Frontiers in immunology · 2026
Duodenal tuberculosis with probable biliary involvement in primary Sjögren's syndrome mimicking pancreatobiliary malignancy: a case report.
Клинический случайСтатьяНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Zhang Jing, Zhou Xucheng, Li Sheng-Guang, Zhang Lina, Shi Wenzai
Аннотация
BACKGROUND: Extrapulmonary tuberculosis can imitate malignancy and systemic autoimmune disease. Concurrent duodenal tuberculosis with probable biliary involvement is exceptionally uncommon and may create a high-stakes pancreatobiliary cancer mimic.
CASE PRESENTATION: A 71-year-old Han Chinese woman with primary Sjögren's syndrome and type 2 diabetes, and no recent immunosuppressive therapy, presented with polyarthralgia, intermittent fever, abdominal discomfort, anorexia, constipation, and weight loss. Laboratory testing showed systemic inflammation and a cholestatic enzyme pattern, whereas bilirubin and tumor markers remained normal. Magnetic resonance cholangiopancreatography revealed diffuse bile-duct wall thickening with severe distal common bile duct stenosis, and positron emission tomography-computed tomography showed hypermetabolic duodenal thickening with multiple fluorodeoxyglucose-avid lymph nodes. The tuberculin skin test measured 15 x 12 mm at 48 and 72 hours, and interferon-gamma release assay was positive (T-N >10.00 IU/mL). Upper endoscopy demonstrated a duodenal ulcer with fistula formation, and biopsy showed ulceration, granulomatous inflammation, and one acid-fast bacillus on staining. Supraclavicular lymph-node aspiration revealed lymphocytes and multinucleated giant cells without malignant cells. Duodenal tuberculosis with nodal disease and probable, non-biopsy-proven biliary involvement was diagnosed. After discharge, she received specialist-supervised antituberculosis therapy including isoniazid 0.3 g daily, rifampicin 0.45 g daily, and levofloxacin 0.5 g daily; by January 2022, treatment had continued for more than 3 months. The initial phase structure and total treatment duration could not be reliably ascertained. Symptoms, inflammatory and cholestatic markers, endoscopic ulceration, fistula, lymph-node size, and common bile duct stenosis improved at reassessment in January 2022.
CONCLUSION: Tuberculosis should remain in the differential diagnosis of fluorodeoxyglucose-avid duodenal and biliary lesions in patients with autoimmune disease, particularly when biochemical obstruction, tumor markers, and tissue pathology do not fit malignancy. Early endoscopic biopsy and accessible nodal sampling can prevent unnecessary surgery and unsafe escalation of immunosuppression.
CASE PRESENTATION: A 71-year-old Han Chinese woman with primary Sjögren's syndrome and type 2 diabetes, and no recent immunosuppressive therapy, presented with polyarthralgia, intermittent fever, abdominal discomfort, anorexia, constipation, and weight loss. Laboratory testing showed systemic inflammation and a cholestatic enzyme pattern, whereas bilirubin and tumor markers remained normal. Magnetic resonance cholangiopancreatography revealed diffuse bile-duct wall thickening with severe distal common bile duct stenosis, and positron emission tomography-computed tomography showed hypermetabolic duodenal thickening with multiple fluorodeoxyglucose-avid lymph nodes. The tuberculin skin test measured 15 x 12 mm at 48 and 72 hours, and interferon-gamma release assay was positive (T-N >10.00 IU/mL). Upper endoscopy demonstrated a duodenal ulcer with fistula formation, and biopsy showed ulceration, granulomatous inflammation, and one acid-fast bacillus on staining. Supraclavicular lymph-node aspiration revealed lymphocytes and multinucleated giant cells without malignant cells. Duodenal tuberculosis with nodal disease and probable, non-biopsy-proven biliary involvement was diagnosed. After discharge, she received specialist-supervised antituberculosis therapy including isoniazid 0.3 g daily, rifampicin 0.45 g daily, and levofloxacin 0.5 g daily; by January 2022, treatment had continued for more than 3 months. The initial phase structure and total treatment duration could not be reliably ascertained. Symptoms, inflammatory and cholestatic markers, endoscopic ulceration, fistula, lymph-node size, and common bile duct stenosis improved at reassessment in January 2022.
CONCLUSION: Tuberculosis should remain in the differential diagnosis of fluorodeoxyglucose-avid duodenal and biliary lesions in patients with autoimmune disease, particularly when biochemical obstruction, tumor markers, and tissue pathology do not fit malignancy. Early endoscopic biopsy and accessible nodal sampling can prevent unnecessary surgery and unsafe escalation of immunosuppression.