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Is fibromyalgia part of the climacteric syndrome?
Juan Enrique Blümel1, Santiago Palacios, Deborah Legorreta
1Departamento de Medicina Sur, Universidad de Chile, Santiago de Chile, Chile. juan.blumel@redsalud.gov.cl
Fibromyalgia syndrome (FMS) is a disorder usually affecting middle aged women, who complain of diffuse musculoskeletal aches, pains or stiffness associated with tiredness, anxiety and poor sleep. Neurotransmission disorders linked both to pain perception as well as mood, sleep and cognition modulation are involved in FMS etiopathogenesys. Treatments that may be effective to decrease pain and fatigue include tricyclic antidepressants, dual reuptake inhibitors of serotonin/noradrenalin and pregabalin. The climacteric syndrome is a set of symptoms caused by the decline of ovarian hormone levels, which alters brain neurotransmission and provokes musculoskeletal pains, mood disorders, poor sleep quality and hot flushes. The hormone therapy reverses those symptoms and its risks are marginal if women's own hormones are used through transdermal route. Some antidepressants may be useful for patients with climacteric symptoms. We have found it surprising the epidemiological, etiopathogenic, symptomatic and therapeutic similarity between FMS and climacteric that could lead us to hypothesize that FMS is a part of the climacteric syndrome. However, the existence of FMS non-climacteric patients points out that hormone deficit is not the only physiopathological mechanism involved in this syndrome's etiopathogenesys. Nevertheless, it is likely that hormone disorders are involved in the symptoms genesis of most middle aged women with FMS. Keeping this in mind, we see the point in considering the use of HT in climacteric patients with FMS. Studies assessing the FMS clinical response to HT in a prospective manner and with the current diagnose criteria are still required.
Fibromyalgia syndrome (FMS) is a disorder usually affecting middle aged women, who complain of diffuse musculoskeletal aches, pains or stiffness associated with tiredness, anxiety and poor sleep. Neurotransmission disorders linked both to pain perception as well as mood, sleep and cognition modulation are involved in FMS etiopathogenesys. Treatments that may be effective to decrease pain and fatigue include tricyclic antidepressants, dual reuptake inhibitors of serotonin/noradrenalin and pregabalin. The climacteric syndrome is a set of symptoms caused by the decline of ovarian hormone levels, which alters brain neurotransmission and provokes musculoskeletal pains, mood disorders, poor sleep quality and hot flushes. The hormone therapy reverses those symptoms and its risks are marginal if women's own hormones are used through transdermal route. Some antidepressants may be useful for patients with climacteric symptoms. We have found it surprising the epidemiological, etiopathogenic, symptomatic and therapeutic similarity between FMS and climacteric that could lead us to hypothesize that FMS is a part of the climacteric syndrome. However, the existence of FMS non-climacteric patients points out that hormone deficit is not the only physiopathological mechanism involved in this syndrome's etiopathogenesys. Nevertheless, it is likely that hormone disorders are involved in the symptoms genesis of most middle aged women with FMS. Keeping this in mind, we see the point in considering the use of HT in climacteric patients with FMS. Studies assessing the FMS clinical response to HT in a prospective manner and with the current diagnose criteria are still required.
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