Viral esophagitis in non-human immunodeficiency virus patients: a case-control study.

Background: Esophagitis, inflammation of the esophagus, can result from various causes, including reflux, infections, food allergies, medications, and trauma. Infectious esophagitis is the third most common cause after gastroesophageal reflux disease (GERD) and eosinophilic esophagitis worldwide. The primary causes of infectious esophagitis are candida esophagitis and viral esophagitis (VE) caused by herpes simplex virus (HSV) or cytomegalovirus (CMV). VE is typically associated with immunosuppression, with risk factors such as malignancy, chemotherapy, organ transplant, and human immunodeficiency virus (HIV). Infectious esophagitis is prevalent in about one-third of untreated acquired immunodeficiency syndrome (AIDS) patients, but recent reports indicate an increase in VE cases among immunocompetent individuals. This study aims to explore risk factors and patient demographics in non-HIV individuals. Methods: A case-control study that included patients 18 years and older diagnosed with HSV or CMV esophagitis who were identified through histopathologic examination or immunohistochemical staining. Cases were obtained by searching pathology reports between 2009-2022 from five MedStar Health Hospitals in the District of Columbia and Maryland. Controls were selected based on International Classification of Diseases (ICD) codes for esophagogastroduodenoscopy (EGD) with negative VE results within the same period. Patient demographics, comorbidities, laboratory parameters, endoscopic findings, and potential risk factors were collected through chart review. Results: Out of 40,224 cases between 2009-2022, 50 cases of VE were identified, with 30 cases attributed to HSV, 19 cases to CMV, and one case of HSV/CMV coinfection. Hematemesis was the predominant symptom in patients with HSV (33%), while dysphagia was more prevalent in CMV patients (42%). The most common finding during EGD was ulceration in HSV patients (67%) and esophagitis in CMV patients (37%). Patients with VE had a higher likelihood of a history of immunosuppressive therapy, organ transplant, active malignancy, and systemic steroid use. However, a significant portion (34%) had no identifiable risk factors. Conclusions: The study's findings contribute to a better understanding of the clinical characteristics and risk factors associated with VE in non-HIV patients. The identification of immunosuppression and specific risk factors can aid in early detection, appropriate management, and targeted interventions for VE. Further research is warranted to explore the rising incidence of VE in immunocompetent individuals and to optimize preventive strategies and treatment approaches for this condition.

PTEN, ERG, SPINK1, and TFF3 Status and Relationship in a Prostate Cancer Cohort from Jordanian Arab Population.

Background and Objectives: Prognostic biomarkers in prostate cancer (PCa) include PTEN, ERG, SPINK1, and TFF3. Their relationships and patterns of expression in PCa in developing countries, including Jordan, have not yet been investigated. Materials and Methods: A tissue microarray (TMA) of PCa patients was taken from paraffin-embedded tissue blocks for 130 patients. PTEN, ERG, SPINK1, and TFF3 expression profiles were examined using immunohistochemistry (IHC) and correlated with each other and other clinicopathological factors. Results: PTEN loss of any degree was observed in 42.9% of PCa cases. ERG and TFF3 were expressed in 59.3% and 46.5% of PCa cases, respectively. SPINK1 expression was observed in 6 out of 104 PCa cases (5.4%). Among all PCa cases (n = 104), 3.8% (n = 4) showed SPINK1+/ERG+ phenotype, 1.9% (n = 2) showed SPINK1+/ERG- phenotype, 56.7% (n = 59) showed SPINK1-/ERG+ phenotype, and 37.5% showed SPINK1-/ERG- phenotype (n = 39). Among ERG positive cases (n = 63), 6.3% were SPINK1 positive. Among SPINK1 positive cases (n = 6), 66.7% were ERG positive. SPINK1 expression was predominantly observed in a subgroup of cancers that expressed TFF3 (6/6). Additionally, a statistically significant loss of PTEN expression was observed from Gleason Score 6 (GS6) (Grade Group 1 (GG1)) to GS9-10 (GG5); (p-value 0.019). Conclusions: This is the first study to look at the status of the PTEN, ERG, SPINK1, and TFF3 genes in a Jordanian Arab population. Loss of PTEN has been linked to more aggressive prostate cancer with high GSs/GGs. SPINK1 expression was predominantly observed in a subgroup of cancers that expressed TFF3. Our results call for screening these biomarkers for grading and molecular subtyping of the disease.

Boerhaave Syndrome: A Report of Two Cases and Literature Review.

Boerhaave's syndrome is a rare yet serious condition associated with high mortality and morbidity. Diagnosis of this syndrome is usually done with the aid of imaging and prompt management should be initiated to improve the outcomes. Treatment for this syndrome has been mainly surgical since its discovery by Herman Boerhaave; however, multiple endoscopic approaches have been successfully used recently with the advancement of this field. Here, we describe two cases of Boerhaave's syndrome that were endoscopically managed along with a brief literature review of the different endoscopic methods used to manage this syndrome.

Dysphagia: A Rare Presentation of Sarcoidosis.

Gastrointestinal (GI) sarcoidosis is a rare manifestation of this multi-systemic granulomatous disorder. Esophageal involvement is extremely rare and there have been few case reports about this. Our article reports a case of esophageal sarcoidosis in which dysphagia was the main presenting symptom. The main initial treatment of symptomatic sarcoidosis in general and pulmonary sarcoidosis in specific usually involves corticosteroids, however, there are no specific guidelines for the management of GI sarcoidosis. Surprisingly, or maybe not, in our case, the dysphagia did not improve with steroid therapy which prompted further investigations as well as endoscopic intervention.

PTEN Loss in a Prostate Cancer Cohort From Jordan.

Deletion of phosphatase and tensin homolog (PTEN) in prostate cancer has been associated with early biochemical recurrence, increased metastatic potential, and androgen independence. We evaluated the status of PTEN loss in a cohort of prostate cancer patients from Jordan. We investigated 71 patients with prostate cancer and 52 control subjects with benign prostatic hyperplasia (BPH). PTEN status was assessed by immunohistochemistry. PTEN mutations on exons 1, 2, 5, and 8 were also evaluated by polymerase chain reaction single-stranded conformation polymorphism (PCR-SSCP). We found PTEN loss in 42 of 71 (59.2%) evaluated prostate cancer cases by immunohistochemistry. In contrast, 51 of 52 BPH (98.1%) cases had an intact PTEN. In a subset of 24 prostate cancer cases evaluated by PCR-SSCP, we found PTEN mutations in 15 (62.5%) cases, whereas 22 (91.7%) of BPH controls lacked PTEN mutations. Exon 5 was the most frequently mutated exon (37.5%). Although the loss of PTEN was not significantly correlated with the Gleason Score (GS) or the World Health Organization (WHO)-International Society of Urological Pathology (ISUP) Grade Group (GG), we found higher frequency of PTEN loss (64%) in patients with GS≥4+3/GG≥3, compared with patients with GS≤3+4/GG≤2 (47.6%). In this first study to address the question of PTEN loss in a predominantly Arab population, we documented the frequency of PTEN loss in prostate cancer patients from Jordan, which was found to be higher than in comparable cohorts from East Asia, and was at the higher end of the range of reported frequency of PTEN loss in respective cohorts from North America and Western Europe. Although there was more frequent PTEN loss in cancers with higher GS/GG, this was not statistically significant.