A Case-Study Report of an Indiscernible Adrenal Myelolipoma - Clinical and Histologic Features

Adrenal myelolipomas are rare, non-functional, benign tumor-like lesions of the adrenal gland. They are usually found to occur alone in one adrenal gland but not both and there may be a right sided predilection. Histological examination demonstrates variable amounts of mature adipocytes (with distended lipid vacuoles) similar to bone marrow and hematopoietic cells (including cells from myeloid, erythroid and megakaryocytic cell lines) [1,2]. The fatty component is often the predominant feature and therefore the most characteristic feature on imaging. The lesions can infrequently contain bone or show partial replacement by haemorrhage or fibrosis. Adrenal myelolipomas are usually indentified in adults, either incidentally or if complicated by haemorrhage [3]. There is no gender predilection. The tumor affects men and women equally and is most commonly found between the fifth and seventh decades of life with a mean age of 62 years. Adrenal myelolipomas can vary widely in size [4]. They are often smaller than 4cm in diameter, with the largest reported adrenal myelolipoma measuring 31x24.5x11.5cm and weighing 6kg. Most of them are small, asymptomatic and may be discovered incidentally when the region is imaged for other reasons. Larger ones (typically over 4cm in size) can present with an acute retroperitoneal haemorrhage and still others (especially when very large, causing pressure of surrounding organs or tissues) with vague mass related symptoms. Symptoms include pain in the abdomen or flank, blood in the urine, a palpable lump or high blood pressure. Some studies suggest surgical intervention if the tumor is symptomatic, growing or larger than 6cm. ultimately, the optimal treatment for myelolipoma depends on size and symptoms of the mass, and the patient’s needs [5]. Although the tumor itself is non-functioning there is a relatively high incidence (10%) of associated endocrine disorders such as the Cushing syndrome, the congenital adrenal hyperplasia (21-hydroxylase deficiency) and the Conn syndrome (primary Abstract