Search

Primary urinary Bladder Adenocarcinoma (PBA) is an uncommon neoplasm and can cause diagnostic difficulties due to histologic similarities with adenocarcinomas of adjacent structures like Gastrointestinal Tract (GIT) and prostate, since involvement of the bladder by metastasis or direct spread can occur. Seven cases of bladder adenocarcinomas were diagnosed during a period of four years in a tertiary care hospital. Patient's age ranged from 26-78 years with a male predilection. Three cases were signet ring type adenocarcinomas, two cases were subtyped as enteric variant, one as mucinous variant and one as adenocarcinoma Not Otherwise Specified (NOS) variant. One case showed urachal involvement. Common site of involvement was the base and posterior wall of the bladder. Three cases had prior history of GIT malignancy. No morphologic difference was identified to differentiate primary from secondary adenocarcinomas. Bladder adenocarcinoma is rare tumours. Primary and secondary adenocarcinomas cannot be distinguished from each other on morphologic grounds. Ancillary studies may have limited role in distinguishing between the two. Hence, clinical correlation has a major role in their evaluation. [ABSTRACT FROM AUTHOR]

Glucose-6-phosphate dehydrogenase (G6PD) deficiency is an X-linked disease responsible for moderate to severe hemolytic anaemia. Despite being the most common erythrocyte enzyme disorder, it is often overlooked in the regular diagnostic parlance. A 40-year-old male patient admitted to the casualty with an acutely exacerbated diabetic ketoacidosis, showed features of hemolytic anaemia on peripheral smear examination. Crucially, the spherocytes and bite cells suggested a possibility of G6PD deficiency. This was substantiated by an increased reticulocyte count (6.8%) and a reduced quantitative G6PD enzyme assay (7.2%). There was no significant family or prior medical/ drug history. Interestingly, the hemolytic features were evidenced when blood glucose levels were returning to normal values. The insulin mediated NADPH loss may have resulted in an increased erythrocyte oxidant sensitivity and a loss of sulfhydryl group availability; causing hemolysis to manifest. G6PD deficiency is conventionally affiliated with drug induced oxidative stress. But an association with a diabetes mellitus is seldom reported. This case is being presented as it highlights the lesser known complication of diabetic crisis such as hemolysis secondary to a G6PD deficiency. [ABSTRACT FROM AUTHOR]