The Schwannoma is a benign growth of the nerve sheath cells most commonly seen in the vestibulocochlear nerve. Its prevalence in the adrenal gland is 1-3%. Here we discuss a case that presented as an incidentaloma of the right adrenal gland in a young male patient who had vague abdominal symptoms and a normal hormonal profile. He underwent an excisional biopsy of the right adrenal gland due to the large size of the lesion (more than 4cm). The histopathology report helped to establish the diagnosis of Schwannoma. Incidentaloma is defined as a lesion of the adrenal gland encountered on any radiological investigation carried out for symptoms that are not associated with adrenal pathologies. After discovering such lesions, it is imperative to perform radiological and hormonal investigations in an organised manner to plan further management of such cases. Keywords: Schwannoma, Adrenal Incidentaloma, Adrenocortical Adenoma, Adrenocortical Carcinoma, Adrenalectomy.
Figure 1. (A) Trichrome stain showing markedly active chronic hepatitis consistent with cirrhosis. (B) Immunohistochemical stains demonstrate patchy staining with HBV surface antigen but (C) negative for HBV core antigen.
Figure 1. a) Ductal polypoid mass near common hepatic duct identified via endoscopic retrograde cholangiopancreatography with cholangioscopy. b) Intrahepatic biliary ductal dilatation seen on magnetic resonance cholangiopancreatography. c) Occlusion cholangiogram during endoscopic retrograde cholangiopancreatography showing a Bismuth Type IV common bile duct stricture. d) Occlusion cholangiogram during endoscopic retrograde cholangiopancreatography showing resolution of the common bile duct stricture after steroid treatment. e) Biliary stricture biopsies showing fragments of bile duct mucosa with acute and chronic inflammation with marked eosinophilia. f) Ductal mass/biliary stricture biopsy demonstrating inflammation and eosinophilia on Hematoxylin-eosin stain.
Introduction: Pancreatic adenocarcinoma, though a relatively uncommon malignancy, is one of the leading causes of cancer mortality. Rarely it metastasizes to the large bowel to present as intestinal obstruction, complicating its diagnosis. Herein we report a case of pancreatic adenocarcinoma presenting as intestinal obstruction due to sigmoid metastasis in a female patient. Case Description/Methods: A 60-year-old female with a past medical history of diabetes presented with constipation for 2 weeks and obstipation for 1 day associated with left lower quadrant abdominal pain. On admission, vital signs were stable and physical examination revealed normal bowel sounds and mild tenderness in the left lower quadrant. CT abdomen revealed an obstructing sigmoid tumor with concerning pancreatic and liver lesions. Subsequently, the patient underwent exploratory laparotomy with en bloc sigmoid colectomy with primary colorectal anastomosis. Pathology report revealed poorly differentiated adenocarcinoma involving the colonic muscularis propria, pericolonic adipose tissue, serosa, and involvement of 5 out of 14 lymph nodes. Since immunohistochemical markers were more consistent with metastatic disease from a pancreatobiliary primary rather than a colorectal primary, an EUS/FNA of the pancreatic lesion was performed, revealing pancreatic adenocarcinoma and confirming the pancreas as the site of primary malignancy. MRI abdomen further elucidated an infiltrative mass at the body and tail of the pancreas with adjacent vessel encasement. Due to the involvement of the celiac axis exceeding 180 degrees, the tumor was deemed unresectable, and patient was started on FOLFIRINOX chemotherapy (Figure). Discussion: Pancreatic adenocarcinoma (PAC) is a rare but ominous diagnosis with less than 20% of patients presenting with an operable tumor and a 5-year survival approaching 5% [3]. PAC rarely presents as large bowel obstruction with 7 cases reported so far [4]. It can therefore be misdiagnosed as primary colorectal cancer. Knowing the true diagnosis beforehand in such a case can guide management, as palliative chemotherapy regimens, instead of local resection of colorectal disease, would be initiated if the pancreatic primary were first identified [5]. In our case, resection of the sigmoid mass was done to relieve symptoms of acute intestinal obstruction. Since patients with PAC are diagnosed after the disease has spread, palliative chemotherapy remains one of the few viable options for treatment.[1950] Figure 1. Focal transmural thickening of the sigmoid colon wall with associated luminal narrowing (apple core lesion).
Introduction: Celiac disease (CD) is a small bowel autoimmune enteropathy mediated by antibodies against dietary gluten. We present a case of a patient with multiple sclerosis with persistently positive IgA antibodies against deamidated gliadin peptide (DGP) who was ultimately demonstrated not to have CD after decades of gluten avoidance. Case Description/Methods: A 64-year-old male with a history of multiple sclerosis (MS) and a family history of celiac disease in his mother presented to clinic to clarify his CD diagnosis. On prior testing he had positive DGP IgA (39 U) and weakly positive tissue transglutaminase (tTG) IgG serologies (8 U/mL, upper limit of normal 5 U/mL). However, prior esophagogastroduodenoscopy (EGD) was reportedly unremarkable. Based on serologies, he had been told he had CD and followed a gluten-free diet for years. On presentation, he denied bloating, diarrhea, abdominal pain, or weight changes. Labs were notable for an elevated DGP IgA level of 38 U with normal DGP IgG, tTG IgA, and tTG IgG serologies. On EGD while on a gluten free diet, the duodenum appeared normal, and pathology showed normal duodenal mucosa without villous atrophy (VA). Studies were repeated after several months of dietary gluten reintroduction. DGP IgA remained persistently elevated at 37 U, DGP IgG and tTG IgA remained within normal limits, and tTG IgG was borderline at 6 U/mL, of questionable significance. Genotyping was positive for HLA-DQ8 but negative for HLA-DQ2. Repeat EGD after gluten reintroduction demonstrated a normal-appearing duodenum without evidence of VA on pathology. The patient was informed that he did not have celiac disease. Discussion: Serologies in CD can be impacted by autoimmune disease. This patient had MS-related immunogenicity to DGP in the absence of CD. Several studies have noted that patients with MS without CD often have higher titers of DGP IgA antibodies, which may be due to antibody cross reactivity or even increased gut permeability to DGP. When serology is discordant, as in this case, duodenal biopsy should be performed, ideally after a gluten challenge. If repeat biopsy and tTG IgA serologies remain negative after gluten challenge, CD is highly unlikely. However, these patients should be closely followed for development of symptoms of CD, as latent CD is also possible.
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