophilic esophagitis codes was noted over time. Esophageal dilation codes were present in ∼50% of stricture cases. The total health care costs associated with esophageal strictures were estimated at $1.39 billion in 2017. CONCLUSIONS: Esophageal strictures are common, affecting between 1/100 and 1/1000 patients in the United States, with the highest rates seen in patients aged 75 years and older. Accordingly, strictures have a significant financial burden on the health care system, with costs greater than $1 billion annually.

A Rare Case of Hydralazine-Induced Diffuse Alveolar Hemorrhage.

Hydralazine-induced anti-neutrophil cytoplasmic antibody (ANCA) vasculitis may occur any time after hydralazine initiation. General internists should recognize diffuse alveolar hemorrhage (DAH) as a rare complication of this condition, as early treatment reduces the associated high risk of mortality. We describe the case of an 82-year-old female with diastolic heart failure who presented with a one-month history of worsening dyspnea on exertion and a one-week history of scant hemoptysis and fatigue. Her medications included aspirin and hydralazine. She was hypoxic with bilateral expiratory wheezes on exam. Labs showed new anemia, elevated creatinine, proteinuria, and hematuria. Chest computed tomography showed asymmetric bilateral upper lobe ground-glass attenuation superimposed on interlobular septal thickening and intralobular lines. Further testing showed anti-nuclear antibody, positive ANCA, perinuclear ANCA (p-ANCA), and anti-myeloperoxidase ANCA (anti-MPO-ANCA). Renal biopsy revealed MPO-ANCA, pauci-immune, necrotizing, and crescentic glomerulonephritis. She was diagnosed with DAH secondary to hydralazine-induced ANCA-associated vasculitis (AAV). Hydralazine is an anti-hypertensive medication with known potential for autoimmune reactions. Of these, AAV is a rare sequela mediated by anti-MPO and most commonly affects the kidneys. In rare circumstances, patients with AAV can develop pulmonary-renal syndrome, resulting in both glomerulonephritis and DAH with an associated high risk of mortality. Diagnosis requires a high index of suspicion in patients with acute kidney injury of unclear etiology. Early diagnosis through immune work-up and kidney biopsy should be pursued, as prompt recognition of the vasculitis, cessation of hydralazine, immunosuppression, and early plasma exchange are essential to an improved prognosis.

A Rare Case of Olmesartan-Associated Enteropathy Successfully Managed With Steroid Taper.

Olmesartan is a commonly used antihypertensive medication belonging to the class of angiotensin II receptor blockers. Though generally well-tolerated, olmesartan can rarely cause olmesartan-associated enteropathy (OAE) with non-bloody diarrhea, weight loss, abdominal pain, and vomiting. Patients may develop enteropathy months to years after drug initiation. In severe cases, patients may develop complications that require hospitalization. Diagnosis is often delayed due to unfamiliarity of OAE, nonspecific presenting symptoms, and normal-appearing gross endoscopic findings. Esophagogastroduodenoscopy (EGD) with biopsy is essential to the diagnosis, showing sprue-like enteropathy with intestinal villous atrophy and mucosal inflammation. This report describes a case of a 70-year-old man who presented with three months of profuse watery diarrhea and 40-pound unintentional weight loss. After an extensive workup, including EGD with duodenal biopsies, the patient was diagnosed with OAE. The biopsies showed findings consistent with acute and chronic duodenitis, mucosal desquamation and ulceration, blunting of villi, and a sprue-like pattern with neutrophils. Celiac serologies and anti-enterocyte antibodies were negative, further supporting the diagnosis of OAE. Complete resolution of symptoms was achieved by discontinuing olmesartan and administering a steroid taper. Considering the frequent use of olmesartan, the increasing occurrence of OAE, and the wide range of associated symptoms, it is crucial for providers to recognize OAE and consider early discontinuation of olmesartan. This approach can help prevent further intestinal damage, protracted symptoms, unnecessary diagnostic tests, and financial burdens on both patients and the healthcare system.

Older patients with eosinophilic esophagitis have high treatment response to topical steroids.

BACKGROUND: There are few data assessing treatment response in older eosinophilic esophagitis (EoE) patients and we evaluated treatment outcomes to topical corticosteroids (tCS) in this older population. METHODS: This retrospective cohort study of the UNC EoE Clinicopathologic database included subjects with a new diagnosis of EoE treated with tCS. Histologic responses, global symptom response, and endoscopic changes were recorded. Older EoE patients (≥65 years) were compared to younger EoE patients (<65). RESULTS: We identified 467 EoE patients treated with tCS, 12 (3%) of whom were ≥65 years. Compared to those <65 years, patients ≥65 had longer symptom duration and worse endoscopy scores, but most clinical features were similar. Post-treatment peak eosinophil counts trended higher in the <65 group (25.0 vs 5.5; p = 0.07). Histological response was greater in the ≥65 population at <15 eos/hpf (92% vs 57%; p = 0.02), ≤6 eos/hpf (83% vs 50%; p = 0.02), and <1 eos/hpf (58% vs 29%; p = 0.03). Older age was independently associated with increased odds of histologic response (adjusted OR 8.48, 95% CI: 1.08-66.4). CONCLUSIONS: EoE patients ≥65 years had a higher likelihood of responding to tCS therapy, suggesting they should be studied more closely and included in future trials.