Osteoporosis
Osteoporosis is defined by the National Institutes of Health as ‘‘a skeletal disorder characterized by compromised bone strength predisposing a person to an increased risk of fracture.’’ Low estrogen levels and poor nutrition, especially low calcium intake, can lead to osteoporosis, the third aspect of the triad. This condition can ruin a female athletes career because it may lead to stress fractures and other injuries.Patients with RED-S get osteoporosis due to hypoestrogenemia, or low estrogen levels. With estrogen deficiency, the osteoclasts live longer and are therefore able to resorb more bone. In response to the increased bone resorption, there is increased bone formation and a high-turnover state develops which leads to bone loss and perforation of the trabecular plates. As osteoclasts break down bone, patients see a loss of bone mineral density. Low bone mineral density renders bones more brittle and hence susceptible to fracture. Because athletes are active and their bones must endure mechanical stress, the likelihood of experiencing bone fracture is particularly high.Additionally, because those suffering with RED-S are also restricting their diet, they may also not be consuming sufficient amounts vitamins and minerals which contribute to bone density; not getting enough calcium or vitamin D further exacerbates the problem of weak bones.Bone mass is now thought to peak between the ages of 18-25. Thus, behaviors which result in low bone density in youth could be detrimental to an athlete’s bone health throughout her lifetime.In addition, ovulation is the primary way that females create the hormone progesterone.
Typically, patients diagnosed with LG (medium age 58 years) have been asymptomatic at presentation with their disease being detected during GI tract examinations done for other reasons. Three of twenty patients diagnosed with LG complained of pain or discomfort in the upper abdominal region. Symptomatic individuals with either disease generally have a long history of persistent or intermittent symptoms. Pathophysiology
NK cells normally occupy the GI tract where they contribute to innate immunity by becoming active in killing pathogen-infected and cancerous cells. The proliferating lymphocytes in NKCE and LG express CD56 and CD7 proteins on their cell surface membrane, CD3γ protein in their cytoplasm, and granzyme B, perforin, and T-cell intracellular antigen-1 cytotoxic proteins within their cytoplasmic granules. This pattern of protein expression identifies these cells as NK cells that, because of their expression of the cytotoxic granule-bound proteins, have been activated. However, the cause(s) for the activation of these cells as wells as for their rapid proliferation to produce NKCE and LG is unknown. To date, no evidence of NK cell clonality (i.e. cells developing from a single precursor) or for these cells to bear gene mutations or chromosome abnormalities have been reported in NKCE or LG. These findings help distinguish LB and NKCE from many lymphomas and support the conclusion that neither disease is malignant. The NK cells in LG and NKCE are not infected with the Epstein-Barr virus (EBV), as evidenced by their failure to express this viruss latency proteins and latency ncRNAs.