Buscar en
Endocrinología y Nutrición
Toda la web
Inicio Endocrinología y Nutrición Evolución del hiperparatiroidismo primario en 56 pacientes. Comparación entre ...
Información de la revista
Vol. 54. Núm. 7.
Páginas 347-353 (Agosto 2007)
Compartir
Compartir
Descargar PDF
Más opciones de artículo
Vol. 54. Núm. 7.
Páginas 347-353 (Agosto 2007)
Originales
Acceso a texto completo
Evolución del hiperparatiroidismo primario en 56 pacientes. Comparación entre hiperparatiroidismo hipercalcémico y normocalcémico
Progression of primary hyperparathyroidism in 56 patients. Comparison between hypercalcemic and normocalcemic hyperparathyroidism
Visitas
5543
Cristina Familiara,
Autor para correspondencia
crisfami@terra.es

Correspondencia: Dra. C. Familiar. Servicio de Endocrinología. Hospital Virgen de la Salud. Av. de Barber, s/n. 45004 Toledo. España.
, Bárbara Cánovasa, Manuel Ángel Gargallob, Julia Sastrea, Amparo Marcoa, Almudena Vicentea, José Lópeza, Enrique Castroa
a Servicio de Endocrinología. Hospital Virgen de la Salud. Toledo. España
b Servicio de Endocrinología. Hospital Virgen de la Torre. Madrid. España
Este artículo ha recibido
Información del artículo
Resumen
Bibliografía
Descargar PDF
Estadísticas
Introducción

Actualmente, el hiperparatiroidismo primario (HPP) se considera una enfermedad escasamente sintomática y poco progresiva. El HPP normocalcémico (HPPN) es una entidad reconocida e identificada esencialmente por complicaciones asociadas al HPP (osteoporosis y urolitiasis).

Pacientes y método

Estudio de 56 pacientes con HPP no operados o con seguimiento mínimo de 1 año previo a la paratiroidectomía. Se subdividió a los pacientes en HPP hipercalcémico (HPPH) (27 pacientes) y HPPN (29 pacientes). Se pretendió analizar las comorbilidades hipertensión arterial [HTA] y nefrolitiasis) en el grupo total y en cada subgrupo, valorar la evolución anual de calcemia, fosfatemia, paratirina PTH) y fosfatasa alcalina séricas, calciuria, filtrado glomerular y densidad mineral ósea lumbar durante un período de 1 a 5 años y hallar posibles diferencias entre HPPH y HPPN para estas variables.

Resultados

El 55,4% de los pacientes presentaban HTA y se registraron episodios de nefrolitiasis en el 37,5% de los casos. No se apreciaron cambios a lo largo del tiempo en los parámetros bioquímicos y densitométricos ni en el grupo total ni por subgrupos. Excepto en los valores de calcio, fósforo y PTH séricos no se hallaron diferencias entre HPPH y HPPN.

Conclusiones

El HPP parece una enfermedad poco progresiva si bien no se incluyó en este estudio a los pacientes remitidos precozmente a cirugía con seguimiento previo escaso que podrían corresponder a casos más agresivos. El HPPN es una entidad asociada a complicaciones similares a las del HPPH por lo que pensamos debería someterse a los mismos criterios de derivación quirúrgica.

Palabras clave:
Hiperparatiroidismo primario
Hiperparatiroidismo normocalcémico
PTH
Paratirina
Calciuria
Calcemia
Fosfatemia
Osteoporosis
Nefrolitiasis
Introduction

Primary hyperparathyroidism (PHP) is considered a relatively stable, asymptomatic disease. Normocalcemic PHP (NPHP) is now a recognized entity that is usually diagnosed through its associated complications (such as osteoporosis and nephrolithiasis).

Patients and method

We studied 56 patients with PHP who did not undergo surgery or who completed a minimum follow-up of 1 year before parathyroid surgery. The group was subdivided into patients with hypercalcemic PHP (HPHP) (27 patients) and those with NPHP (29 patients). The presence of comorbidities (hypertension, nephrolithiasis) was analyzed in the whole group and in each subset of patients, as was yearly progression of calcemia, phosphatemia, serum parathyroid hormone (PTH) and alkaline phosphatase, urinary calcium, glomerular filtration rate and bone mineral density in the lumbar spine during a follow-up period ranging from 1 to 5 years. Possible differences in these variables between HPHP and NPHP were also studied.

Results

A total of 55.4% of the patients were hypertensive and nephrolithiasis events were reported in 37.5%. No changes were observed in biochemical or densitometric variables over time or in the whole group or in the subgroups. Except for serum calcium, phosphate and PTH values, no differences were found between HPHP and NPHP.

Conclusions

PHP seems to be a relatively stable disease, although patients referred early to surgery with a short follow-up, who could have had more aggressive kinds of PHP, were not included in this study. The complications of NPHP are similar to those of HPHP and therefore we believe the same recommendations for surgery should be followed in both forms.

Key words:
Primary hyperparathyroidism
Normocalcemic hyperparathyroidism
PTH
Parathyroid hormone
Calciuria
Calcemia
Phosphatemia
Osteoporosis
Nephrolithiasis
El Texto completo está disponible en PDF
Bibliografía
[1.]
S.J. Silverberg, J.P. Bilezikian.
Evaluation and management of primary hyperparathyroidism.
J Clin endocrinol Metab, 81 (1996), pp. 2036-2040
[2.]
G. Albright, J. Aub, W. Bauer.
Hyperparathyroidism. A common and polymorphic condition as illustrated by seventeen proved cases from one clinic.
JAMA, 102 (1934), pp. 1276-1287
[3.]
O. Cope.
The study of hyperparathyroidism at the Massachusetts General Hospital.
N Engl J Med, 274 (1966), pp. 1174-1182
[4.]
S.J. Silverberg, E. Shane, T.P. Jacobs, E. Siris, J.P. Bilezikian.
A 10-year prospective study of hyperparathyroidism with or without parathyroid surgery.
N Engl J Med, 341 (1999), pp. 1249-1255
[5.]
D.A. Sholz, D.C. Purnell.
Asymptomatic primary hyperparathyroidism: 10-year prospective study.
Mayo Clin Proc, 56 (1981), pp. 473-478
[6.]
M. Palmer, H.O. Adami, R. Bergstrom, G. Akerstrom, H. Adami, S. Jakobsson, et al.
Survival and renal function in persons with untreated hypercalcemia. Population-based cohort study with 14 years of follow up.
Lancet, 1 (1987), pp. 59-62
[7.]
D.S. Rao, R.J. Wilson, M. Kleerekoper.
Lack of biochemical progression or continuation of accelerated bone loss in mild asymptomatic primary hyperparathyroidism: evidence for biphasic disease course.
J Clin Endocrinol Metab, 67 (1988), pp. 1294-1298
[8.]
L. Lind, S. Jacobsson, M. Palmer, H. Lithell, B. Wengle, S. Ljunghall.
Cardiovascular risk factors in primary hyperparathyroidism: a 15-year follow-up of operated and unoperated cases.
J Intern Med, 230 (1991), pp. 29-35
[9.]
NIH Consensus Development Panel: Diagnosis and management of asymptomatic primary hyperparathyroidism: Consensus Development Conference Statement.
Ann Intern Med, 114 (1991), pp. 593-597
[10.]
J.P. Bilezikian, J.T. Potts Jr, G. Fuleihan, M. Kleerekoper, R. Neer, M. Peacock, et al.
Summary statement from a workshop on asymptomatic primary hyperparathyroidism: a perspective for the 21st century.
J Clin Endocrinol Metab, 87 (2002), pp. 5353-5361
[11.]
R.A. Wermers, S. Khosla, E. Atkinson, C. Grant, S. Hodgson, M. O’Fallon, et al.
Survival after the diagnosis oh hyperparathyroidism. A population-based study.
Am J Med, 104 (1998), pp. 115-122
[12.]
R.A. Wermers, S. Khosla, E. Atkinson, S.F. Hodgson, W.M. O’Fallon, L.J. Melton.
The rise and fall of primary hyperparathyroidism: a population-based study in Rochester, Minnesota,1965-1992.
Ann Intern Med, 126 (1997), pp. 433-440
[13.]
A.G. Bondeson, L. Bondeson, N.W. Thompson.
Clinicopathological peculiarities in parathyroid disease with hypercalcaemic crisis.
Eur J Surg, 159 (1993), pp. 613-617
[14.]
I. Hajjar, T.A. Kotchen.
Trends in prevalence, awareness, treatment and control of hypertension in the United States,1988-2000.
JAMA, 290 (2003), pp. 199-206
[15.]
T. Stefenelli, C. Abela, H. Frank, J. Koller-Strametz, S. Globits, J. Bergjer-Klein, et al.
Cardiac abnormalities in patients with primary hiperparathyroidism: implications for follow-up.
J Clin Endocrinol Metab, 82 (1997), pp. 106-112
[16.]
L. Lind, A. Hvarfner, M. Palmer.
Hypertension in primary hyperparathyroidism in relation to histopathology.
Eur J Surg, 157 (1991), pp. 457-459
[17.]
L. Lind, S. Ljunghall.
Pre-operative evaluation of risk factors for complications in pacients with primary hiperparathyroidism.
Eur J Clin Invest, 25 (1995), pp. 955-958
[18.]
S.J. Silverberg, F. Gartenberg, T.P. Jacobs, E. Shane, E. Siris, R.B. Staron, et al.
Increased bone mineral density after parathyroidectomy in primary hyperparathyroidism.
J Clin Endocrinol Metab, 80 (1995), pp. 729-734
[19.]
P. Glendenning, B.G. Stuckey, D.H. Gutteridge, R.W. Retallach, B.G. Stuckey, D.G. Kermode, et al.
High prevalence of normal total calcium and intact PTH in 60 patients with proven primary hyperparathyroidism: a challenge to current diagnostic criteria.
Aust N Z J Med, 28 (1998), pp. 173-178
[20.]
H. Oberleithner, R. Greger, F. Lang.
The effect of respiratory and metabolic acid-base changes on ionized calcium concentration.
Eur J Clin Invest, 12 (1982), pp. 451-455
[21.]
S. Wang, E.H. McDonnell, F.A. Sedor, J.G. Toffaletti.
pH effects on measurements of ionized calcium and ionized magnesium in blood.
Arch Pathol Lab Med, 126 (2002), pp. 947-950
[22.]
V. LoCascio, S. Adami, G. Galvanini.
Substrate-product relation of 1-hydroxilase activity in primary hiperparathyroidism.
N Engl J Med, 313 (1985), pp. 1123-1125
[23.]
E. Lundgren, D.G. Hagstrom, J. Lundin.
Primary hyperparathyroidism revisited in menopausal women with serum calcium in the upper normal range at population-based screening 8 years ago.
World J Surg, 26 (2002), pp. 931-936
[24.]
E. Lundgren, P. Ridefelt, G. Akerstrom, S. Ljunhall, J. Rastad.
Parathyroid tissue in normocalcemic primary hyperparathyroidism recruited by health sceeening.
World J Surg, 20 (1996), pp. 727-735
[25.]
K.M. Tordjman, Y. Greenman, O.E. Osher, G. Shenkerman, N. Stern.
Characterization of normocalcemic primary hyperparathyroidism.
Am J Med, 117 (2004), pp. 861-863
[26.]
G. Maruani, A. Hertig, M. Paillard, P. Houillier.
Normocalcemic primary hyperparathyroidism: evidence for a generalized target-tissue resistance to parathyroid hormone.
J Clin Endocrinol Metab, 88 (2003), pp. 4641-4648
[27.]
S.J. Silverberg, J.P. Bilezikian.
“Incipient” primary hyperparathyroidism: a forme “frustre” of an old disease.
J Clin Endocrinol Metab, 88 (2003), pp. 5348-5352
[28.]
H. Murer.
Cellular mechanisms in proximal tubular Pi reabsortion: some answers and more questions.
J Am Soc Nephrol, 2 (1992), pp. 1649-1665
[29.]
S.H. Silvelberg, E. Shane, T.P. Jacobs, E.S. Siris, F. Gartemberg, D. Seldin, et al.
Nephrolithiasis and bone involvement in primaryhyperparathyroidism.
Am J Med, 89 (1990), pp. 327-334
[30.]
J.P. Bilezikian, S.H. Silverberg, F. Gartenberg.
Clinical presentation of primary hyperparathyroidism.
The parathyroids: basic and clinical concepts, pp. 457-470
[31.]
J. Parks, F. Coe, M. Favus.
Hyperparathyroidism in nephrolitiasis.
Arch Intern Med, 140 (1980), pp. 1479-1481
[32.]
A.E. Broadus, R.L. Horst, R. Lang, E.T. Littledike, H. Rasmussen.
The importance of circulating 1 25-dihydroxivitamin D in the pathogenesis of hypercalciuria and renal stone in primary hyperparathyroidism.
N Engl J Med, 302 (1980), pp. 421-426
[33.]
S.J. Silverberg, J.P. Bilezikian.
Primary hyperparathyroidism stillevolving?.
J Bone Miner Res, 12 (1997), pp. 856-862
[34.]
C.Y.C. Pak, K. Holt.
Nucleation and growth of brushite and calcium in urine of stone formers.
Metabolism, 25 (1976), pp. 665-673
[35.]
C.L. Mollerup, P. Vestergaard, V.G. Frokjaer, L. Mosekilde, P. Christiansen, M. Blichert-Toft.
Risk of renal stones events in primary hyperparathyroidism before and after parathyroid surgery: controlled retrospective follow-up study.
BMJ, 325 (2002), pp. 807
[36.]
A. Piovesan, N. Molieri, F. Cassaso, I. Emmolo, G. Ugliengo, F. Cesario, et al.
Left ventricular hypertrophy in primary hyperparathyroidism Effects of successful parathyroidectomy.
Clin Endocrinol, 50 (1999), pp. 321-328
[37.]
A.E. Siperstein, W. Shen, A.K. Chan, Q.Y. Duh, O.H. Clark.
Normocalcemic hyperparthyroidism Biochemical and symptom profiles before and after surgery.
Arch Surg, 127 (1992), pp. 1157-1166
[38.]
E.R. Yendt, R.J. Gagne.
Detection of primary hyperparthyroidism, with special reference to its occurrence in hypercalciuric females with normal or borderline serum calcium.
CMAJ, 98 (1968), pp. 331-336
[39.]
V.M. Duncombe, R.W.E. Watts, T.J. Peters.
Studies on intestinal calcium absorption in patients with idiopathic hypercalciuria.
Q J Med, 209 (1984), pp. 69-79
[40.]
P. Bataille, J.M. Achard, A. Fournier, B. Boudailliez, P.F. Westeel, N. el Esper, et al.
Diet, vitamin D and vertebral mineral density in hypercalciuric calcium stone formers.
Kidney Int, 39 (1991), pp. 1193-1205
[41.]
K.L. Insogna, A.E. Broadus, B.E. Dreyer, A.F. Ellison, J.M. Gertner.
Elevated production rate of 1,25 dihydroxyvitamin D in patients with absortive hypercalciuria.
J Clin Endocrinol Metab, 61 (1985), pp. 490-495
[42.]
F.L. Coe, J.M. Canterbury, J.J. Firpo, E. Reiss.
Evidence for secondary hyperparathyroidism in idiopathic hypercalciuria.
J Clin Invest, 52 (1973), pp. 134-142
[43.]
J.E. Zerwekh, C.Y.C. Pak.
Selective effects of thiazide therapy on serum 1 25-dihydroxy-vitamin D and intestinal calcium absorption in renal and absortive hypercalciurias.
Metabolism, 29 (1980), pp. 13-17
[44.]
D.C. Purnell, D.A. Scholz, L.H. Smith, G.W. Sizemore, M.B. Black, R.S. Glodsmith, et al.
Treatment of primary hyperparathyroidism.
Am J Med, 56 (1974), pp. 800-809
[45.]
J. Coresh, B.C. Astor, T. Greene, G. Eknoyan, A.S. Levey.
Prevalence of chronic kidney disease and decreased kidney function in the adult US population: third National Health and Nutrition Examination Survey.
Am J Kidney Dis, 41 (2003), pp. 1-12
[46.]
D.F. Davies, N.W. Shoch.
Age changes in glomerular filtration rate, effective renal plasma flow and tubular excretory capacity in adult males.
J Clin Invest, 29 (1950), pp. 496-507
[47.]
S.J. Silverberg, E. Shane, L. De la Cruz, D.W. Dempster, F. Feldman, D. Seldin, et al.
Skeletal disease in primary hyperparathyroidism.
J Bone Miner Res, 4 (1989), pp. 283-291
[48.]
C.R. Parker, P.J. Blackwell, K.J. Fairbairn, D.J. Hosking.
Alendronate in the treatment of primary hyperparthyroidim-related osteoporosis: a 2-year study.
J Clin Endocrinol Metab, 87 (2002), pp. 4482-4489
[49.]
C.C. Chow, W.B. Chan, J.K. Li, N.N. Chan, M.H. Chan, G.T. Ko, et al.
Oral alendronate increases bone mineral density in potmenopausal women with primary hyperparathyroidism.
J Clin Endocrinol Metab, 88 (2003), pp. 581-587
[50.]
S.J. Silverberg, E. Shane, D.W. Dempster, J.P. Bilezikian.
The effect of vitamin insufficiency in pacients with primary hyperparathyroidism.
Am J Med, 107 (1999), pp. 561-567
[51.]
V. Kantorovich, M.A. Gacad, L.L. Seeger, J.S. Adams.
Bone mineral density increases with vitamin D repletion in pacients with coexistent vitamin D insufficiency and primary hyperparathyroidism.
J Clin Endocrinol Metab, 85 (2000), pp. 3541-3543
[52.]
P. Christiansen, T. Steiniche, K. Brixen, I. Hessov, F. Melsen, L. Heickendorff, et al.
Primary hyperparathyroidism: Biochemical markers and bone mineral density at multiple skeletal sites in Danish patients.
Bone, 21 (1997), pp. 93-99
[53.]
S.J. Silverberg, F. Gartenberg, T.P. Jacobs, E. Shane, E. Siris, R.B. Staron, et al.
Longitudinal measurements of bone mineral density and biochemical indices in untreated primary hyperparathyroidism.
J Clin Endocrinol metab, 80 (1995), pp. 723-728
[54.]
M. Parisien, F. Cosman, R.W. Mellish, M. Schnitzer, J. Nieves, S.J. Silverberg, et al.
Bone structure in postmenopausal hyperparathyroidism, osteoporotic, and normal women.
J Bone Miner Res, 10 (1995), pp. 1393-1399
[55.]
D.W. Dempster, M. Parisien, S.J. Silverberg, X.G. Liang, M. Schintzer, V. Sher, et al.
On the mechanisms of cancellous bone preservation in potmenopausal women with primary hyperparathyroidism.
J Clin Endocrinol Metab, 84 (1999), pp. 1562-1566
[56.]
S. Khosla, L.J. Melton, R.A. Wermers, C.S. Crowson, W.M. O’Fallon, B.L. Riggs.
Primary hyperparathyroidism and the risk of fracture: a population-based study.
J Bone Miner Res, 14 (1999), pp. 1700-1707
[57.]
A.M. Kenny, D.C. MacGillivray, C.C. Pilbeam, H.D. Crombie, L.G. Raisz.
Fracture incidence in postmenopausal women with primary hyperparathyroidism.
Surgery, 118 (1995), pp. 109-114
[58.]
S.J. Silverberg, F.G. Locker, J.P. Bilezikian.
Vertebral osteopenia: a new indication for surgery in primary hyperparathyroidism.
J Clin Endocrinol Metab, 81 (1996), pp. 4007-4012
[59.]
P. Vestergaard, C.L. Mollerup, V.G. Frokjaer, P. Christiansen, M. Blichert-Joft, L. Mosekilde.
Cohort study of risk fracture before and after surgery for primary hyperparathyroidism.
BMJ, 321 (2000), pp. 598-602
Copyright © 2007. Sociedad Española de Endocrinología y Nutrición
Opciones de artículo
Herramientas
es en pt

¿Es usted profesional sanitario apto para prescribir o dispensar medicamentos?

Are you a health professional able to prescribe or dispense drugs?

Você é um profissional de saúde habilitado a prescrever ou dispensar medicamentos