Adenomatous Polyposis in a Young Jamaican Male of African Descent

Abstract

inhibitor and repeat haematinics (Hb plus), his prior haemoglobin of 3.8 g/dL failed to improve. His past medical history included three years of chronic headaches. At that time, he had also complained of anal pruritus and investigations revealed iron deficiency anaemia and giardiasis. Haemoglobin (Hb) was 3.3 g/dL. He received metronidazole and oral iron therapy and after a few months, his subsequent haemoglobin was 8 g/dL. He subsequently defaulted from follow-up.He had no chronic illnesses, no known significant family history and was a non-smoker. On examination, he was asthenic and pale. General examination revealed no lymphadenopathy. Cardiorespiratory examination was normal. On abdominal examination, a liver span of 12 cm was noted. Digital rectal examination was negative for any masses and blood. Neurological examination was normal. He was assessed and admitted for inpatient evaluation. During this admission, investigations revealed:C Hb 3.8 (14-17) g/dL, mean corpuscular volume (MCV) 63 (80-95) fl, white blood cells 15.1 (4-10) x 10 9 /L, platelets 1618 (150-400) x 10 9 /L, absolute reticulocyte count 19.4 (23-90) x 10 9 /L C Blood film showed hypochromasia, microcytosis, fragmented red blood cells, giant platelets and thrombocytosis Adenomatous Polyposis in a Young Jamaican Male of African Descent

Clinicopathological Characteristics and Mutational Landscape of APC, HOXB13, and KRAS among Rwandan Patients with Colorectal Cancer

“…Germline mutations in APC are also key factors in familial adenomatous polyposis syndrome. This syndrome is quasi-nonexistent in African populations, with only a few cases having ever been reported in the literature [54][55][56][57][58][59][60][61][62][63]. Mutations in the APC gene in CRC have been reported in more than 50% of cases [44].…”