The vanishing bile duct syndrome (VBDS) is a condition secondary to inciting triggers resulting in destruction and eventual disappearance of intrahepatic bile ducts leading to cholestasis. The overall outcome varies and often depends on the nature of the precipitating cause. VBDS has been found to be associated with adverse drug reactions, infectious diseases, autoimmune diseases, ischemia, and humoral factors associated with malignancies and is often irreversible. The objective of this clinical case report is to highlight the need for a broad differential to include VBDS in similar scenarios to aid rapid diagnosis and management. We hope this could lead to a more favourable outcome for patients presenting with VBDS such as the one described in this case report with concurrent non-Hodgkin's lymphoma and infection with hepatitis E virus. To the best of our knowledge, this is the first ever reported case of VBDS associated with non-Hodgkin's lymphoma and hepatitis E virus infection.
A 64-year-old man was admitted with fever, weight loss, fatigue and night sweats. He was known to have rheumatoid arthritis and had been taking methotrexate for 1 year. He had worked in Saudi Arabia until 1994 and had been living in Spain for 6 months every year. Clinical examination showed an enlarged spleen. Routine investigations showed pancytopaenia. Serial blood cultures were negative. CT scan confirmed splenomegaly and was otherwise unremarkable. Bone marrow biopsy revealed Leishmania amastigote consistent with a diagnosis of visceral leishmaniasis. After discussing with the hospital for tropical diseases (HTD), he was started on liposomal amphotericin B. Following two infusions of amphotericin B, he started improving as his fever, night sweats and weakness had settled. He was then discharged and followed up in HTD clinic 4 weeks later where he was found to be consistently improving.
A Caucasian man in early 80s was seen in Gastroenterology Clinic, following, referral from the Endocrinology Clinic for concerns for CT Abdomen requested for tiredness and weight loss of three kilograms. The patient also had microcytic picture with low MCV and Ferritin and hypomagnesemia. The CT suggested gross circumferential thickening of the wall of stomach with advice for invasive investigations to further characterise the CT findings. The Endoscopy suggested grossly enlarged rugae in the stomach, and enlarged gastric polyps. Patient was assured no new sinister abnormality.
Treatment challenges to consider were to stop acid suppression by prescribing Proton Pump Inhibitors (PPIs) which would lead to stomach ulcers, or to continue with PPIs with sequalae of worsening of hypertrophic gastric folds, enlarged gastric polyps and hypomagnesemia. It would be necessary to consider risk versus benefits in either situation to determine an appropriate treatment plan in the long term.
With background of Zollinger-Ellison Syndrome and MEN1 with heterozygous mutation with gastrinoma of the duodenum, and frailty he was advised to continue with Proton Pump Inhibitors with twice weekly correction of Magnesium infusions, and Iron tablets following Multi-disciplinary meeting.
doi: https://doi.org/10.12669/pjms.37.4.3984
How to cite this:Zafar M, Muhammad T, Najam-us-Saher, Toqeer M. Hypertrophic Gastric folds with Hypomagnesemia, linking the dots. Pak J Med Sci. 2021;37(4):1237-1240. doi: https://doi.org/10.12669/pjms.37.4.3984
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