Association of primary hyperparathyroidism and humoral hypercalcemia of malignancy in a patient with clear cell renal carcinoma.

Hypercalcemia is found frequently in patients with cancer. Besides the etiology related to the malignancy, other causes should be considered in the differential diagnostic, as primary hyperparathyroidism, granulomatous diseases and the use of thiazide diuretics. We present a case report of a severe hypercalcemia due to a rare association and review the relevant literature. A female patient, 57 years old, sent to the Endocrinology Service of Hospital das Clínicas da Universidade do Paraná (SEMPR) in order to investigate severe hypercalcemia with frequent need of hospitalization. The patient was in chemotherapy treatment for recurrence of clear cell renal cancer. During the investigation she presented high level of parathyroid hormone (PTH) and parathyroid scintigraphy suggestive of hyperplasia/ adenoma of parathyroid, histopathological diagnosis was confirmed after parathyroidectomy. After surgery the patient presented undetectable levels of PTH. However, she continued with progressive increase of serum calcium, with no signs of bone metastases or change in vitamin D metabolism. The investigation showed high levels of PTH-related protein (PTHrP), leading us to the diagnosis of hypercalcemia of malignancy. The patient presented severe hypercalcemia due to the rare association of primary hyperparathyroidism and humoral hypercalcemia of malignancy due to secretion of PTHrP by tumor cells. The presence of isolated primary hyperparathyroidism, as a cause of hypercalcemia in cancer patients, has been described in approximately 5-10% of the patients. However, the association of primary hyperparathyroidism and humoral hypercalcemia of malignancy (which means with concomitant elevation of PTH and PTHrP) is rare, only three cases have been described in the literature.

Association of primary hyperparathyroidism and humoral hypercalcemia of malignancy in a patient with clear cell renal carcinoma

Hypercalcemia is found frequently in patients with cancer. Besides the etiology related to the malignancy, other causes should be considered in the differential diagnostic, as primary hyperparathyroidism, granulomatous diseases and the use of thiazide diuretics. We present a case report of a severe hypercalcemia due to a rare association and review the relevant literature. A female patient, 57 years old, sent to the Endocrinology Service of Hospital das Clínicas da Universidade do Paraná (SEMPR) in order to investigate severe hypercalcemia with frequent need of hospitalization. The patient was in chemotherapy treatment for recurrence of clear cell renal cancer. During the investigation she presented high level of parathyroid hormone (PTH) and parathyroid scintigraphy suggestive of hyperplasia/ adenoma of parathyroid, histopathological diagnosis was confirmed after parathyroidectomy. After surgery the patient presented undetectable levels of PTH. However, she continued with progressive increase of serum calcium, with no signs of bone metastases or change in vitamin D metabolism. The investigation showed high levels of PTH-related protein (PTHrP), leading us to the diagnosis of hypercalcemia of malignancy. The patient presented severe hypercalcemia due to the rare association of primary hyperparathyroidism and humoral hypercalcemia of malignancy due to secretion of PTHrP by tumor cells. The presence of isolated primary hyperparathyroidism, as a cause of hypercalcemia in cancer patients, has been described in approximately 5-10% of the patients. However, the association of primary hyperparathyroidism and humoral hypercalcemia of malignancy (which means with concomitant elevation of PTH and PTHrP) is rare, only three cases have been described in the literature. Arch Endocrinol Metab. 2015;59(1):84-8.

[Clinical heterogeneity of atypical fractures during prolonged use of bisphosphonates--risk factors and bone turnover markers]. / Heterogeneidade na apresentação clínica de fraturas atípicas após uso prolongado de bisfosfonatos--fatores de risco e marcadores de remodelação óssea.

We describe four cases of atypical femoral fractures treated at the Department of Endocrinology, Hospital de Clínicas, Federal University of Paraná (SEMPR) which, although characteristic of this type of fracture, presented clinical peculiarities that should be considered and serve as a warning in these patients, such as: late diagnosis with maintenance of bisphosphonates; absence of co-morbidities with excellent result; failure of fracture healing; use of anabolic medication after the fracture and the use of bone turnover markers at the follow up.

Osteocalcin, energy and glucose metabolism.

Osteocalcin is a bone matrix protein that has been associated with several hormonal actions on energy and glucose metabolism. Animal and experimental models have shown that osteocalcin is released into the bloodstream and exerts biological effects on pancreatic beta cells and adipose tissue. Undercarboxylated osteocalcin is the hormonally active isoform and stimulates insulin secretion and enhances insulin sensitivity in adipose tissue and muscle. Insulin and leptin, in turn, act on bone tissue, modulating the osteocalcin secretion, in a traditional feedback mechanism that places the skeleton as a true endocrine organ. Further studies are required to elucidate the role of osteocalcin in the regulation of glucose and energy metabolism in humans and its potential therapeutic implications in diabetes, obesity and metabolic syndrome.

Bone disease after transplantation: osteoporosis and fractures risk.

Organ transplantation is the gold standard therapy for several end-stage diseases. Bone loss is a common complication that occurs in transplant recipients. Osteoporosis and fragility fractures are serious complication, mainly in the first year post transplantation. Many factors contribute to the pathogenesis of bone disease following organ transplantation. This review address the mechanisms of bone loss including the contribution of the immunosuppressive agents as well as the specific features to bone loss after kidney, lung, liver, cardiac and bone marrow transplantation. Prevention and management of bone loss in the transplant recipient should be included in their post transplant follow-up in order to prevent fractures.

Osteocalcin, energy and glucose metabolism / Osteocalcina, metabolismo energético e da glicose

Osteocalcin is a bone matrix protein that has been associated with several hormonal actions on energy and glucose metabolism. Animal and experimental models have shown that osteocalcin is released into the bloodstream and exerts biological effects on pancreatic beta cells and adipose tissue. Undercarboxylated osteocalcin is the hormonally active isoform and stimulates insulin secretion and enhances insulin sensitivity in adipose tissue and muscle. Insulin and leptin, in turn, act on bone tissue, modulating the osteocalcin secretion, in a traditional feedback mechanism that places the skeleton as a true endocrine organ. Further studies are required to elucidate the role of osteocalcin in the regulation of glucose and energy metabolism in humans and its potential therapeutic implications in diabetes, obesity and metabolic syndrome.

A osteocalcina é uma proteína da matriz óssea que tem sido implicada com várias ações hormonais relacionadas à homeostase de glicose e ao metabolismo energético. Modelos animais e experimentais têm demonstrado que a osteocalcina é liberada do osso para a circulação sanguínea e age nas células betapancreáticas e no tecido adiposo. A osteocalcina decarboxilada é a isoforma hormonalmente ativa e estimula a secreção e sensibilidade à insulina no tecido adiposo e muscular. A insulina e a leptina, por sua vez, atuam no tecido ósseo modulando a secreção da osteocalcina, formando uma alça de retroalimentação tradicional em que o esqueleto torna-se um órgão endócrino. Novos estudos ainda são necessários para elucidar o papel da osteocalcina na regulação glicêmica e no metabolismo energético em humanos, com potenciais implicações terapêuticas no tratamento de diabetes, obesidade e síndrome metabólica.

Bone disease after transplantation: osteoporosis and fractures risk / Doença óssea pós-transplante: risco de osteoporose e fraturas

Organ transplantation is the gold standard therapy for several end-stage diseases. Bone loss is a common complication that occurs in transplant recipients. Osteoporosis and fragility fractures are serious complication, mainly in the first year post transplantation. Many factors contribute to the pathogenesis of bone disease following organ transplantation. This review address the mechanisms of bone loss including the contribution of the immunosuppressive agents as well as the specific features to bone loss after kidney, lung, liver, cardiac and bone marrow transplantation. Prevention and management of bone loss in the transplant recipient should be included in their post transplant follow-up in order to prevent fractures.

Transplantes de órgão é terapia padrão-ouro para várias doenças em estágio terminal. Perda óssea é uma complicação comum que ocorre em pacientes transplantados. Osteoporose e fraturas por fragilidade são complicações sérias, principalmente no primeiro ano pós-transplante. Muitos fatores podem contribuir para patogênese da doença óssea nesses pacientes. Esta revisão aborda os mecanismos de perda óssea incluindo o papel dos agentes imunossupressores, bem como os fatores específicos da perda óssea após rim, pulmão, fígado, coração e transplante de medula óssea. A prevenção e o tratamento da perda óssea nos pacientes transplantados devem ser realizados para evitar fraturas.

Responses of urinary N-telopeptide and renal calcium handling to PTH infusion after treatment with estrogen, raloxifene, and tamoxifen.

This prospective, randomized, placebo-controlled study investigated whether estrogen, tamoxifen, and raloxifene protect the skeleton from the acute catabolic effects of continuous PTH(1-34) infusion. It was infused over 24 h in 25 postmenopausal women both before and while on medication for 16-20 weeks (estrogen n = 7, raloxifene n = 5, tamoxifen n = 7, placebo n = 6). Blood and urine samples were collected at baseline and every 4 h during the PTH(1-34) infusion and analyzed for calcium homeostasis, bone remodeling, and specific cytokines. Data for the premedication PTH(1-34) infusions were pooled. During the premedication PTH(1-34) infusions, serum calcium and urine phosphorus increased, while serum phosphorus and urine calcium declined. Osteocalcin decreased (mean 18%), while urine NTX increased (mean 315%). Serum IL-6 increased 260%, but there were no other cytokine changes as a result of the PTH(1-34) infusion. On medication, the mean peak change in NTX with PTH(1-34) infusion was less (77, 59, and 31 nM/mM with raloxifene, tamoxifen, and estrogen, respectively). The reduction in urine calcium excretion was prolonged with each agent but only significantly with estrogen. There was no reduction in the IL-6 elevation induced by PTH(1-34) with any medication. The differential skeletal resorption response to PTH(1-34) infusion after the treatments may reflect different potencies of these agents or variability in interaction with the estrogen receptor. Renal calcium conservation and the blunted response of bone resorption to PTH(1-34) infusion may be mechanisms by which estrogen and estrogen agonist/antagonist agents preserve bone mass.

Skeletal microstructural abnormalities in postmenopausal women with chronic obstructive pulmonary disease.

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.

[Endocrine and metabolic effects of antiepileptic drugs]. / Efeitos endócrinos e metabólicos das drogas antiepilépticas.

The antiepileptic drugs (AED) have been widely used for a great deal of people--in the treatment of epilepsy and other diseases--throughout the world. Continuous and prolonged use of AED may be associated with adverse effects in different systems, including a variety of endocrine and metabolic abnormalities. In this review, the relationship of AED with alterations in bone mineral metabolism, energy balance and body weight, gonadal function and thyroid metabolism was revised, as well as their clinical utility in the treatment of diabetic neuropathy.

Efeitos endócrinos e metabólicos das drogas antiepilépticas / Endocrine and metabolic effects of antiepileptic drugs

As drogas antiepilépticas (DAE) são utilizadas por um enorme contingente de pessoas em todo o mundo - tanto no tratamento das epilepsias como para outros fins - frequentemente por um longo tempo. Por essas razões, torna-se fundamental o conhecimento sobre os potenciais efeitos adversos desses medicamentos, muitos deles envolvendo vários aspectos hormonais e metabólicos que devem ser do conhecimento do endocrinologista. Nesta revisão, foi abordada a relação das DAE com anormalidades no metabolismo mineral ósseo, balanço energético e peso corporal, eixo gonadal e função tireoideana, além de ter sido revisado o papel terapêutico dessas medicações no tratamento da neuropatia diabética.

The antiepileptic drugs (AED) have been widely used for a great deal of people - in the treatment of epilepsy and other diseases - throughout the world. Continuous and prolonged use of AED may be associated with adverse effects in different systems, including a variety of endocrine and metabolic abnormalities. In this review, the relationship of AED with alterations in bone mineral metabolism, energy balance and body weight, gonadal function and thyroid metabolism was revised, as well as their clinical utility in the treatment of diabetic neuropathy.

Efeitos endócrinos e metabólicos dos antiepilépticos / Endocrine and metabolic effects of antiepileptics drugs

As drogas antiepilépticas (DAE) são utilizadas por um enorme contingente de pessoas em todo o mundo - seja no tratamento das epilepsias como para outros fins - freqüentemente por longo tempo. Por estas razões, os médicos que utilizam DAE no seu arsenal terapêutico, devem estar atentos para os potenciais efeitos adversos do uso prolongado destes medicamentos. O objetivo desta revisão é analisar a relação das DAE com anormalidades no metabolismo mineral ósseo, balanço energético e peso corporal, função gonadal e tireoideana e suas aplicações no tratamento da neuropatia diabética.

The antiepileptic drugs (AEDs) have been widely used for treatment of epilepsy and other diseases. Continuous and prolonged use of AEDs might be associated with potential adverse effects in different systems, including endocrine and metabolic abnormalities. The purpose of this review was to examine the relationship of AEDs with alterations in bone mineral metabolism, energy balance and body weight, gonadal function and thyroid metabolism, as well as their implications in the treatment of diabetic neuropathy.

[Bone mineral density of children and adolescents with congenital hypothyroidism]. / Densidade mineral óssea de crianças e adolescentes com hipotireoidismo congênito.

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.

Densidade mineral óssea de crianças e adolescentes com hipotireoidismo congênito / Bone mineral density of children and adolescents with congenital hypothyroidism

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.

Bone density and bone turnover markers in patients with epilepsy on chronic antiepileptic drug therapy.

In this comparative, cross-sectional study, we evaluated 55 patients with epilepsy on chronic use of antiepileptic drugs (AED); [(38 females and 17 males, 35 +/- 6 years (25 to 47)] and compared to 24 healthy subjects (17 females/7 males). Laboratorial evaluation of bone and mineral metabolism including measurements of bone specific alkaline phosphatase (BALP) and carboxyterminal telopeptide of type I collagen (CTX-I) were performed. Bone mineral density (BMD) was measured by DXA. BALP and CTX-I levels did not differ significantly between the groups. CTX-I levels were significantly higher in patients who were exposed to phenobarbital (P< 0.01) than those who were not. Patients presented BMD of both sites significantly lower than the controls (0.975 +/- 0.13 vs. 1.058 +/- 0.1 g/cm(2); p= 0.03; 0.930 +/- 0.1 vs. 0.988 +/- 0.12 g/cm(2); p= 0.02, respectively). Total hip BMD (0.890 +/- 0.10 vs. 0.970 +/- 0.08 g/cm(2); p< 0.003) and femoral neck (0.830 +/- 0.09 vs. 0.890 +/- 0.09 g/cm(2); p< 0.03) were significantly lower in patients who had been exposed to phenobarbital, in comparison to the non-phenobarbital users. In conclusion, patients on AED demonstrate reduced BMD. Among the AED, phenobarbital seems to be the main mediator of low BMD and increases in CTX-I.

Bone density and bone turnover markers in patients with epilepsy on chronic antiepileptic drug therapy

In this comparative, cross-sectional study, we evaluated 55 patients with epilepsy on chronic use of antiepileptic drugs (AED); [(38 females and 17 males, 35 ± 6 years (25 to 47)] and compared to 24 healthy subjects (17 females/7 males). Laboratorial evaluation of bone and mineral metabolism including measurements of bone specific alkaline phosphatase (BALP) and carboxyterminal telopeptide of type I collagen (CTX-I) were performed. Bone mineral density (BMD) was measured by DXA. BALP and CTX-I levels did not differ significantly between the groups. CTX-I levels were significantly higher in patients who were exposed to phenobarbital (P< 0.01) than those who were not. Patients presented BMD of both sites significantly lower than the controls (0.975 ± 0.13 vs. 1.058 ± 0.1 g/cm²; p= 0.03; 0.930 ± 0.1 vs. 0.988 ± 0.12 g/cm²; p= 0.02, respectively). Total hip BMD (0.890 ± 0.10 vs. 0.970 ± 0.08 g/cm²; p< 0.003) and femoral neck (0.830 ± 0.09 vs. 0.890 ± 0.09 g/cm²; p< 0.03) were significantly lower in patients who had been exposed to phenobarbital, in comparison to the non-phenobarbital users. In conclusion, patients on AED demonstrate reduced BMD. Among the AED, phenobarbital seems to be the main mediator of low BMD and increases in CTX-I.

Neste estudo comparativo, transversal, 55 pacientes com epilepsia [38 mulheres e 17 homens; 35 ± 6 anos (25 a 47anos)] foram comparados com 24 indivíduos normais (17 mulheres / 7 homens). Foi realizada uma avaliação laboratorial do metabolismo ósseo e mineral incluindo a dosagem de fosfatase alcalina específica óssea (BALP) e telopeptídeo carboxiterminal do colágeno tipo I (CTX-I). Densidade mineral óssea (DMO) da coluna lombar e do fêmur foi medida por DXA. BALP e CTX-I não foram diferentes entre os grupos. CTX-I foi significativamente mais elevado nos pacientes expostos ao fenobarbital do que os que não usaram essa medicação (p< 0,01). DMO de ambos os sítios foi menor no grupo de pacientes (0,975 ± 0,13 vs. 1,058 ± 0,1 g/cm²; p= 0,03; 0,930 ± 0,1 vs. 0,988 ± 0,12 g/cm²; p= 0,02, respectivamente). DMO do fêmur total (0,890 ± 0,10 vs. 0,970 ± 0,08 g/cm²; p< 0,003) e colo do fêmur (0,830 ± 0,09 vs. 0,890 ± 0,09 g/cm²; p< 0,03) foi significativamente menor nos pacientes que usaram fenobarbital. Em conclusão, pacientes portadores de epilepsia em uso crônico de drogas antiepilépticas (DAE) demonstraram uma redução da DMO. Entre as DAE, o fenobarbital parece ser o principal mediador da diminuição da DMO e do aumento do CTX-I.

[Main causes of low bone mass in premenopausal women referred to a Metabolic Bone Clinic of Curitiba]. / Principais causas de diminuição da massa óssea em mulheres na pré-menopausa encaminhadas ao ambulatório de doenças ósteo-metabólicas de um Hospital Terciário de Curitiba.

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.

Transplantation osteoporosis.

In the past two decades, there has been a rapid increase in the number of organ transplanted worldwide, including Brazil, along with an improvement in survival and quality of life of the transplant recipients. Osteoporosis and a high incidence of fragility fractures have emerged as a complication of organ transplantation. Many factors contribute to the pathogenesis of osteoporosis following organ transplantation. In addition, most patients have some form of bone disease prior to transplantation, which is usually related to adverse effects of end-stage organ failure on the skeleton. This chapter reviews the mechanisms of bone loss that occur both in the early and late post-transplant periods, as well as the features specific to bone loss after kidney, lung, liver, cardiac and bone marrow transplantation. Prevention and treatment for osteoporosis should be instituted prior and in the early and late phase after transplantation, and will also be addressed in this article.

Principais causas de diminuição da massa óssea em mulheres na pré-menopausa encaminhadas ao ambulatório de doenças ósteo-metabólicas de um Hospital Terciário de Curitiba / Main causes of low bone mass in premenopausal women referred to a Metabolic Bone Clinic of Curitiba / Main causes of low bone mass in premenopausal women referred to a Metabolic Bone Clinic of Curitiba

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.

Transplantation osteoporosis / Osteoporose pós transplante

In the past two decades, there has been a rapid increase in the number of organ transplanted worldwide, including Brazil, along with an improvement in survival and quality of life of the transplant recipients. Osteoporosis and a high incidence of fragility fractures have emerged as a complication of organ transplantation. Many factors contribute to the pathogenesis of osteoporosis following organ transplantation. In addition, most patients have some form of bone disease prior to transplantation, which is usually related to adverse effects of end-stage organ failure on the skeleton. This chapter reviews the mechanisms of bone loss that occur both in the early and late post-transplant periods, as well as the features specific to bone loss after kidney, lung, liver, cardiac and bone marrow transplantation. Prevention and treatment for osteoporosis should be instituted prior and in the early and late phase after transplantation, and will also be addressed in this article.

Nas últimas décadas houve um grande aumento no número de transplantes realizados no Brasil e no mundo, o que proporcionou uma melhora na sobrevida e qualidade de vida dos pacientes transplantados. A osteoporose e o aumento da prevalência de fraturas por fragilidade óssea têm se mostrado como uma complicação do transplante. Muitos fatores contribuem para a patogênese da osteoporose relacionada ao transplante. Além disso, a maioria dos pacientes apresenta doença óssea antes do transplante, a qual é secundária à doença grave de base. Este artigo revisa os mecanismos da perda óssea que ocorre tanto na fase precoce quanto na fase tardia após o transplante, como também os fatores específicos envolvidos na perda óssea relacionados ao transplante renal, pulmonar, cardíaco, hepático e de medula óssea. A prevenção e o tratamento da osteoporose em todas as fases do transplante também são abordados neste artigo.