Osteoporosis en el varón / Osteoporosis in men

La osteoporosis en hombres continúa estando infradiagnosticada e infratratada. Su presencia obliga a descartar condiciones o enfermedades predisponentes. Se deben recomendar medidas de prevención generales y cuando sea necesario también suplementación con 1.200mg/día de calcio y, al menos, 800UI/día de vitamina D. Los bisfosfonatos (BF), específicamente alendronato y risedronato, son el tratamiento de elección en los varones con osteoporosis. En los casos graves con alto riesgo de fractura y en los pacientes con fallo terapéutico con los BF o que no toleren estos fármacos puede estar aconsejado el uso de teriparatida (TRPT) . La evidencia disponible sugiere que la eficacia antifractura del tratamiento con alendronato, risedronato y TRPT es similar en ambos sexos. Los andrógenos solo están justificados si existe hipogonadismo clínico. Aun en ese caso, probablemente deban asociarse BF o TRPT si el riesgo de fractura es muy elevado a pesar de la sustitución androgénica(AU)

Osteoporosis in men continues to be underdiagnosed and undertreated. Its presence makes it necessary to rule out predisposing conditions and diseases. General prevention measures should be recommended and when necessary also supplementation with 1200mg/day of calcium and at least 800IU/day of vitamin D. Bisphosphonates, specifically alendronate (ALN) and risedronate (RSN), are the treatment of choice in men with osteoporosis. In severe cases with high risk of fracture and in patients with therapeutic failure with the bisphosphonates or who do not tolerate these drugs, the use of teriparatide may be recommended. The evidence available suggests that anti-fracture efficacy of treatment with ALN, RSN and teriparatide is similar in both genders. Androgens are only justified if there is clinical hypogonadism. Even in this case, bisphosphonates or teriparatide should probably be associated if the risk of fracture is very high in spite of androgen replacement(AU)

[Osteoporosis in men]. / Osteoporosis en el varón.

Osteoporosis in men continues to be underdiagnosed and undertreated. Its presence makes it necessary to rule out predisposing conditions and diseases. General prevention measures should be recommended and when necessary also supplementation with 1200mg/day of calcium and at least 800IU/day of vitamin D. Bisphosphonates, specifically alendronate (ALN) and risedronate (RSN), are the treatment of choice in men with osteoporosis. In severe cases with high risk of fracture and in patients with therapeutic failure with the bisphosphonates or who do not tolerate these drugs, the use of teriparatide may be recommended. The evidence available suggests that anti-fracture efficacy of treatment with ALN, RSN and teriparatide is similar in both genders. Androgens are only justified if there is clinical hypogonadism. Even in this case, bisphosphonates or teriparatide should probably be associated if the risk of fracture is very high in spite of androgen replacement.

Bone disease induced by phenytoin therapy: clinical and experimental study.

Previous studies have made references to prolonged treatment with phenytoin as a possible risk factor in the development of osteoporosis and/or osteomalacia. We studied a group of 30 epileptic patients who were under long-term treatment with phenytoin (DPH) in an ambulatory regimen. We found the prevalence of osteoporosis to be 3.3% and of osteopenia to be 56.6%, affecting predominantly the femur, without any significant decrease in bone mineral density of the lumbar spine. These patients were showing signs of bone turnover uncoupling with increases in bone resorption markers. At this time, they also exhibited slight alterations in their phosphocalcium metabolism with trends to hypocalcemia and secondary hyperparathyroidism that was found not to be caused by a vitamin D deficiency as the serum levels of 25(OH)D and 1,25(OH)(2)D were normal. With the aims of corroborating these results and to investigate the physiopathological effects on the bone induced by anticonvulsant drugs we developed a further experimental study in which we administered DPH over a 6-week period with a dose of 5 g/kg/day to male Wistar rats that were in the growth phase. This treatment produced a decrease in overall BMD and bone mineral content in the femur. We did not find osteomalacia in the vertebral biopsy, but the administration of DPH to these animals decreased trabecular volume as well as lessened the thickness of osteoid edges together with an uncoupling in bone turnover. There was also a marked decrease in bone formation and a tendency towards increased bone resorption. We have also found a decrease in resistance to fracture by torsion in the biomechanical assay, which translates into an increase in bone fragility. In these male Wistar rats, the administration of DPH produced a tendency towards increasing the markers of resorption and, though changes in serum levels of calcium and phosphorus were not observed, to provoke an increase in the parathyroid hormone levels; with normal levels of 1,25(OH)(2)D which has produced the same inclination in rats as in humans.

[Benign familial hyperphosphatasemia. A report of one case and diagnostic considerations]. / Hiperfosfatasemia familiar. Reporte de un caso y consideraciones diagnósticas.

Benign familial hyperphosphatasemia is a rare biochemical abnormality characterized by the presence of persistently elevated levels of serum alkaline phosphatase in several members of the same familiy, in the absence of disease or any known cause of hyperphosphatasemia. We describe one family affected with this biochemical abnormality and the epidemiology, genetic, isoenzymatic patterns and clinical significance of this entity are discussed.A 61-year-old man was referred to the Unit of Metabolic Bone Diseases for investigation of a lumbar pain with a history of urolithiasis and inguinofemoral hernia repair. The results of the physical examination and laboratory analysis were normal except for a high serum alkaline phosphatase level of 690 UI/l (reference range 40-129 UI/l). Isoenzymatic profile showed a 50% of intestinal variant, 33% of bone variant and 17% of liver variant isoenzymes. Skeletal radiographs and lumbar magnetic resonance imaging showed signs of osteoarthritis in the spine, bone scan showed a skeletal distribution of the radioisotope.One year later the biochemical exams showed similar raised levels of alkaline phosphatase. Family investigation revealed that one of the three sons of the patient had the same biochemical disorder.

Hiperfosfatasemia familiar. Reporte de un caso y consideraciones diagnósticas / Benign familial hyperphosphatemia. A report of one case and diagnostic considerations

La hiperfosfatasemia benigna familiar es una rara anomalía bioquímica caracterizada por la presencia de niveles persistentemente elevados de fosfatasa alcalina sérica en varios miembros de una misma familia en ausencia de una enfermedad o causa conocida de hiperfosfatasemia. Describimos un caso y discutimos todos los aspectos epidemiológicos, genéticos, patrones isoenzimáticos y significado clínico asociados a esta entidad. Varón de 61 fue remitido a la consulta de enfermedades metabólicas óseas para valoración de lumbalgia y con antecedentes personales de urolitiasis y herniorrafia inguinal. La exploración física y análisis de laboratorio resultaron normales excepto por niveles elevados de fosfatasa alcalina total de 690 UI/l (rango de referencia 40-129 UI/l). El perfil de las isoenzimas era de 50% isoenzima intestinal, 33% isoenzima ósea y 17% de isoenzima hepática. Radiografias y resonancia magnética nuclear de la columna lumbar mostraron signos de espondiloartrosis y la gammagrafía ósea resultó normal en la distribución del radioisótopo. Un año más tarde la bioquímica mostraba niveles similarmente aumentados de fosfatasa alcalina. El estudio familiar encontró que uno de los tres hijos del paciente presentaba el mismo trastorno bioquímico

Benign familial hyperphosphatasemia is a rare biochemical abnormality characterized by the presence of persistently elevated levels of serum alkaline phosphatase in several members of the same familiy, in the absence of disease or any known cause of hyperphosphatasemia. We describe one family affected with this biochemical abnormality and the epidemiology, genetic, isoenzymatic patterns and clinical significance of this entity are discussed. A 61-year-old man was referred to the Unit of Metabolic Bone Diseases for investigation of a lumbar pain with a history of urolithiasis and inguinofemoral hernia repair. The results of the physical examination and laboratory analysis were normal except for a high serum alkaline phosphatase level of 690 UI/l (reference range 40-129 UI/l). Isoenzymatic profile showed a 50% of intestinal variant, 33% of bone variant and 17% of liver variant isoenzymes. Skeletal radiographs and lumbar magnetic resonance imaging showed signs of osteoarthritis in the spine, bone scan showed a skeletal distribution of the radioisotope. One year later the biochemical exams showed similar raised levels of alkaline phosphatase. Family investigation revealed that one of the three sons of the patient had the same biochemical disorder

Fármacos que inducen osteomalacia / Osteomalacia inducing drugs

No disponbile (AU)

Fármacos que afectan el metabolismo del hueso / Drugs affecting bone metabolism

No disponible

Los inhibidores de la hmg-coa reductasa en el tratamiento de la osteoporosis / HMG-CoA reductase inhibitors in the therapy of the osteoporosis

No disponible

[Spontaneous bacterial peritonitis in the cirrhotic patient]. / Peritonitis bacteriana espontánea en el paciente cirrótico.

Spontaneous bacterial peritonitis in cirrhotic patients is a severe complication which frequently decompensate the underlying disease and which is associated, even in our days, to a 50% mortality. Hence, the relevance of an adequate exploration, as weil as an early treatment. The acknowledge of several variants, as are the concepts of bacterascites and neutrocytic ascites with negative culture required the use of updated diagnostic criteria. In addition to the already known clinical and bacteriological characteristics of the ascitic fluid infection, we have also intended to review new aspects of this entity referred to in the literature published in the past years, as are the followings; study of possible predictive factors of this complication and factors which have an influence on its mortality, in order to be able to implement the most adequate preventive its mortality, in order to be able to implement the most adequate preventive its mortality, in order to be able to implement the most adequate preventive and curative therapeutics.

[Pseudo-thrombophlebitis syndrome: diagnostic and therapeutic considerations of 2 cases]. / Síndrome pseudotromboflebítico: consideraciones diagnósticas y terapéuticas a propósito de dos casos.

Pseudo-thrombophlebitic syndrome is a frequent clinical entity but many times insufficiently diagnosed. Described more than a century ago by Baker it is characterized for being clinically undistinguishable from a true thrombophlebitis, being its cause the presence of a synovial cyst in the knee joint (Baker's cyst) which can be complicated or not (breakage or dissection). Diagnosis is easy and is based mainly in echography and arthrography. The anticoagulant therapy used in true thrombophlebitis is contraindicated in this syndrome.