Update on trabecular bone score.

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.

Update on trabecular bone score

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.

Effect of soft tissue noise on trabecular bone score in postmenopausal women with diabetes: A cross sectional study.

BACKGROUND: Type 2 diabetes (T2D) is associated with increased fracture risk, despite similar or greater BMD compared to nondiabetics. TBS predicts fracture risk in T2D and nondiabetics. However, increased abdominal thickness, a common feature in T2D, may reduce TBS values. AIM: To study the relationship among glycemic status, BMD and TBS, considering abdominal soft tissue thickness (STT) interference. METHODS: Cross-sectional analysis of 493 women ≥65 years, with simultaneous DXA scans and HbA1c measures. STT and TBS (iNsight Software, v3.0) were derived from lumbar spine (LS) scans. Subjects were divided according to HbA1c levels: 1 (≥6.5%; n = 116), 2 (5.7-6.4%; n = 217) and 3 (≤5.6%; n = 160). Group 1 was further divided based on HbA1c and/or disease duration: 1a (HbA1c ≥ 7.5%; n = 42), 1b (HbA1c ≥ 6.5% and disease duration ≥5 years; n = 63) and 1c (HbA1c ≥ 7.5% and disease duration ≥5 years; n = 30). FINDINGS: For the entire cohort, mean age, TBS, BMI and STT were 71.8 ± 6.0 years, 1.299 ± 0.101, 26.9 ± 4.1 kg/m2, and 21.4 ± 2.9 cm, respectively. LS-BMD was similar among groups. BMD in hip sites and STT were higher in group 1. TBS was lower in patients with higher HbA1c (P = 0.020), with a mean TBS in groups 1, 2, and 3 of 1.280, 1.299 and 1.314, respectively. This difference remained after adjusting for age, LS-BMD and BMI (P = 0.010). After replacing BMI with STT, TBS differences were no longer significant (P = 0.270). The same was observed when subgroups 1a and 1b were compared to group 3. However, for subgroup 1c, TBS remained lower compared to group 3, even after adjusting for age, LS-BMD and STT, with a borderline P-value (1.275 vs. 1.308; P = 0.047). CONCLUSION: Higher HbA1c levels were associated with greater BMD in hip sites, higher abdominal STT and lower TBS values. However, after including the STT in the adjustment, TBS differences among groups disappeared, except in women with higher HbA1c levels and longer disease duration.

[Diabetes insipidus in a pacient with multiple sclerosis]. / Diabetes insípido em paciente com esclerose múltipla.

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.

Diabetes insípido em paciente com esclerose múltipla / Diabetes insipidus in a pacient with multiple sclerosis

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.