SEL is a condition that causes neural symptoms by the growth of mature adipose tissue without a capsule in the epidural space . The pathogenesis of SEL is not yet clear. Frogel et al.  classified SEL into the following four categories: (1) exogenous steroid use, 55.3%; (2) obesity only, 24.5%; (3) endocrinopathy or endogenous steroid group, 3.2%; and (4) non-obese idiopathic group, approximately 17%. Depending on these classified causes, the predominant site of SLE tends to be different. Exogenous steroid-induced SEL more often involves the thoracic spine, whereas idiopathic SEL more often involves the lumbar spine, i.e., LEL . LEL is more likely to occur in older men and our cases were also all males over the age of 62. Our patients included 3 with exogenous steroid use (Category 1) and 3 with overweight only (Category 4).
MRI is the most useful diagnostic imaging tool for both LEL and spinal lipoma. Both LEL and lipoma are exhibited as hyperintensity masses on T1- and T2-weighted imaging. Therefore, it can be difficult to distinguish between LEL and lipomas [18–20]. Although lipoma, unlike LEL, is a mass lesion enveloped by a capsule identification of the capsule may be sometimes difficult . Therefore, the terms lipoma and lipomatosis are sometimes applied ambiguously . On the other hand, epidural hematoma, tumor, and abscess typically show signal hyperintensity on T1-weighted imaging and intermediate signal intensity on T2-weighted imaging, making differentiation from SEL less difficult .
It has been reported that there are no morphological differences between normal and epidural adipocytes in LEL . However, there are few reports that have analyzed the size of epidural adipocytes in LEL [9, 28]. One case study showed adipocyte hypertrophy in an obese patient with idiopathic LEL . Fujita et al.  also reported that epidural adipocytes in obese patients with LEL were significantly larger than those in patients with lumbar spinal stenosis (LSS). The mechanism was thought to be adipocyte hypertrophy associated with obesity in LEL. In the present study, the size of the epidural adipocytes was smaller than that of subcutaneous adipocytes in the same patient; this result is contradictory to the previous report. However, only epidural adipocytes were examined in the previous report. Differences in the methods of analysis may have led to the different results.
Typically, the diameter of adipocytes in normal-weight adults is 70–90 µm, and adipocytes do not usually exceed 130 µm . If an adipocyte is assumed to be circular, the size should be approximately 3500–6500 µm2 in a normal-weight adult, and adipocytes are not larger than 13,200 µm2. In this study, the size of the subcutaneous adipocytes was found to be within the normal range. However, the size of the epidural adipocytes was significantly smaller than that of the subcutaneous adipocytes. This finding suggests that adipocytes in LEL are changed by exogenous and/or endogenous factors. One possible exogenous factor is the fact that epidural adipocytes are present in the spinal canal, which is an enclosed space. Barz et al.  reported that epidural pressure in patients with LSS increases substantially compared with individuals without stenosis. We have previously reported the detailed imaging findings and epidural pressure measurements in LEL . We showed that epidural pressure is higher in LEL than in LSS. Furthermore, epidural pressure is higher than the subarachnoid space pressure in patients with LEL. Therefore, adipocytes in LEL might decrease in size because of high epidural pressure due to the proliferation of adipocytes in the enclosed space. As another possibility, adipocytes might be newly produced in LEL. Additionally, chromosomal aberrations are an endogenous factor that might influence cellular morphology and function.
To the best of our knowledge, there are no reports on cytogenetic analysis in LEL. In this study, all patients showed solitary loss of the Y chromosome. In humans, the Y chromosome is one of two sex chromosomes found only in males. The Y chromosome is functionally composed of three regions: (1) male‑specific region of Y chromosome (MSY), (2) pseudoautosomal regions (PAR1 and PAR2), and (3) heterochromatin region on Yq. PAR is the lesion on Y and X chromosomes where homology remains, and heterochromatin region does not have a valid gene. The Y chromosome contains over 200 genes, of which at least 72 encode proteins. Some cells, especially those in elder men and smokers, lack a Y chromosome . It has been found that men with a high proportion of hematopoietic stem cells in the peripheral blood that loss of the Y chromosome have been found to be at increased risk of non-blood cancer. . Although the mechanism linking loss of the Y chromosome in peripheral blood and cancer mortality is not yet understood, these observations strongly suggest that the Y chromosome is involved in a wide variety of biological processes that have not yet been fully explored . LEL occurs in middle and older age and is most often seen in men [33, 34]. Loss of the Y chromosome might partially contribute to the pathological mechanism or expression of LEL, although this may be an effect rather than a cause. To explore the role of the Y chromosome in LEL further, cytogenetic analysis in women with LEL will also be necessary.
In lipomas, various chromosomal aberrations such as 12q13-15 (65% of all cases), loss of 13q (10%), 6p21-23 (5%), and others (20%) have been reported . With regard to the Y chromosome, only one case has been reported, i.e., t(Y;12) in a lipoma ; however, there are no reports of loss of the Y chromosome. Therefore, it is thought that there is no connection between lipomas and SEL based on cytogenetics. On the other hand, loss of the Y chromosome has been reported in various tumors, such as papillary renal cell carcinoma , urothelial bladder cancer , and hepatocellular carcinoma . In this study, the size of epidural adipocytes was significantly smaller than that of subcutaneous adipocytes. In other words, the number of epidural adipocytes might be higher than the number of subcutaneous adipocytes. Therefore, although a mechanism for the pathogenesis of Y chromosome has not been elucidated, the Y chromosome might play a role in the pathogenesis of LEL.
The present study has several limitations. First, all patients evaluated with LEL were men, because LEL is more common in men. We have cytogenetic results for one woman, but the data cannot be presented here as they pertain to only one case. Second, cytogenetic analysis was performed only with epidural lipomatous tissue, not with subcutaneous lipomatous tissue. Therefore, we cannot definitively determine whether the loss of the Y chromosome is specific to EF in LEL. Third, the cohort was relatively small. Future studies examining larger sample sizes are needed.