ABSTRACT
ABSTRACT Trabecular bone score (TBS) is an indirect and noninvasive measure of bone quality. A low TBS indicates degraded bone microarchitecture, predicts osteoporotic fracture, and is partially independent of clinical risk factors and bone mineral density (BMD). There is substantial evidence supporting the use of TBS to assess vertebral, hip, and major osteoporotic fracture risk in postmenopausal women, as well as to assess hip and major osteoporotic fracture risk in men aged > 50 years. TBS complements BMD information and can be used to adjust the FRAX (Fracture Risk Assessment) score to improve risk stratification. While TBS should not be used to monitor antiresorptive therapy, it may be potentially useful for monitoring anabolic therapy. There is also a growing body of evidence indicating that TBS is particularly useful as an adjunct to BMD for fracture risk assessment in conditions associated with increased fracture risk, such as type-2 diabetes, chronic corticosteroid excess, and other conditions wherein BMD readings are often misleading. The interference of abdominal soft tissue thickness (STT) on TBS should also be considered when interpreting these findings because image noise can impact TBS evaluation. A new TBS software version based on an algorithm that accounts for STT rather than BMI seems to correct this technical limitation and is under development. In this paper, we review the current state of TBS, its technical aspects, and its evolving role in the assessment and management of several clinical conditions.
ABSTRACT
A esclerose múltipla (EM) é uma doença crônica e progressiva que se caracteriza por surtos de desmielinização que podem atingir qualquer topografia do cérebro, medula espinhal e nervo óptico. Sendo o diabetes insípido (DI) central causado, principalmente, em virtude de danos do sistema nervoso central (tais como trauma, cirurgia, tumor, infecção, sarcoidose), a EM está inclusa entre suas possíveis etiologias. Entretanto, a ocorrência dessa associação não é comumente descrita. A suspeita clínica deve ser feita na presença de poliúria e polidipsia ou hipernatremia refratária (em pacientes privados do acesso à água) durante a evolução da EM. Descreveremos um caso em que essa associação ocorreu e, após o início da terapêutica com desmopressina, a paciente reverteu o quadro clínico.
Multiple Sclerosis (ME) is a chronic progressive disease characterized by relapses of demyelination that can occur anywhere in the brain stem, spinal cord and optic nerve. Since central diabetes insipidus (DI) is mainly caused by central nervous system damage (such as trauma, surgery, tumor, infection, sarcoidosis), ME is included among its possible etiologies. However, this association is not commonly described. The clinical suspicion must be made in the presence of polyuria and polydipsia or refractory hypernatremia (in patients without free access to water) during the evolution of ME. We will describe a clinical report in which this association occurred and, after the beginning of desmopressin therapy, the clinical findings were reverted.