Local ethanol injection for the treatment of deltoid parathyroid cell hyperplasia.

Secondary hyperparathyroidism (SHPT) is a serious complication in dialysis patients and is routinely managed with medical therapy. Refractory disease is usually treated either surgically or by local ethanol injection into the parathyroid glands. Total parathyroidectomy with deltoid implant can be successful; however, recurrent, resistant disease is not uncommon. Local ethanol injection was applied to the deltoid autoimplant of a patient with recurrent, resistant SHPT, which had not been resolved with surgical treatment. Serum intact parathyroid hormone (iPTH) levels subsequently decreased from 1,400 to 219 pg/dl and remained stable for the next 6 months. To our knowledge, this procedure has not been previously described in the literature. Local injection of ethanol may represent an interesting alternative to surgery for the treatment of deltoid parathyroid cell hyperplasia in patients in which surgical treatment is not an option.

Osteoporosis regional transitoria y distrofia simpática refleja: una misma enfermedad? / Regional transient osteoporosis, and reflex sympathetic dystrophy: the same disease?

Complex regional pain syndrome, reflex sympathetic dystrophy, regional, transient and migratory osteoporosis, are known as a spectrum of medical conditions that present with pain, edema, erythema, localized osteoporosis and sometimes sympathetic dysfunction. Many factors which are present in these conditions, such as clinical presentation, radiologic findings and a variety of still unclear physiopathologic mechanisms are correlated. We propose that all these conditions are different periods of the same pathology.

Síndrome doloroso regional complejo, distrofia simpática refleja, osteoporosis regional, transitoria, y migratriz, representan un espectro de alteraciones que se presentan con dolor, edema, eritema, osteoporosis localizada y en ocasiones disfunción simpática descripta en muchos sitios esqueléticos. Muchosfactores, tales como la forma de presentación clínica, los hallazgos radiológicos y la fisiopatología desconocida de estas enfermedades las correlacionan íntimamente. Proponemos entonces, mediante la presentación de uncaso clínico, que dichas entidades son estadios y presentaciones diferentes de una misma enfermedad.

Osteoporosis regional transitoria y distrofia simpática refleja: una misma enfermedad? / Regional transient osteoporosis, and reflex sympathetic dystrophy: the same disease?

Complex regional pain syndrome, reflex sympathetic dystrophy, regional, transient and migratory osteoporosis, are known as a spectrum of medical conditions that present with pain, edema, erythema, localized osteoporosis and sometimes sympathetic dysfunction. Many factors which are present in these conditions, such as clinical presentation, radiologic findings and a variety of still unclear physiopathologic mechanisms are correlated. We propose that all these conditions are different periods of the same pathology.(AU)

Síndrome doloroso regional complejo, distrofia simpática refleja, osteoporosis regional, transitoria, y migratriz, representan un espectro de alteraciones que se presentan con dolor, edema, eritema, osteoporosis localizada y en ocasiones disfunción simpática descripta en muchos sitios esqueléticos. Muchosfactores, tales como la forma de presentación clínica, los hallazgos radiológicos y la fisiopatología desconocida de estas enfermedades las correlacionan íntimamente. Proponemos entonces, mediante la presentación de uncaso clínico, que dichas entidades son estadios y presentaciones diferentes de una misma enfermedad.(AU)

Resultados iniciales con criopreservación de glándulas paratiroides y potenciales aplicaciones / Histological integrity and functional viability results of previously cryopreserved human para thyroid tissue

Objetivo: Analizar la integridad histológica y viabilidad funcional de tejido paratiroideo criopreservado, con miras a un potencial trasplante futuro. Material y método: Se criopreservaron muestras de tejido paratiroideo proveniente de 14 pacientes operados por HPT (8 secundarios, 3 terciarios , 1 primario recidivado y dos hiperplasias primarias). Fraccionado en porciones de 2 x 3 mm, el material fue preservado en suero + solución de Hanks + DMSO y congelados hasta -90ºC, conservándolo en nitrógeno líquido. Luego de seis meses, el material de 4 pacientes fue parcialmente descongelado y estimulado con solución de Cloruro de Ca++, midiéndose la secreción de PTH y estudiando la histología con H y E y con el método de Tunne

Resultados iniciales con criopreservación de glándulas paratiroides y potenciales aplicaciones / Histological integrity and functional viability results of previously cryopreserved human para thyroid tissue

Objetivo: Analizar la integridad histológica y viabilidad funcional de tejido paratiroideo criopreservado, con miras a un potencial trasplante futuro. Material y método: Se criopreservaron muestras de tejido paratiroideo proveniente de 14 pacientes operados por HPT (8 secundarios, 3 terciarios , 1 primario recidivado y dos hiperplasias primarias). Fraccionado en porciones de 2 x 3 mm, el material fue preservado en suero + solución de Hanks + DMSO y congelados hasta -90°C, conservándolo en nitrógeno líquido. Luego de seis meses, el material de 4 pacientes fue parcialmente descongelado y estimulado con solución de Cloruro de Ca++, midiéndose la secreción de PTH y estudiando la histología con H y E y con el método de Tunnel para apoptosis. Resultados: Se observó en las cuatro muestras un patrón similar de respuesta, con un pico inicial de secreción, un descenso a la hora, y un nuevo ascenso a las dos horas del estímulo. El estudio histológico de las piezas mostró integridad histológica luego de seis meses de criopreservación, pero importante depauperización celular luego del estímulo. Conclusiones: En la muestra analizada, la criopreservación del tejido paratiroideo ha permitido conservar su integridad histológica, así como sus capacidades secretorias básicas. El fenómeno apoptótico que invariablemente acompaña a la estimulación prolongada in vitro, requiere nuevas investigaciones que permitan controlarlo

High prevalence of vitamin D insufficiency in healthy elderly people living at home in Argentina.

OBJECTIVE: To evaluate the nutritional status of vitamin D in urban populations of healthy elderly people living at home, in different regions of Argentina. DESIGN: Cross-sectional study. SUBJECTS: In total, 386 ambulatory subjects over 65 y of age from seven cities (between latitude 26 degrees S and 55 degrees S) were asked to participate between the end of winter and the beginning of spring. Of these, 369 accepted, 30 were excluded because of medical history or abnormal biochemical determinations. Finally, 339 subjects (226 women and 113 men) (X+/-s.d.) (71.3+/- 5.2 y) were included. RESULTS: Serum 25OHD levels were lowest in the South (latitude range: 41 degrees S-55 degrees S): 14.2+/-5.6 ng/ml (P<0.0001vs North and Mid regions); highest in the North (26 degrees S-27 degrees S): 20.7+/-7.4 ng/ml (P<0.03 vs Mid, P<0.0001vs South); and intermediate in the Mid region (33 degrees S-34 degrees S) 17.9+/-8.2 ng/ml. Serum mid-molecule PTH (mmPTH) and 25OHD were inversely related: (r=-0.24, P<0.001). A cutoff level of 25OHD at which serum mmPTH levels began to increase was established at 27 ng/ml. A high prevalence (87-52%) of subjects with 25OHD levels in the deficiency-insufficiency range (25OHD levels <20 ng/ml) was detected. CONCLUSION: This study shows that vitamin D deficiency/insufficiency in the elderly is a worldwide problem. Correction of this deficit would have a positive impact on bone health of elderly people.

Papel del calcio y de la vitamina D en la salud ósea (parte II) / Role of calcium and vitamin D in bone health (Part II)

No disponible

Papel del calcio y de la vitamina D en la salud ósea (parte I) / Role of calcium and vitamin D in bone health

No disponible

[Vertebral osteoporosis induced by corticoids and cyclosporine ina a patient with Still disease]. / Osteoporosis vertebral inducida por corticoides y ciclosporina en una paciente con enfermedad de Still.

We report on a 29-year-old patient who received high doses of prednisone and cyclosporine for the treatment of Still disease. She consulted about dorsolumbar pain leading to physical disability. She presented multiple vertebral fractures, decreased lumbar bone mineral density in the rank of osteoporosis, high bone turnover, and associated hypercalciuria. Cyclosporine and corticoids induced severe changes in bone and mineral metabolism. All patients in treatment with these drugs should undergo radiology, bone densitometry and biochemical determinations of mineral metabolism at the beginning of therapy. Treatment with high doses of intravenous pamidronate (225 mg in 3 months), calcitonin (200/400 IU daily), tiazide (25 mg/daily), and kinesiotherapy mitigated the pain quickly and she recovered motility. We discuss this approach of treating osteoporosis with corticoids and immunosuppressors according to the present knowledge of bone biology.

Osteoporosis vertebral inducida por corticoides y ciclosporina en una paciente con enfermedad de Still. / [Vertebral osteoporosis induced by corticoids and cyclosporine ina a patient with Still disease]

We report on a 29-year-old patient who received high doses of prednisone and cyclosporine for the treatment of Still disease. She consulted about dorsolumbar pain leading to physical disability. She presented multiple vertebral fractures, decreased lumbar bone mineral density in the rank of osteoporosis, high bone turnover, and associated hypercalciuria. Cyclosporine and corticoids induced severe changes in bone and mineral metabolism. All patients in treatment with these drugs should undergo radiology, bone densitometry and biochemical determinations of mineral metabolism at the beginning of therapy. Treatment with high doses of intravenous pamidronate (225 mg in 3 months), calcitonin (200/400 IU daily), tiazide (25 mg/daily), and kinesiotherapy mitigated the pain quickly and she recovered motility. We discuss this approach of treating osteoporosis with corticoids and immunosuppressors according to the present knowledge of bone biology.

[Osteoporosis in pregnancy and lactation]. / Osteoporosis en embarazo y lactancia.

Normal pregnancy and lactation lead to a combination of adaptive metabolic responses, the end result of which is to assure adequate delivery of mineral to the fetus while affording protection to the maternal skeleton. Elevated circulating levels of 1.25-OH vitamin D lead to increased efficiency of maternal intestinal calcium absorption and possibly lead to hypersecretion of calcitonin. Although serum concentrations of parathyroid hormone do not change during pregnancy, increased levels of a related hormone, PTH-related peptide, seem to contribute to a state of maternal functional hyperparathyroidism and maintain the fetal-maternal calcium gradient necessary to provide calcium to the fetus. Bone turnover increases during lactation and diminishes urinary calcium loss mobilizing mineral for the milk. Elevated levels of ionized calcium and phosphorus possibly correlate with increased bone resorption and decreased urinary excretion of these minerals. Bone mass is not normally lost during pregnancy but may decrease with sustained lactation for as long as six months. If lactation ceases before nine months, however, bone mass usually is restored. However, several rare forms of osteoporosis have been associated with pregnancy and lactation.

Osteoporosis en embarazo y lactancia. / [Osteoporosis in pregnancy and lactation]

Normal pregnancy and lactation lead to a combination of adaptive metabolic responses, the end result of which is to assure adequate delivery of mineral to the fetus while affording protection to the maternal skeleton. Elevated circulating levels of 1.25-OH vitamin D lead to increased efficiency of maternal intestinal calcium absorption and possibly lead to hypersecretion of calcitonin. Although serum concentrations of parathyroid hormone do not change during pregnancy, increased levels of a related hormone, PTH-related peptide, seem to contribute to a state of maternal functional hyperparathyroidism and maintain the fetal-maternal calcium gradient necessary to provide calcium to the fetus. Bone turnover increases during lactation and diminishes urinary calcium loss mobilizing mineral for the milk. Elevated levels of ionized calcium and phosphorus possibly correlate with increased bone resorption and decreased urinary excretion of these minerals. Bone mass is not normally lost during pregnancy but may decrease with sustained lactation for as long as six months. If lactation ceases before nine months, however, bone mass usually is restored. However, several rare forms of osteoporosis have been associated with pregnancy and lactation.

[Post-transplantation osteoporosis]. / Osteoporosis postrasplante.

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.

Osteoporosis postrasplante. / [Post-transplantation osteoporosis]

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.

[Hypervitaminosis D in institutionalized elderly in Buenos Aires]. / Hipovitaminosis D en ancianos institucionalizados de Buenos Aires.

Several studies have shown that vitamin D (Vit. D) deficiency in elderly people enhances bone mass loss. Most of these studies have been carried out in areas of low solar irradiation. In order to establish Vit. D circulating levels in elderly people in our community (34 degrees S) and their relationship with bone metabolism, 34 men and 33 women were studied at the end of the summer. These subjects, all residents of nursing homes, had a mean age of 81.9 + 8.1 years (range 69-99). Calcemia, parathyroid hormone (PTH and 25-hydroxyvitamin D (25(HO)D) were measured in serum and bone markers in serum and urine. Bone densitometry (BMD) of cortical and trabecular bone in the forearm (distal third of the radius (R33%) and ultradistal (RUD), respectively) were performed using X-ray absorptiometry. We found: 1) Low serum 25(HO)D (14.4 + 1.7 ng/ml) at summer's end. 40.5% showed levels < 10 ng/ml. 2) Secondary hyperparathyroidism (PTH: 169.4 + 30.9 pg/ml), 3) Hypocalcemia was observed in 34.5% of elderly people, 4) increased bone turnover in the subpopulation with hypovitaminosis D. 5) The serum levels of 25(HO)D correlated with BMD R33% (r = 0.55, n = 54, P < 0.001), with BMD RUD (r = 0.50, n = 54, P < 0.001) and with PTH (r = -0.44, n = 42, P < 0.01). A deficiency of Vit.D was found in our population of elderly people, probably due to diminished epidermic production of its precursors and/or to scant exposure to sunlight in the elderly. The decrease is associated to age. The positive correlation of 25(HO)D with bone mass (cortical and trabecular bone) underscores its importance for the preservation of bone mass. Hyperparathyroidism, triggered by Vit. D deficit, enhances bone loss.

Impairment of gamma carboxylation of circulating osteocalcin (bone gla protein) in elderly women.

Osteocalcin, also called bone gla protein, is a unique noncollagenous protein of the extracellular matrix of bone that circulates in blood. Oseteocalcin contains three residues of the vitamin K-dependent gamma-carboxyglutamic acid (gla) responsible for the affinity of osteocalcin for bone mineral. In animals treated with the vitamin K antagonist warfarin, the osteocalcin content of bone is markedly reduced and the fraction of osteocalcin released into the circulation is increased. Most studies have shown that osteocalcin increases with aging in women, reflecting an increase in bone turnover, especially after the menopause. To determine if this increase in osteocalcin could be associated with impaired carboxylation, we measured total and noncarboxylated osteocalcin in the serum of 72 women of various ages: 22 premenopausal (31 +/- 7 years old), 20 early postmenopausal (54 +/- 3 years), and 30 elderly women (85 +/- 8 years). As previously reported, total serum osteocalcin was significantly increased in early postmenopausal and elderly women. Noncarboxylated serum osteocalcin was slightly increased in early postmenopausal women (0.95 +/- 0.4 versus 0.65 +/- 0.5 ng/ml in premenopausal women), markedly elevated in elderly women (1.59 +/- 1.1 ng/ml, p less than 0.001), and correlated with age (r = 0.47, p less than 0.001). Elderly women had values of the same magnitude as in 10 patients on chronic warfarin therapy (1.94 +/- 1.1 ng/ml). As a consequence, the increase in carboxylated serum osteocalcin was significant in early postmenopausal women but not in elderly women. Serum levels of vitamin K1 and of menaquinones 6, 7, and 8 were measured in some of the young and elderly women.(ABSTRACT TRUNCATED AT 250 WORDS)

Differential action of pamidronate on trabecular and cortical bone in women with involutional osteoporosis.

Since osteoporotic fractures are mainly related to the diminution of the bone mineral density (BMD), the effect of pamidronate (3-amino-1-hydroxy-propylidene) 1,1-bisphosphonate on the BMD of the spine, proximal femur and radius shaft was evaluated in an initial cohort of 35 postmenopausal women with at least one vertebral fracture due to involutional osteoporosis. Pamidronate was given continuously during 18 months in a daily oral dose of 4.8 to 6.0 mg/kg supplemented with calcium (1 g/day). BMD--measured by dual photon absorptiometry--increased after one year 5.3 +/- 1.0% (P less than 0.001) in lumbar spine and 5.3 +/- 1.5% (P less than 0.001) over trochanter. However no significant changes were observed in the BMD of the femoral neck, Ward's triangle or in the cortical bone of the radius shaft measured by single photon absorptiometry. Pamidronate also decreased significantly urinary hydroxyproline-creatinine excretion after 6 months and thereafter maintained a plateau. After 18 months of treatment the diminution was 42.6 +/- 4.9% (P less than 0.001). The differing effects of pamidronate on the BMD of lumbar spine and proximal femur might be ascribed to dissimilarities between the proportions of trabecular and cortical bone in these. These results suggest that pamidronate may be prescribed to prevent fractures in cases of involutional osteoporosis with a significant decrease of BMD in lumbar spine and/or trochanter.