RESUMEN

The aim of this study was to evaluate the effect of denosumab (Dmab) on bone mineral density (BMD) and bone turnover markers after 1 year of treatment. Additionally, the effect of Dmab in bisphosphonate-naïve patients (BP-naïve) compared to patients previously treated with bisphosphonates (BP-prior) was analyzed. This retrospective study included 425 postmenopausal women treated with Dmab for 1 year in clinical practice conditions in specialized centers from Argentina. Participants were also divided according to previous bisphosphonate treatment into BP-naïve and BP-prior. A control group of patients treated with BP not switched to Dmab matched by sex, age, and body mass index was used. Data are expressed as mean ± SEM. After 1 year of treatment with Dmab the bone formation markers total alkaline phosphatase and osteocalcin were significantly decreased (23.36% and 43.97%, resp.), as was the bone resorption marker s-CTX (69.61%). Significant increases in BMD were observed at the lumbar spine, femoral neck, and total hip without differences between BP-naïve and BP-prior. A better BMD response was found in BP-prior group compared with BP treated patients not switched to Dmab. Conclusion. Dmab treatment increased BMD and decreased bone turnover markers in the whole group, with similar response in BP-naïve and BP-prior patients. A better BMD response in BP-prior patients versus BP treated patients not switched to Dmab was observed.

RESUMEN

The intravertebral vacuum cleft sign (VCS) is an uncommon radiological sign, characterized by a radiolucent zone in the vertebral body. It is composed of 95% nitrogen and small amounts of oxygen and carbon dioxide. Post-traumatic ischemic necrosis could be its physiopathological mechanism, along with other pathologies like osteoporosis, corticosteroid therapy, diabetes, arteriosclerosis, alcoholism, multiple myeloma, bone metastasis and osteomyelitis. The broad diagnosis is made by antero-posterior X-ray, but computed tomography scan (CT scan) and magnetic resonance imaging (MRI) may help with the differential diagnosis. The aims of this paper are, on one hand, to communicate the clinical case of a 73-year-old osteoporotic woman with traumatic vertebral fractures who developed this sign in her radiological survey. On the other hand, its secondary aims are to review the medical literature about this sign and to show the clinical and radiological evolution after a percutaneous vertebroplasty.

Asunto(s)

Gases/análisis , Osteoporosis Posmenopáusica/complicaciones , Fracturas de la Columna Vertebral/diagnóstico por imagen , Fracturas de la Columna Vertebral/etiología , Anciano , Densidad Ósea , Diagnóstico Diferencial , Femenino , Humanos , Vértebras Lumbares/diagnóstico por imagen , Imagen por Resonancia Magnética , Osteonecrosis/diagnóstico por imagen , Osteonecrosis/etiología , Osteoporosis Posmenopáusica/diagnóstico , Osteoporosis Posmenopáusica/diagnóstico por imagen , Fracturas de la Columna Vertebral/diagnóstico , Tomografía Computarizada por Rayos X

RESUMEN

Durante el embarazo y la lactancia la mujer debe formar y mantener el esqueleto del feto y del neonato, lo que demanda importantes adaptaciones hormonales y metabólicas. La absorción intestinal de calcio aumenta desde el inicio del embarazo siendo máxima en los últimos trimestres. Se produceuna hipercalciuria que desaparece al suspender la lactancia. El calcio de la leche proviene de la reducción ensu excreción urinaria y de un aumento de la resorción ósea. Las oncentraciones de 1,25 (OH)(2) D(3) se duplican desde el comienzo del embarazo manteniéndose elevadas hasta el parto, debido a un aumento de la actividad de la 1-alfa-hidroxilasa placentaria, normalizándose durante la lactancia. Los estrógenos, prolactina y lactógeno placentario, hormonas implicadas en el aumento de la absorción intestinal de calcio, aumentan conjuntamente.La parathormona (PTH) se mantiene en rango normal o bajo, por lo tanto sus acciones fisiológicas serían ejercidas por el péptido relacionado con la PTH (PTHrP), cuyos niveles aumentan tardíamente en el embarazo y permanecen elevados durante el parto y la lactancia. La calcitonina se eleva durante el embarazo, cae durante la lactancia, y se normaliza al finalizar la misma. El papel fisiológico del factor de necrosis tumoral, interleuquina 1, interleuquina 6 y osteoprotegerina todavía no han sido aclarados. Los cambios analizados favorecen,en casos excepcionales, el desarrollo de osteoporosis generalizada y regional. El objetivo de este trabajo es revisar la bibliografía publicada sobre la fisiopatología y clínica de estas entidades.

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During pregnancy and lactation women have to form and maintain fetus and newborn skeleton. These processes require maternal hormonal and metabolic adjustments. During the first weeks of pregnancy, calcium intestinal absorption rise and reach a maximum in the last trimester. Hypercalciuria can be detected until lactation is stopped. During lactation, calcium that is present in maternal milk, results from lowering maternal calcium excretion and increasing bone resorption. Plasma 1,25 (OH)(2) D(3) levels increase two-fold early in pregnancy due to high placental 1-alpha-hydroxilase activity, remain high until delivery and decline to normal values during lactation. Estrogen, prolactin and placental lactogen, which are involved in calcium absorption, increase at the same time. Normal or even low levels of parathyroid hormone (PTH) can be detected during pregnancy. This suggests that their physiological actions could be mimicked by the parathyroid- related-peptide (PTHrP), which increases in late stages of pregnancy and remain high during delivery and lactation. Calcitonin levels increase during pregnancy, decline during lactation and return to normal values after lactation is stopped. The physiological roll of tumor necrosis factor, interleukin 6 and osteoprotegerin has not been elucidated yet. The above mentioned changes can exceptionally lead to generalized or regional osteoporosis. The aim of this article is to review the published bibliography concerning the physiopathology of these diseases.

Asunto(s)

Humanos , Femenino , Embarazo , Adulto , Complicaciones del Embarazo/metabolismo , Lactancia/metabolismo , Osteoporosis/metabolismo , Absorciometría de Fotón , Absorción Intestinal/fisiología , Calcio/metabolismo , Calcio/uso terapéutico , Complicaciones del Embarazo/fisiopatología , Complicaciones del Embarazo , Densidad Ósea/fisiología , Fósforo/metabolismo , Hormona Paratiroidea/metabolismo , Lactancia/fisiología , Osteoporosis/fisiopatología , Osteoporosis , Resorción Ósea/etiología , Resorción Ósea/metabolismo , Tasa de Filtración Glomerular/fisiología , Vitamina D/metabolismo , Vitamina D/uso terapéutico

RESUMEN

Tanto la osteoporosis generalizada como la regional son enfermedades que excepcionalmente seasocian con el embarazo. El objetivo de este trabajo es revisar nuestra experiencia en el diagnósticoy tratamiento de estas afecciones. Entre 1984 y 2004 consultaron seis puérperas por osteoporosis y dospor osteoporosis regional. En el primer grupo tres pacientes refirieron fracturas vertebrales y las restantes gravedesmineralización detectada por densitometría ósea (DEXA). Los síntomas comenzaron en el tercer trimestre o en el posparto inmediato. Cinco eran primíparas mientras que una era multípara y había amamantado porun tiempo prolongado. Los factores de riesgo detectados fueron: baja ingesta láctea, delgadez, osteoporosisfamiliar, amenorreas, tabaquismo y corticoterapia. El laboratorio mostró recambio óseo acelerado. La DEXAdocumentó marcada desmineralización especialmente en esqueleto axial. En todas se interrumpió la lactanciay se indicaron drogas anti-resortivas en cuatro, estrógenos en una y sólo calcio y vitamina D en otra. Todas, menos una, evolucionaron favorablemente independientemente del tratamiento utilizado. Dos pacientes consultaronpor dolor y limitación funcional progresiva durante el embarazo, en cadera izquierda y pie derecho respectivamente. La DEXA mostró desmineralización del lado afectado. El diagnóstico de osteoporosis regionalse confirmó por resonancia magnética nuclear. Los informes de laboratorio indicaron aumento del turnover óseo.Ambas fueron tratadas exitosamente con reposo y bifosfonatos.

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Both generalized and regional osteoporosis exceptionally occur during pregnancy and lactation. The aim of this paper is to show our experience in the diagnosis and treatment of these diseases. From 1984 to 2004 six lactating women with osteoporosis and two with regional osteoporosis consulted us. In the former group, three patients had vertebral fractures and the others experienced substantial demineralization detected by dual-energy X-ray absorptiometry (DXA). In all cases, symptoms began during the third trimester of pregnancy or immediately after delivery. Five of them were primiparous and one was multiparous with a long period of lactation. Risk factors were: low calcium intake, low weight, family history of osteoporosis, amenorrhea, cigarette consumption and corticosteroid therapy. Laboratory tests evidenced increased bone turnover. DXA scan showed substantial demineralization, particularly in axial skeleton. Lactation was interrupted in all women and four received anti-resorptive drugs, one estrogen and only calcium plus vitamin D the remaining. All of them, but one, evolved successfully. The women affected by regional osteoporosis complained of unilateral pain and progressive functional limitation of right foot and left hip respectively. Reduced bone mineral density at symptomatic sites was seen by DXA. Diagnosis was confirmed by typical magnetic resonance imaging pattern. Both patients cured with rest and bisphosfonates treatment.

Asunto(s)

Humanos , Embarazo , Adulto , Femenino , Complicaciones del Embarazo/fisiopatología , Lactancia/fisiología , Osteoporosis/fisiopatología , Absorciometría de Fotón , Lactancia Materna/efectos adversos , Calcio/análisis , Calcio/uso terapéutico , Complicaciones del Embarazo/tratamiento farmacológico , Deficiencia de Vitamina D/tratamiento farmacológico , Densidad Ósea/fisiología , Cuello Femoral , Estudios de Seguimiento , Osteoporosis/tratamiento farmacológico , Columna Vertebral , Vitamina D/uso terapéutico

RESUMEN

Durante el embarazo y la lactancia la mujer debe formar y mantener el esqueleto del feto y del neonato, lo que demanda importantes adaptaciones hormonales y metabólicas. La absorción intestinal de calcio aumenta desde el inicio del embarazo siendo máxima en los últimos trimestres. Se produceuna hipercalciuria que desaparece al suspender la lactancia. El calcio de la leche proviene de la reducción ensu excreción urinaria y de un aumento de la resorción ósea. Las oncentraciones de 1,25 (OH)(2) D(3) se duplican desde el comienzo del embarazo manteniéndose elevadas hasta el parto, debido a un aumento de la actividad de la 1-alfa-hidroxilasa placentaria, normalizándose durante la lactancia. Los estrógenos, prolactina y lactógeno placentario, hormonas implicadas en el aumento de la absorción intestinal de calcio, aumentan conjuntamente.La parathormona (PTH) se mantiene en rango normal o bajo, por lo tanto sus acciones fisiológicas serían ejercidas por el péptido relacionado con la PTH (PTHrP), cuyos niveles aumentan tardíamente en el embarazo y permanecen elevados durante el parto y la lactancia. La calcitonina se eleva durante el embarazo, cae durante la lactancia, y se normaliza al finalizar la misma. El papel fisiológico del factor de necrosis tumoral, interleuquina 1, interleuquina 6 y osteoprotegerina todavía no han sido aclarados. Los cambios analizados favorecen,en casos excepcionales, el desarrollo de osteoporosis generalizada y regional. El objetivo de este trabajo es revisar la bibliografía publicada sobre la fisiopatología y clínica de estas entidades.(AU)

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During pregnancy and lactation women have to form and maintain fetus and newborn skeleton. These processes require maternal hormonal and metabolic adjustments. During the first weeks of pregnancy, calcium intestinal absorption rise and reach a maximum in the last trimester. Hypercalciuria can be detected until lactation is stopped. During lactation, calcium that is present in maternal milk, results from lowering maternal calcium excretion and increasing bone resorption. Plasma 1,25 (OH)(2) D(3) levels increase two-fold early in pregnancy due to high placental 1-alpha-hydroxilase activity, remain high until delivery and decline to normal values during lactation. Estrogen, prolactin and placental lactogen, which are involved in calcium absorption, increase at the same time. Normal or even low levels of parathyroid hormone (PTH) can be detected during pregnancy. This suggests that their physiological actions could be mimicked by the parathyroid- related-peptide (PTHrP), which increases in late stages of pregnancy and remain high during delivery and lactation. Calcitonin levels increase during pregnancy, decline during lactation and return to normal values after lactation is stopped. The physiological roll of tumor necrosis factor, interleukin 6 and osteoprotegerin has not been elucidated yet. The above mentioned changes can exceptionally lead to generalized or regional osteoporosis. The aim of this article is to review the published bibliography concerning the physiopathology of these diseases.(AU)

Asunto(s)

Humanos , Femenino , Embarazo , Adulto , Lactancia/metabolismo , Osteoporosis/metabolismo , Complicaciones del Embarazo/metabolismo , Densidad Ósea/fisiología , Resorción Ósea/etiología , Resorción Ósea/metabolismo , Calcio/metabolismo , Calcio/uso terapéutico , Absorciometría de Fotón , Tasa de Filtración Glomerular/fisiología , Absorción Intestinal/fisiología , Lactancia/fisiología , Osteoporosis/fisiopatología , Osteoporosis/diagnóstico por imagen , Hormona Paratiroidea/metabolismo , Fósforo/metabolismo , Complicaciones del Embarazo/fisiopatología , Complicaciones del Embarazo/diagnóstico por imagen , Vitamina D/metabolismo , Vitamina D/uso terapéutico

RESUMEN

Tanto la osteoporosis generalizada como la regional son enfermedades que excepcionalmente seasocian con el embarazo. El objetivo de este trabajo es revisar nuestra experiencia en el diagnósticoy tratamiento de estas afecciones. Entre 1984 y 2004 consultaron seis puérperas por osteoporosis y dospor osteoporosis regional. En el primer grupo tres pacientes refirieron fracturas vertebrales y las restantes gravedesmineralización detectada por densitometría ósea (DEXA). Los síntomas comenzaron en el tercer trimestre o en el posparto inmediato. Cinco eran primíparas mientras que una era multípara y había amamantado porun tiempo prolongado. Los factores de riesgo detectados fueron: baja ingesta láctea, delgadez, osteoporosisfamiliar, amenorreas, tabaquismo y corticoterapia. El laboratorio mostró recambio óseo acelerado. La DEXAdocumentó marcada desmineralización especialmente en esqueleto axial. En todas se interrumpió la lactanciay se indicaron drogas anti-resortivas en cuatro, estrógenos en una y sólo calcio y vitamina D en otra. Todas, menos una, evolucionaron favorablemente independientemente del tratamiento utilizado. Dos pacientes consultaronpor dolor y limitación funcional progresiva durante el embarazo, en cadera izquierda y pie derecho respectivamente. La DEXA mostró desmineralización del lado afectado. El diagnóstico de osteoporosis regionalse confirmó por resonancia magnética nuclear. Los informes de laboratorio indicaron aumento del turnover óseo.Ambas fueron tratadas exitosamente con reposo y bifosfonatos.(AU)

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Both generalized and regional osteoporosis exceptionally occur during pregnancy and lactation. The aim of this paper is to show our experience in the diagnosis and treatment of these diseases. From 1984 to 2004 six lactating women with osteoporosis and two with regional osteoporosis consulted us. In the former group, three patients had vertebral fractures and the others experienced substantial demineralization detected by dual-energy X-ray absorptiometry (DXA). In all cases, symptoms began during the third trimester of pregnancy or immediately after delivery. Five of them were primiparous and one was multiparous with a long period of lactation. Risk factors were: low calcium intake, low weight, family history of osteoporosis, amenorrhea, cigarette consumption and corticosteroid therapy. Laboratory tests evidenced increased bone turnover. DXA scan showed substantial demineralization, particularly in axial skeleton. Lactation was interrupted in all women and four received anti-resorptive drugs, one estrogen and only calcium plus vitamin D the remaining. All of them, but one, evolved successfully. The women affected by regional osteoporosis complained of unilateral pain and progressive functional limitation of right foot and left hip respectively. Reduced bone mineral density at symptomatic sites was seen by DXA. Diagnosis was confirmed by typical magnetic resonance imaging pattern. Both patients cured with rest and bisphosfonates treatment.(AU)

Asunto(s)

Humanos , Embarazo , Adulto , Humanos , Femenino , Lactancia/fisiología , Osteoporosis/fisiopatología , Complicaciones del Embarazo/fisiopatología , Densidad Ósea/fisiología , Lactancia Materna/efectos adversos , Calcio/análisis , Calcio/uso terapéutico , Absorciometría de Fotón , Cuello Femoral , Estudios de Seguimiento , Osteoporosis/tratamiento farmacológico , Complicaciones del Embarazo/tratamiento farmacológico , Columna Vertebral , Vitamina D/uso terapéutico , Deficiencia de Vitamina D/tratamiento farmacológico

RESUMEN

In the last two decades organ transplantation has become an effective and established therapy for end-stage disease of various organs. The increase in survival has been due to the greater immunosuppressive capacity of regimens that include cyclosporin. During the first few months after transplantation cyclosporin is associated with high-dose steroids, which produce deleterious effects on bone and mineral metabolism. These effects are superimposed on the previous bone lesions produced by the underlying chronic diseases. Rapid bone loss occurs specially during the first 6 to 12 months after transplantation, when the incidence of fractures is greater. The majority of the fractures involve the spine. Fracture rates are lower after renal transplantation (7 to 11% in nondiabetic renal transplant recipients) and higher in the recipients of other organ transplants: 17.2 to 42% after liver transplantation, 18 to 50% after cardiac transplantation and 25 to 29% after lung transplantation. No pretransplant densitometric or biochemical parameter can adequately predict fracture risk in the individual patient. Despite this, patients with low bone mineral density at the hip, particularly in women, tend to have an increased risk of fracture. Patients can have vertebral fractures despite normal bone mineral density at the spine. Pathogenesis of bone loss is multifactorial. Patients with renal and liver diseases have either renal or hepatic osteodystrophy prior to transplantation that predispose to bone loss, and many patients awaiting pulmonary transplantation already have osteoporosis due to the use of corticosteroids for their lung disease. Rapid bone loss after transplantation depends, as suggested by prospective biochemical parameters, on a decrease in bone formation (reduction in osteocalcin levels) and an increase in bone resorption. Steroids seem to be the principal determinants of these derangements, although some role of cyclosporin cannot be excluded. Other factors that contribute to bone loss are secondary hyperparathyroidism and hypogonadism. Calcium supplementation and vitamin D administration as the only preventive measures do not seem to reduce fracture risk. The most promising regimens to prevent bone loss after transplantation seem to be the use of bisphosphonates immediately prior to and during the first year after transplantation.

Asunto(s)

Inmunosupresores/efectos adversos , Osteoporosis/inducido químicamente , Inmunología del Trasplante , Huesos/efectos de los fármacos , Ciclosporinas/efectos adversos , Femenino , Trasplante de Corazón , Humanos , Trasplante de Hígado , Trasplante de Pulmón , Masculino

RESUMEN

In the last two decades organ transplantation has become an effective and established therapy for end-stage disease of various organs. The increase in survival has been due to the greater immunosuppressive capacity of regimens that include cyclosporin. During the first few months after transplantation cyclosporin is associated with high-dose steroids, which produce deleterious effects on bone and mineral metabolism. These effects are superimposed on the previous bone lesions produced by the underlying chronic diseases. Rapid bone loss occurs specially during the first 6 to 12 months after transplantation, when the incidence of fractures is greater. The majority of the fractures involve the spine. Fracture rates are lower after renal transplantation (7 to 11

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in nondiabetic renal transplant recipients) and higher in the recipients of other organ transplants: 17.2 to 42

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after liver transplantation, 18 to 50

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after cardiac transplantation and 25 to 29

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after lung transplantation. No pretransplant densitometric or biochemical parameter can adequately predict fracture risk in the individual patient. Despite this, patients with low bone mineral density at the hip, particularly in women, tend to have an increased risk of fracture. Patients can have vertebral fractures despite normal bone mineral density at the spine. Pathogenesis of bone loss is multifactorial. Patients with renal and liver diseases have either renal or hepatic osteodystrophy prior to transplantation that predispose to bone loss, and many patients awaiting pulmonary transplantation already have osteoporosis due to the use of corticosteroids for their lung disease. Rapid bone loss after transplantation depends, as suggested by prospective biochemical parameters, on a decrease in bone formation (reduction in osteocalcin levels) and an increase in bone resorption. Steroids seem to be the principal determinants of these derangements, although some role of cyclosporin cannot be excluded. Other factors that contribute to bone loss are secondary hyperparathyroidism and hypogonadism. Calcium supplementation and vitamin D administration as the only preventive measures do not seem to reduce fracture risk. The most promising regimens to prevent bone loss after transplantation seem to be the use of bisphosphonates immediately prior to and during the first year after transplantation.

RESUMEN

Pamidronate is an effective inhibitor of bone resorption; for this reason it is used in the treatment of high bone turnover diseases and osteoporosis. Because of potential gastric and esophagic side effects their oral use is limited in patients with active pathology in these organs. With the aim to evaluate the usefulness and to establish the ideal schedule of treatment of intravenous pamidronate, we assayed pamidronate infusions (APDIV) in 20 postmenopausal women with active gastroesophagical diseases. Ten of these patients received 30 or 45 mg weekly until they achieved an average dose of 157.50 +/- 9.28 mg/year in one month (range: 120-180 mg) (Group A). Another comparable ten women's group received 30 or 45 mg every three months or 90 mg every six months; the achieved average dose in this group was 166.50 +/- 6.87 mg/year (range: 120-180 mg) (Group B). All patients received 1,000 mg elemental calcium daily. Bone mineral density in lumbar spine significantly increased in both groups, but this increment (delta DMO%) was higher in group B. Bone mineral density in femoral neck was only increased in group A. Parathyroid hormone (iPTH) significantly increased at the third month but returned to basal values at the end of the year in both groups. Parameters of bone remodeling such as osteocalcin (BGP), pyridinoline and deoxipyridinolin decreased progressively and remained low at the end of the year. The treatment was well tolerated: only two patients in group A and one in Group B experienced fever and pseudoflu syndrome; phlebitis was present in one patient in the second group. In conclusion, intravenous Pamidronate is an effective and safe treatment for postmenopausal osteoporosis specially in these patients with esophagicor gastric disorders. Future trials are needed to clarify the ideal dose and schedule of treatment.

Asunto(s)

Difosfonatos/uso terapéutico , Enfermedades del Esófago/complicaciones , Osteoporosis Posmenopáusica/tratamiento farmacológico , Gastropatías/complicaciones , Anciano , Femenino , Humanos , Infusiones Intravenosas , Persona de Mediana Edad , Osteoporosis Posmenopáusica/complicaciones , Pamidronato , Estudios Prospectivos , Resultado del Tratamiento

RESUMEN

Association between primary hyperparathyroidism and Paget's disease of bone is extremely uncommon, despite the relatively high incidence of both entities. The mechanism of this association remains unknown. Dramatic changes in parathyroid function are found in patients with Paget's disease and, on the other hand, the evolution of Paget's disease is influenced by parathyroid functional disorders. We reviewed 175 patients with Paget's disease and 60 with primary hyperparathyroidism, followed during 10 years. We only found 5 cases with the association of the two diseases. Approximately equal number were male and female (ratio: 1.5/1) patients and the average age was 63.60 +/- 2.65 years. Hypercalcemia in Paget's patients, and in increase in alkaline phosphatase in post parathyroid adenoma surgery patients were the clues that suggested the presence of the second disease. Surgical treatment was indicated in 3 patients, and the others were treated with antiresorptive drugs. We also reviewed the cases published since 1934, comparing their diagnostic, clinical, treatment and evolution features with our own cases.

Asunto(s)

Hiperparatiroidismo/complicaciones , Osteítis Deformante/complicaciones , Anciano , Femenino , Humanos , Hiperparatiroidismo/diagnóstico , Hiperparatiroidismo/tratamiento farmacológico , Masculino , Persona de Mediana Edad , Osteítis Deformante/diagnóstico , Osteítis Deformante/tratamiento farmacológico , Estudios Retrospectivos

RESUMEN

In osteoporotic women (n:163), 63.8 (+/- 8.1) years old and 15.2 (+/- 8.3) years since menopause, oral (200 mg/day) pamidronate was administered during protracted periods, up to 6 years. During the first 4 years of therapy significant increases from basal in both, lumbar spine and femoral neck were reported (p < 0.01). Patients who underwent to 5-6 years of treatment also showed positive results in both skeletal sites. Whole body mineral content estimated a 23.8 g/year mean gain during a 4-year period. Biochemical bone markers of resorption and formation reflected a variable degree of bone turnover decrease. Such changes were more pronounced at the beginning, and remained steady after the first year of continuous therapy. Calcemia remained between normal range without any hypocalcemic episode being reported. Phosphatemia, within normal range, showed a smooth trend to increase. PTH remained within normal range and vitamin D tended to slightly increase. The total number of new bone fractures and total number of patients with new fractures were less frequent during the pamidronate treatment period than before (p < 0.01). Indeed, the relative risk (RR) of fracture was estimated comparing the treatment lapse, 495 patient/year, vs a pretreatment period of 1,814 patient/year. Overall RR resulted less than 1 (RR = 0.83; CI 95% = 0.53-1.26). In total, hip, forearm and "other" fractures, RR was also less than 1 and remained over 1 in vertebral fractures. The latter can be explained because our sample started its treatment probably in a period of increased spine crushing. Overall fracture results, in a sample of patients as own controls and in spite of differences in ages, suggested that during treatment, patients improved their skeletal biomechanical competence, mainly in sites where cortical bone plays a meaningful role, as in femoral neck. It is concluded that pamidronate is an effective tool to ameliorate the skeletal conditions of postmenopausal osteoporotic women.

Asunto(s)

Densidad Ósea/efectos de los fármacos , Difosfonatos/uso terapéutico , Fracturas Óseas/prevención & control , Osteoporosis Posmenopáusica/tratamiento farmacológico , Administración Oral , Resorción Ósea , Tolerancia a Medicamentos , Femenino , Estudios de Seguimiento , Humanos , Estudios Longitudinales , Persona de Mediana Edad , Pamidronato , Factores de Tiempo

RESUMEN

Alcohol intake is one of the multiple risk factors for developing osteoporosis. Alcohol has direct toxic effects on osteoblasts which determines lower osteocalcin levels at an early stage, and histomorphometric changes later on. Some authors found not only diminished bone formation in alcoholics, but also increased bone resorption. The effect of alcoholism on calciotropic hormones includes fall of PTH serum levels after an acute or moderate alcohol intake, causing transient hypoparathyroidism. In chronic alcoholism, serum levels of vitamin D and its metabolites are decreased independently of any liver disease, probably related to alcohol influence on enzymatic systems. The mineral homeostasis of alcoholics is affected: hypocalcemia is found in acute intoxication, with hypo or hypermagnesemia. In chronic alcoholism the serum calcium values tend to be normal. Alcohol intake causes multiple endocrine changes that lead to hypogonadism in both sexes. The stimulation of hypothalamus-hypophyseal-adrenal axis contributes to the alcoholic bone disease, because of the adverse effects of corticoids on bone. Caloric and protein malnutrition, in addition to a dissipated life style are additional risk factors for the development of osteoporosis.

Asunto(s)

Alcoholismo/complicaciones , Osteoporosis/etiología , Alcoholismo/metabolismo , Animales , Densidad Ósea/efectos de los fármacos , Glándulas Endocrinas/efectos de los fármacos , Etanol/farmacología , Homeostasis/efectos de los fármacos , Humanos , Osteoporosis/metabolismo , Ratas

RESUMEN

El consumo de alcohol constituye un factor de riesgo para el desarrollo de osteoporosis. Actúa como un tóxico celular directo sobre los osteoblastos, lo que se evidencia precozmente por un descenso de la osteocalcina (BGP), y se confirma por histomorfometría ósea. Algunos autores también encontraron evidencias de aumento de la reabsorción ósea, y no únicamente disminución de la formación. Los efectos sobre las hormonas calciotrópicas incluyen una caída de PTH luego de una ingesta aguda y moderada de alcohol, pudiendo llegar en algunos casos a producir verdaderos cuadros de hipoparatiroidismo transitorio. La vitamina D y sus metabolitos están afectados en los alcohólicos crónicos sin relación con su disfunción hepática, probablemente debido a modulación de los sistemas enzimáticos de síntesis y catabolización. La homeostasis mineral sufre modificaciones: la hipocalcemia es la regla en las intoxicaciones agudas, con hipo o hipermagnesemia, tendiendo a normalizarse en los alcohólicos crónicos. Los cambios en el eje hipotálamo-hipofiso-gonadal llevan al hipogonadismo en el varón y la mujer alcoholicos crónicos por múltiples mecanismos. La hipercortisolemia secundaria al estímulo del eje hipotálamo-hipófiso-adrenal también acarrea daños en la calidad ósea. La desnutrición proteica y vitamínica sumada a modificaciones en el estilo de vida constituyen factores adicionales de riesgo para el desarrollo de osteoporosis (AU)

Asunto(s)

Ratas , Humanos , Animales , Osteoporosis/etiología , Alcoholismo/complicaciones , Osteoporosis/metabolismo , Alcoholismo/metabolismo

RESUMEN

El consumo de alcohol constituye un factor de riesgo para el desarrollo de osteoporosis. Actúa como un tóxico celular directo sobre los osteoblastos, lo que se evidencia precozmente por un descenso de la osteocalcina (BGP), y se confirma por histomorfometría ósea. Algunos autores también encontraron evidencias de aumento de la reabsorción ósea, y no únicamente disminución de la formación. Los efectos sobre las hormonas calciotrópicas incluyen una caída de PTH luego de una ingesta aguda y moderada de alcohol, pudiendo llegar en algunos casos a producir verdaderos cuadros de hipoparatiroidismo transitorio. La vitamina D y sus metabolitos están afectados en los alcohólicos crónicos sin relación con su disfunción hepática, probablemente debido a modulación de los sistemas enzimáticos de síntesis y catabolización. La homeostasis mineral sufre modificaciones: la hipocalcemia es la regla en las intoxicaciones agudas, con hipo o hipermagnesemia, tendiendo a normalizarse en los alcohólicos crónicos. Los cambios en el eje hipotálamo-hipofiso-gonadal llevan al hipogonadismo en el varón y la mujer alcoholicos crónicos por múltiples mecanismos. La hipercortisolemia secundaria al estímulo del eje hipotálamo-hipófiso-adrenal también acarrea daños en la calidad ósea. La desnutrición proteica y vitamínica sumada a modificaciones en el estilo de vida constituyen factores adicionales de riesgo para el desarrollo de osteoporosis

Asunto(s)

Ratas , Humanos , Animales , Alcoholismo/complicaciones , Osteoporosis/etiología , Alcoholismo/metabolismo , Osteoporosis/metabolismo

RESUMEN

Alcohol intake is one of the multiple risk factors for developing osteoporosis. Alcohol has direct toxic effects on osteoblasts which determines lower osteocalcin levels at an early stage, and histomorphometric changes later on. Some authors found not only diminished bone formation in alcoholics, but also increased bone resorption. The effect of alcoholism on calciotropic hormones includes fall of PTH serum levels after an acute or moderate alcohol intake, causing transient hypoparathyroidism. In chronic alcoholism, serum levels of vitamin D and its metabolites are decreased independently of any liver disease, probably related to alcohol influence on enzymatic systems. The mineral homeostasis of alcoholics is affected: hypocalcemia is found in acute intoxication, with hypo or hypermagnesemia. In chronic alcoholism the serum calcium values tend to be normal. Alcohol intake causes multiple endocrine changes that lead to hypogonadism in both sexes. The stimulation of hypothalamus-hypophyseal-adrenal axis contributes to the alcoholic bone disease, because of the adverse effects of corticoids on bone. Caloric and protein malnutrition, in addition to a dissipated life style are additional risk factors for the development of osteoporosis.