Peppered and rare - gastric and duodenal pseudomelanosis: a case series

Upper Gastrointestinal [GI] pseudomelanosis is an uncommon entity characterized by endoscopic visualization of speckled dark mucosal pigmentation. While described in the rectum and colon, 'melanosis' or more aptly 'pseudomelanosis' is rare in the duodenum and exceedingly rare in the stomach. Five cases of pseudomelanosis were encountered at our department. Four females and one male were diagnosed, with a mean age of 70 years. All patients exhibited duodenal pseudomelanosis, with one demonstrating gastric antral pseudomelanosis as well. Common features among these patients included iron deficiency anemia, hypertension, chronic kidney disease, hydralazine use and iron supplementation. Biopsy specimens stained at least partially positive for iron and stains for calcium and copper were negative. Histochemical analysis revealed the pigment of pseudomelanosis to be mainly iron sulfide, exhibiting unpredictable staining patterns, hypothesized to be secondary to varying sulfur content and iron oxidation. It is visualized as dark deposits in macrophages at the tips of the duodenal villi. Upper GI pseudomelanosis remains a poorly understood finding, weakly associated with chronic kidney disease, diabetes, hypertension, iron supplements and anti-hypertensive medications. While the pathogenesis, clinical and prognostic significance remains unclear, it is thus far considered a benign condition

Myocardial ischaemia and reperfusion injury: reactive oxygen species and the role of neutrophil

A growing body of evidence suggests that oxygen radicals can mediate myocardial tissue injury during ischaemia and, in particular, during reperfusion. This review focuses on the role of neutrophil as a mediator of myocardial damage. Upon reperfusion, neutrophils accumulate and produce an inflammatory response in the myocardium that is responsible, in part, for the extension of tissue injury associated with reperfusion. It has shown that the inhibition of neutrophil accumulation and adhesion is associated with decreased infarct size. This strongly suggests that myocardial cells at risk region undergo irreversible changes upon reperfusion and accumulation of neutrophils. Several pharmacological agents [ibuprofen, allopurinol, prostacyclin, and prostaglandin E analogues] protect the myocardium from reperfusion injury. In addition, the mechanisms by which these agents act and directions of research that may lead to therapeutically useful approaches are also discussed in this review