RESUMO

Chronic obstructive pulmonary disease (COPD) is associated with osteoporosis and fragility fractures. The objectives of this study were to assess static and dynamic indices of cancellous and cortical bone structure in postmenopausal women with COPD. Twenty women with COPD who had not received chronic oral glucocorticoids underwent bone biopsies after double tetracycline labeling. Biopsies were analyzed by histomorphometry and µCT and compared with age-matched controls. Distribution of the patients according to the Global Initiative for Chronic Obstructive Lung Disease (GOLD) was: Type I (15%), Type II (40%), Type III (30%), and Type IV (15%). Mean (±SD) cancellous bone volume (15.20 ± 5.91 versus 21.34 ± 5.53%, p = .01), trabecular number (1.31 ± 0.26 versus 1.77 ± 0.51/mm, p = .003), and trabecular thickness (141 ± 23 versus 174 ± 36 µm, p = .006) were lower in patients than in controls. Connectivity density was lower in COPD (5.56 ± 2.78 versus 7.94 ± 3.08/mm, p = .04), and correlated negatively with smoking (r = -0.67; p = .0005). Trabecular separation (785 ± 183 versus 614 ± 36 µm, p = .01) and cortical porosity (4.11 ± 1.02 versus 2.32 ± 0.94 voids/mm(2); p < .0001) were higher in COPD while cortical width (458 ± 214 versus 762 ± 240 µm; p < .0001) was lower. Dynamic parameters showed significantly lower mineral apposition rate in COPD (0.56 ± 0.16 versus 0.66 ± 0.12 µm/day; p = .01). Patients with more severe disease, GOLD III and IV, presented lower bone formation rate than GOLD I and II (0.028 ± 0.009 versus 0.016+ 0.011 µm(3)/µm(2)/day; p = 04). This is the first evaluation of bone microstructure and remodeling in COPD. The skeletal abnormalities seen in cancellous and cortical bone provide an explanation for the high prevalence of vertebral fractures in this disease.

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RESUMO

UNLABELLED: A cross sectional study was made on 60 patients (9.9 +/- 1.8 yr-old) with congenital hypothyroidism (CH) (group A): 40 girls (23 prepubertal) and 20 boys (18 prepubertal). Control group (group B) was constituted of 28 healthy children (10.4 +/- 2.1 yr-old): 18 girls (8 prepubertal) and 10 boys (9 prepubertal). AIMS: To evaluate bone mineral density (BMD) and content (BMC) and to correlate them with chronological and bone age (BA), sex, sexual maturation, l-T4 dose, TSH, TT4, FT4, and CH etiology. BA, total body BMD, and BMC (DXA) were obtained of both groups. TSH, TT4, and FT4 were measured in patients only. BMD was lower in group A (0.795 +/- 0.075 g/cm(2) vs. 0.832 +/- 0.092; p = 0.04) and higher in pubertal than in prepubertal girls (p = 0.004). There was no significant difference between BMD and BMC related to sex and CH etiology. Our data demonstrated that BMD was significantly lower in children with CH, different from what has been published in the literature.

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Realizou-se estudo transversal com 60 pacientes (9,9 ± 1,8 anos) com hipotireoidismo congênito (HC) (grupo A): 40 meninas (23 pré-púberes) e 20 meninos (18 pré-púberes), com grupo controle (grupo B) constituído por 28 indivíduos (10,4 ± 2,1 anos): 18 meninas (8 pré-púberes) e 10 meninos (9 pré-púberes). OBJETIVOS: Avaliar a densidade (DMO) e o conteúdo mineral ósseo (CMO) e correlacioná-los com idade cronológica e óssea (IO), sexo, maturação sexual, dose de l-T4, TSH, TT4, FT4, e etiologia do HC. IO, DMO e CMO de corpo total (DXA) foram obtidos dos 2 grupos; TSH, TT4 e FT4, apenas dos pacientes. DMO foi menor no grupo A (0,795 ± 0,075 g/cm² vs. 0,832 ± 0,092; p = 0,04) e maior nas meninas púberes do que nas pré-púberes (p = 0,004). Não houve diferença significativa de DMO e CMO quanto ao sexo e etiologia do HC. Nosso estudo mostra que a DMO foi significativamente menor no grupo com HC, diferente dos dados da literatura.

A cross sectional study was made on 60 patients (9.9 ± 1.8 yr-old) with congenital hypothyroidism (CH) (group A): 40 girls (23 prepubertal) and 20 boys (18 prepubertal). Control group (group B) was constituted of 28 healthy children (10.4 ± 2.1 yr-old): 18 girls (8 prepubertal) and 10 boys (9 prepubertal). AIMS: To evaluate bone mineral density (BMD) and content (BMC) and to correlate them with chronological and bone age (BA), sex, sexual maturation, l-T4 dose, TSH, TT4, FT4, and CH etiology. BA, total body BMD, and BMC (DXA) were obtained of both groups. TSH, TT4, and FT4 were measured in patients only. BMD was lower in group A (0.795 ± 0.075 g/cm² vs. 0.832 ± 0.092; p = 0.04) and higher in pubertal than in prepubertal girls (p = 0.004). There was no significant difference between BMD and BMC related to sex and CH etiology. Our data demonstrated that BMD was significantly lower in children with CH, different from what has been published in the literature.

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RESUMO

We conducted a chart review of premenopausal women with low bone mineral density referred to the Metabolic Bone Clinic of Federal University of Paraná, to determine the outline of these patients regarding their risk factors and secondary causes of osteoporosis. Thirty-four women (19-48 years old) were evaluated. Twenty nine (85.3%) patients presented a low bone mineral density (BMD) in lumbar spine, 8 (23.5%) had Z-score < -2.5 and 21 (61.8%) had Z-score between -1.0 and -2.5. Twenty patients (58.8%) had a low bone mass in total femur, 2 (6.2%) with Z-score < -2.5 and 18 (56.2%) with Z-score between -1.0 and -2.5. A secondary cause could be identified in 26 patients (76.5%). This study shows that DMO is important in premenopausal women with risk factors of low BMD because it leads to the best treatment option and follow-up.

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The principal function of the parathyroid hormone (PTH) is maintenance of calcium plasmatic levels, withdrawing the calcium from bone tissue, reabsorbing it from the glomerular filtrate, and indirectly increasing its intestinal absorption by stimulating active vitamin D (calcitriol) production. Additionally, the PTH prompts an increase in urinary excretion of phosphorus and bicarbonate, seeking a larger quantity of free calcium available in circulation. Two mechanisms may alter its function, limiting its control on calcium: insufficient PTH production by the parathyroids (hypoparathyroidism), or a resistance against its action in target tissues (pseudohypoparathyroidism). In both cases, there are significantly reduced levels of plasmatic calcium associated with hyperphosphatemia. Clinical cases are characterized by nervous hyperexcitability, with paresthesia, cramps, tetany, hyperreflexia, convulsions, and tetanic crisis. Abnormalities such as cataracts and basal ganglia calcification are also typical of these diseases. Treatment consists of oral calcium supplementation associated with increased doses of vitamin D derivatives.

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Selecionamos mulheres pré-menopausadas com redução da DMO encaminhadas ao ambulatório de Metabolismo Osseo do Hospital de Clínicas da UFPR, com o objetivo de definirmos o perfil destas pacientes em relação aos fatores de risco e prováveis causas secundárias de osteoporose. Trinta e quatro mulheres foram estudadas (19­48 anos). Em 29 pacientes (85,3 por cento) a coluna lombar estava acometida, 8 (23,5 por cento) apresentaram Z-score < -2,5 e 21 (61,8 por cento) Z-score entre -1,0 e -2,5. Vinte pacientes (58,8 por cento) apresentaram redução da DMO em fêmur, 2 (6,2 por cento) com Z-score < -2,5 e 18 (56,2 por cento) com Z-score entre -1,0 e -2,5. Causa secundária foi identificada em 26 pacientes (76,5 por cento). Este estudo demonstra que a realização de densitometria óssea é importante em mulheres na pré-menopausa com fatores de risco para redução da massa óssea, uma vez que permite o início precoce do tratamento e a prevenção das complicações relacionadas.

We conducted a chart review of premenopausal women with low bone mineral density referred to the Metabolic Bone Clinic of Federal University of Paraná, to determine the outline of these patients regarding their risk factors and secondary causes of osteoporosis. Thirty-four women (19­48 years old) were evaluated. Twenty nine (85.3 percent) patients presented a low bone mineral density (BMD) in lumbar spine, 8 (23.5 percent) had Z-score < -2.5 and 21 (61.8 percent) had Z-score between -1.0 and -2.5. Twenty patients (58.8 percent) had a low bone mass in total femur, 2 (6.2 percent) with Z-score < -2.5 and 18 (56.2 percent) with Z-score between -1.0 and -2.5. A secondary cause could be identified in 26 patients (76.5 percent). This study shows that DMO is important in premenopausal women with risk factors of low BMD because it leads to the best treatment option and follow-up.

Assuntos

RESUMO

The principal function of the parathyroid hormone (PTH) is maintenance of calcium plasmatic levels, withdrawing the calcium from bone tissue, reabsorbing it from the glomerular filtrate, and indirectly increasing its intestinal absorption by stimulating active vitamin D (calcitriol) production. Additionally, the PTH prompts an increase in urinary excretion of phosphorus and bicarbonate, seeking a larger quantity of free calcium available in circulation. Two mechanisms may alter its function, limiting its control on calcium: insufficient PTH production by the parathyroids (hypoparathyroidism), or a resistance against its action in target tissues (pseudohypoparathyroidism). In both cases, there are significantly reduced levels of plasmatic calcium associated with hyperphosphatemia. Clinical cases are characterized by nervous hyperexcitability, with paresthesia, cramps, tetany, hyperreflexia, convulsions, and tetanic crisis. Abnormalities such as cataracts and basal ganglia calcification are also typical of these diseases. Treatment consists of oral calcium supplementation associated with increased doses of vitamin D derivatives.

A principal função do paratormônio (PTH) é a manutenção dos níveis plasmáticos de cálcio, retirando-o do tecido ósseo, reabsorvendo-o do filtrado glomerular e, indiretamente, aumentando sua absorção intestinal através do estímulo para a produção de vitamina D ativa (calcitriol). Além disso, o PTH promove um aumento na excreção urinária de fósforo e bicarbonato, objetivando uma maior quantidade de cálcio livre disponível na circulação. Dois mecanismos podem alterar sua função, limitando seu controle sobre o cálcio: produção insuficiente de PTH pelas paratiróides (hipoparatiroidismo), ou uma resistência à sua ação nos órgãos-alvo (pseudohipoparatiroidismo). Em ambos os casos, ocorre uma redução significativa dos níveis plasmáticos de cálcio em associação com hiperfosfatemia. Manifestações clínicas características são: hiperexcitabilidade nervosa, com parestesia, cãimbras, tetania, hiperreflexia, convulsões e crise tetânica. Catarata e calcificação dos gânglios basais são anormalidades típicas dessas doenças. O tratamento consiste da suplementação oral de cálcio, associada com doses elevadas de derivados da vitamina D.

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