Case Reports in Gastroenterology最新文献

Introduction: Primary peritoneal clear cell carcinoma (PPCCC) is a rare abdominal tumor, affecting 7 out of every million people. Its vague presenting signs and symptoms often lead to delayed diagnosis and poor prognosis. We present a case involving a young woman with anemia and abdominal discomfort who on further investigation had a 26-cm abdominal tumor identified to be PPCCC. Multimodal therapy with tumor debulking and chemotherapy was pursued. Given the aggressive nature of PPCCC, any clinical suspicion of peritoneal carcinoma should prompt thorough diagnostic evaluation.

Case presentation: A 39-year-old woman with menorrhagia and peptic ulcer disease presented with abdominal discomfort of 2 days duration. She initially had headaches managed with ibuprofen. Following this, she had generalized abdominal pain with bloating that worsened with food and had no relief with use of stool softeners. She had associated dizziness with palpitations, chest pressure, and exertional dyspnea. In the emergency department, the patient was mildly tachycardic but otherwise stable. On exam, she had a distended abdomen with generalized tenderness and normoactive bowel sounds. Labs showed normocytic anemia with a hemoglobin of 5.2 mg/dL. Electrocardiogram and abdominal and chest X-rays were normal. A non-contrast computed tomography of the abdomen and pelvis showed a fibroid uterus and posterior displacement of multiple bowel loops by a large septate cystic mass (13.5 × 26.0 × 26.7 cm) occupying the entire abdominal cavity. Elevated CA 125 and CA 19-9 were also noted. She underwent exploratory laparotomy with mass resection, partial omentectomy, left colectomy (given extension into transverse colon), appendectomy, and total abdominal hysterectomy with bilateral salpingectomy. Biopsy and immunohistochemical staining (positive for PAX-8, ER, P53, P16, Napsin A and negative for PR and WT-1) confirmed mass as stage IIIB PPCCC. There was no evidence of malignancy in other tissue samples. The patient was discharged with a plan for outpatient chemotherapy and genetic counseling.

Conclusion: Given the rarity of PPCCC, our case highlights how increased clinical vigilance and prompt multidisciplinary efforts are essential for an accurate diagnosis, especially in younger patients to not delay management. Currently, there are no established management guidelines; however, initial treatment with surgical debulking followed by chemotherapy is often practiced.

Introduction: Gastroesophageal reflux disease (GERD) is diagnosed based on bothersome symptoms, such as heartburn, and the presence of mucosal breaks endoscopically. Treatments that suppress gastric acid, such as proton pump inhibitor (PPI) and vonoprazan, are frequently administered. Several studies reported regarding the safety and side effects of long-term PPI administration, including an association with gastric polyps. We report a case of maintained symptom resolution and significantly shrank gastric polyps by performing step-down therapy, which is minimal acid-suppressing treatment.

Case presentation: A female patient in her 60s had been taking PPI for reflux esophagitis for >10 years. An upper gastrointestinal endoscopy revealed two gastric polyps measuring 20 mm and 10 mm. She was referred to our hospital for resection, but narrow-band imaging revealed a nonneoplastic lesion. PPI was discontinued, and step-down therapy using vonoprazan was performed. During the treatment, a lifestyle guidance app (Muneyake PRO) was used to record daily heartburn symptoms, oral medication status, and daily life status. She was worried that her symptoms would worsen due to discontinuation, but she gained her understanding when the use of the app to monitor her symptoms was explained. The app was useful for understanding the progress of symptoms and the status of oral medication. Step-down therapy was performed only twice after PPI discontinuation, symptoms have not worsened, and follow-up endoscopy revealed significant gastric polyp shrinkage.

Conclusion: We experienced a case in which minimal acid-suppression treatment and step-down therapy using vonoprazan resulted in GERD symptom control and significant gastric polyp shrinkage.

Introduction: Erosive damage to the upper gastrointestinal (GI) tract caused by therapeutic oral iron supplements is relatively uncommon. While such injuries are frequently linked to overdoses of oral iron, they can also occur with doses within the standard therapeutic range. Cases have highlighted GI complications caused by iron, predominantly involving the stomach and sometimes the esophagus. During absorption, iron is initially processed as ferrous iron, which, when bound to proteins, can lead to cellular injury. Additionally, ferric iron exerts a corrosive effect on the GI mucosa and disrupts cellular processes by generating free radicals and triggering lipid peroxidation.

Case presentation: A 55-year-old female with dysphagia, pain, and anorexia showed linear to circumferential ulcers covered with white slough extensively around central esophagus with thickened and erythematous mucosa with focal erosions on esophagogastroduodenoscopy.

Conclusion: This case highlights a rare case report of iron-induced esophageal ulcer found incidentally and the significance of acknowledging that iron preparations can harm the esophageal mucosa, especially in an Indian population where anemia is fairly predominant.

Introduction: We report an exceedingly rare case of hepatocellular carcinoma (HCC) associated with an idiopathic congenital forearm arteriovenous fistula (AVF). Given the absence of previous reports addressing the treatment of HCC in patients with AVF, we evaluate HCC treatment strategies, including the appropriateness of using angiogenesis inhibitors.

Case presentation: A 74-year-old man was admitted for the evaluation of liver tumors. His medical history included a chronic, intractable idiopathic right forearm AVF, for which he had undergone multiple surgical interventions. Abdominal EOB-MRI revealed multiple small focal lesions across both liver lobes during the hepatobiliary phase, indicative of multiple HCC, and liver biopsy confirmed early-stage HCC. Considering the potential presence of additional vascular anomalies similar to the forearm AVF, local hepatic artery chemoembolization was performed. Since there is still insufficient discussion about the systemic administration of angiogenesis inhibitors to patients with vascular abnormalities such as AVF, we discuss the treatment options for HCC with AVF, including its strategies in the progressed HCC stage.

Conclusion: As molecularly targeted therapies continue to evolve, recognizing the unique aspects of cases like ours is crucial. Establishing an appropriate treatment strategy for HCC patients with AVF is imperative, highlighting the need for tailored therapeutic approaches based on individual vascular profiles.

Introduction: Most patients with compensated cirrhosis remain asymptomatic. However, with the onset of decompensation, electrolyte and acid-base disturbances are frequent in patients with chronic liver disease, including hypokalemia. We encountered a case of chronic liver disease with portal hypertension, primarily presenting with motor weakness caused by intractable hypokalemia, hypoxia-associated respiratory alkalosis, and chronic diarrhea.

Case presentation: A 54-year-old male presented to the emergency department with motor weakness. He reported experiencing exertional dyspnea and watery diarrhea for the past 3 months, approximately ten times daily. Arterial blood gas analysis indicated hypoxia and hypocapnia compatible with chronic respiratory alkalosis. The transtubular potassium gradient was 1.69, and the aldosterone/renin ratio was 17.6 (ng/dL)/(ng/mL/h). The patient had a 30-year history of consuming 360-720 mL of 20% alcohol almost daily. Abdominal computed tomography revealed multiple regenerative and dysplastic nodules in the liver, splenomegaly, ascites, esophageal varices, and diffuse edematous wall thickening in the bowel, suggesting portal hypertensive enteropathy. Computed tomography of the lungs showed no specific abnormalities in the lungs, pleura, or thoracic wall.

Conclusion: We present a case of liver cirrhosis complicated by intractable hypokalemia, respiratory alkalosis, portal hypertension, and chronic diarrhea. A 24-h urine analysis showed renal excretion levels of Na⁺, K⁺, and Cl^- at 6.0, 2.5, and 11.0 mmol, respectively, suggesting renal retention of these electrolytes. Meanwhile, the serum levels of Na⁺, K⁺, and Cl^- were 136, 1.8, and 98 mEq/L, respectively, indicating a preserved balance of sodium and chloride but not potassium. This case underscores the importance of clinicians considering both liver cirrhosis-associated hypoxia and chronic liver disease-induced chronic diarrhea as potential underlying causes, especially when more common causes of hypokalemia have been excluded.

Introduction: Gall stone ileus is a rare complication of cholelithiasis which typically presents with obstruction in the small intestine. However, it can rarely mimic a mass when it presents in unusual sites like the sigmoid colon as in our case.

Case presentation: We present a 42-year-old woman with a history of bariatric surgery, diverticulitis status post sigmoid colectomy and decompensated cirrhosis complicated by hepatic encephalopathy who presented to the hospital with concern for altered mental status and was diagnosed with grade III hepatic encephalopathy due to lactulose non adherence. During the hospitalization, patient developed rectal bleeding with suspected colonic mass on imaging that was ultimately identified as a large sigmoid gallstone ileus on endoscopic evaluation.

Conclusion: Our report aimed to highlight the importance of considering gallstone ileus in the differential diagnosis of colonic masses, especially in patients with relevant clinical history.

Introduction: Inflammatory bowel disease-primary sclerosing cholangitis (IBD-PSC) is a unique disease entity that has very poorly understood pathogenesis and unique clinical presentation. Patients with this disease may eventually require liver transplantation as there is no current curative treatment for PSC to halt disease progression for liver failure. Thirty percent of patients with IBD may experience recurrence despite being on immunosuppression. Few studies have shown that vancomycin has been used as a salvage treatment for patients with refractory ulcerative colitis (UC) exacerbation refractory to conventional and biological agents. In this report, we discuss the case of 25-year-old female with a prior history of sickle cell disease (SCD), UC, post-liver transplant secondary to PSC, who developed UC exacerbation refractory to conventional therapies and most biological agents and was induced and maintained in remission with oral vancomycin (OV).

Case presentation: This is the case of 25-year-old female with a history of SCD, UC, and primary sclerosing cholangitis (PSC) who developed liver cirrhosis and underwent liver transplantation. Prior to liver transplantation, she had recurrent exacerbations of UC, refractory conventional therapies, and most biological agents. Post-liver transplantation, she developed another UC flare despite being treated with ustekinumab. OV 125 mg four times daily was used as salvage therapy post-liver transplantation to control her UC.

Conclusion: This report supports the use of OV in patient with SCD who had UC exacerbation refractory to conventional and biological agents.

Introduction: Esophageal leiomyomas are relatively common benign esophageal submucosal tumors (SMTs). Generally, benign tumors do not accumulate fluorine-18-fluorodeoxyglucose (FDG), but it is not rare for FDG to accumulate in uterine, duodenal, or esophageal leiomyomas. In our case, we performed peroral endoscopic tumor resection (POET) for an esophageal leiomyoma with FDG accumulation.

Case presentation: A 40-year-old female with a history of surgery for right breast cancer underwent fluorine-18-fluorodeoxyglucose-positron emission tomography for surveillance examination and had no specific symptoms or notable clinical findings. A subepithelial tumor with intense FDG uptake (SUVmax, 5.49) was detected in the middle thoracic esophagus. The lesion appeared as a low-absorption area on contrast-enhanced CT and was confirmed to have an equivalent signal level as muscle tissue on MRI T2WI. Endoscopic examination revealed SMT 25 cm from the incisors. Endoscopic ultrasonography (EUS) revealed a 20 mm low-luminance mass, mainly located in the second and third layers. The histopathology diagnosis by EUS-fine-needle aspiration was leiomyoma. We decided to treat it with POET because malignancy could not be ruled out. The tumor was excised en bloc using POET without severe complications. The tumor diameter was 19 × 15 mm, and disordered spindle cells were observed. Desmin and αSMA were positive, and S100 protein was negative on immunohistochemical study. Therefore, the pathological diagnosis was a leiomyoma.

Conclusion: In the present case, glucose transporter 1 expression was negative; however, we examined why the leiomyoma accumulated FDG. We suggest that awareness of leiomyoma with the accumulation of FDG exists in clinical practice.

Introduction: We present the first published case of turmeric-associated drug-induced liver injury (DILI) accompanied by significant ferritin elevation.

Case presentation: Our patient, a 59-year-old female with DILI caused by long-term ingestion of oral turmeric supplements, presented with painless jaundice on an annual exam. The patient's liver function tests exhibited a hepatocellular pattern and hyperferritinemia (>2,000 ng/dL). Additional testing was negative except for heterozygosity for the H63D allele associated with hemochromatosis. A liver biopsy indicated acute hepatitis without fibrosis or stainable iron.

Conclusion: Upon discontinuation of the supplement, liver enzymes normalized within a month. This case highlights the potential for hepatotoxicity and hyperferritinemia from curcumin toxicity, particularly when combined with additives like black pepper that enhance its bioavailability. Awareness of this phenomenon, particularly in heterozygous carriers of hemochromatosis, is crucial for diagnosis and optimal management.

Introduction: We present the case of a patient with Crohn's disease who experienced recurrent pneumothorax after starting treatment with ustekinumab.

Case presentation: A patient with Crohn's disease started an induction regimen with intravenous ustekinumab, and 2 months later he presented a left-sided pneumothorax. It had an atypical evolution that required surgical management. The medication was withdrawn and the pneumothorax resolved completely. One year later, he had a new flare-up of Crohn's disease and ustekinumab therapy was restarted, presenting a new episode of pneumothorax.

Conclusion: To our knowledge, this is the first report of recurrent pneumothorax following two separate attempts to initiate ustekinumab.