Pseudomelanosis Duodeni: Is It the Iron? A Case Series and Review of the Literature

Abstract

Purpose: Pseudomelanosis duodeni (PD) appears strikingly endoscopically as speckled black pigmentation of the duodenal mucosa due to pigment laden macrophages and is an exceedingly rare endoscopic finding. In two small retrospective studies at Rush and Yale Universities it was hypothesized that oral iron intake in combination with hypertension, diabetes, chronic kidney disease and gastrointestinal bleed, could increase the risk of developing PD. Herein, we report two cases of PD. Case 1: A 66-year-old male with a history of orthotopic heart transplant on immunosuppressive therapy, hypertension, chronic kidney disease, and anemia on oral iron therapy presented with diarrhea, melena, nausea and vomiting. Vital signs were stable and physical examination was unremarkable. Laboratory data: WBC 2.54/UL, Hgb:12.4 g/dl, and CMV PCR 1618 copies/100 ng. He was empirically treated for CMV gastroenteritis with gancicyclovir and discharged. However, readmitted two days later for persistent symptom and epigastric abdominal pain. WBC: 5.9/UL and Hgb:11.1 g/dl, creatinine 2.1 mg/dl, stool occult blood negative. Esophagogastroduodenoscopy demonstrated small punctate-pigmented lesions diffusely throughout the gastric antrum, duodenal bulb and second portion. Colonoscopy illustrated small punctate erythematous mucosa and healing ulcers. Biopsies showed active gastritis, CMV infection in stomach and colon, and focal hemosiderin laden macrophages in the antrum and duodenum consistent with PD. Case 2: An 85-year-old male with a history of myocardial infarction, gastric ulcers, hypertension, chronic kidney disease, diabetes and iron deficiency anemia on oral iron presented with burning epigastric pain and melena. Vital signs were stable and physical examination was significant for epigastric tenderness. Laboratory data: Hgb 9.8 g/dl (baseline of 12 g/dl), creatinine 1.36 mg/dl. Esophagogastroduodenoscopy discovered esophagitis dessicans, antral erosions, a pyloric fistula to the duodenal bulb, black pigmentation of the gastric antrum, duodenal bulb, second and third portion of the duodenum. Colonoscopy showed melanosis coli throughout. Capsule endoscopy illustrated pseudomelanosis of the proximal duodenum, as well as oozing angioectasia of the duodenum and jejunum. Discussion: We present two cases of PD. Interestingly, both patients had a history of oral iron intake, hypertension and chronic kidney disease, and in one case also diabetes mellitus and gastrointestinal bleed. Although it would be hard to prove this with anecdotal evidence, our results correlate with the findings in the prior studies that have shown this association. Prospective studies are needed to further understand the etiology and pathogenesis of PD.