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Hiperparatiroidismo asociado a hipovitaminosis D
- 1. HIPERPARATIROIDISMO PRIMARIO e HIPOVITAMINOSIS D Dr. Pablo Potthoff Residente Medicina Interna Universidad de la Frontera, Enero 2010
- 3. RECEPTOR SENSOR DE CALCIO VESICULA DE PTH CELULA PRINCIPAL RECEPTOR SENSOR DE CALCIO
- 5. SANGRE CELULA PARATIROIDEA REGULACION DEL METABOLISMO DEL CALCIO AUMENTO REABSORCION DE CALCIO SINTESIS 1-25 OH VITAMINA D AUMENTO RESORCION OSEA AUMENTO ABSORCION INTESTINAL DE CALCIO MODIFICADO – NEJM- Volume 343 Number 25 CALCIO
- 6. NEJM - Volume 343 Number 25 - DIAGNOSTICO DIFERENCIAL PTH - CALCEMIA HIPOPARATIROISDISMO PRIMARIO
- 7. GRADO DE HIPERCALCEMIA 8,5 A 10,5 mg % NORMAL 10,5 A 12 mg% LEVE 12 A 14 mg% MODERADA > 14 mg% CRITICA
- 8. DISTRIBUCION DEL CALCIO EN EL PLASMAA CALCIO UNIDO A PROTEÍNAS (40%) ALBUMINA 80% GLOBULINA 20% CALCIO LIBRE IÓNICO (50%) FORMANDO COMPLEJOS (10%) CALCIO TOTAL CALCIO IONICO SULFATO CITRATO LACTATO CALCEMIA CORREGIDA: 4 – Albúmina Pl x 0,8 + Ca Sérico
- 9. EL HIPERPARATIROIDISMO PRIMARIO ES UNA ENTIDAD CARACTERIZADA POR HIPERCALCEMIA ATRIBUIBLE A UNA SECRECIÓN AUTÓNOMA Y EXCESIVA DE PARATHORMONA HIPERPARATIROIDISMO PRIMARIO DEFINICIÓN AACE/AAES Position Statement, Endocr Pract. 2005;11(No. 1 )
- 10. AACE/AAES Position Statement, Endocr Pract. 2005;11(No. 1) 51 REGULACION CALCIO – PTH NORMAL - HIPERPARATIROIDISMO
- 12. HIPERCALCEMIA Leve o Moderada Intermitente A veces requiere multiples determinaciones ENFERMEDAD OSEA LITIASIS RENAL SINTOMAS Y SIGNOS POR EXCESO DE PTH SINTOMAS Y SIGNOS POR HIPERCALCEMIA ANOREXIA NAUSEAS CONSTIPACION POLIURIA POLIDIPSIA
- 19. HPPT Asintomatico - Review - Clinical Endocrinology (2008) 58 , 155–164 EPIDEMIOLOGÍA 12.000 X AÑO CIRUGIA (USA) 1,5% > 65 AÑOS (USA) 3/1000 PREVALENCIA POBLACION GENERAL 20-30/1000 PREVALENCIA EN MUJERES POSMENOPAUSIA 20/100.000 INCIDENCIA ANUAL
- 20. INCIDENCIA HPPT SEGÚN SEXO Y EDAD MUJERES VARONES S W I S S M E D W K LY 2 0 0 9 ; 1 3 9 ( 2 7 – 2 8 ) : 4 0 0 – 4 0 4 Hospitalizacion media anual de pactes. con HPPT-1º x 100.000 hab. En Suiza 2000-2004
- 21. INCIDENCIA POBLACIONAL PARATIROIDECTOMIAS INCIDENCIA HISTORICA DE HPPT-1º Y CIRUGIAS PT
- 23. HIPERPARATIROIDISMO PRIMARIO INCIDENCIA -AUMENTO DE LA INCIDENCIA EN ULTIMOS AÑOS -16/100000 EN 1974 A 112/100000 EN 1992 (20/100000 EN 2002) - DETECCCION RUTINARIA DE CALCIO -CAMBIOS EN LA FORMA DE PRESENTACION AL DIAGNOSTICO -ANTES LITIASIS Y ENFERMEDAD OSEA Y AHORA ASINTOMATICO
- 24. N Engl J Med 1966 - 274:1174 Heath, H III, et al, N Engl J Med 1980 - 302:189 Silverberg, SJ, et al, - Am J Med 1990; 89:327. CAMBIOS EN LA PRESENTACION DEL HPPT LITIASIS RENAL ENFERMEDAD OSEA ASINTOMATICO
- 29. PTH ELEVADA + CALCIO NORMAL. - Hiperparatiroidismo Normocalcémico? - Hiperparatiroidismo Secundario por Hipovitaminosis D - Hiperparatiroidismo Primario + Hipovitaminosis D
- 31. Holick M, Vit D Defiency Review NEJM 2007;357:266-281
- 32. Holick M, Vit D Defiency Review NEJM 2007;357:266-281
- 33. Holick M, Vit D Defiency Review NEJM 2007;357:266-281
- 34. Uptodate: Holick M, Vit D Defiency Review NEJM 2007;357:266-281
- 37. HPPT ASINTOMATICO INDICACIONES DE CIRUGIA THE THIRD INTERNATIONAL WORKSHOP GUIDELINES (2009)
- 42. HIPERCALCEMIA PTH CALCIURIA PTH BAJA (<20 pg/ml) HIPERCALCEMA NO MEDIADA POR PTH HPPT-1º PTH ALTA CALCIURIA <200 mg/24hs HPPT + < VIT D HHF PTH ALTA O NORMAL ALTA CALCIURIA > 200 mg/24hs
- 43. Gracias por su atención…
Notas del editor
- PTH מורכב מ -84 ח &quot; א , אך החלק האקטיבי הוא 34 הח . הראשונות , המסומנות בצהוב . חומצות אמינו 1-6 ב PTH הן אלו הדרושות להפעלת הרצפטור . אנאלוגים 7-34 יכולים להיקשר לרצפטור אך לא מפעילים אותו . משמשים לכם כ competitive antagosints . האתר הדרוש לקישור הנו 18-34
- קלציום משפיע על הפרשת ה - PTH ע &quot; י ה - CSR ( Ca sensing receptor , סוג של GPCR ) – בהיפרקלצמיה הוא משתק הפרשת PTH מהבלוטה , וכאשר יש היפוקלצמיה , השיתוק נעלם .
- Figure 1. The Parathyroid Axis. The synthesis of parathyroid hormone (PTH) and parathyroid hormone–related peptide (PTHrP) is shown on the left, and their target sites of action are shown on the right. Both act by means of the same receptor (also termed the type 1 PTH receptor). Negative feedback of 1,25-dihydroxyvitamin D is not shown. See the text for further descriptions. An excess or deficiency of parathyroid hormone may be treated either at the level of parathyroid hormone release (and the parathyroid hormone receptors) or at selected sites distal to the parathyroid hormone receptors. Blue arrows indicate extracellular calcium flow.
- Figure 2. Serum Calcium and Parathyroid Hormone Concentrations in Patients with Hypercalcemia and Hypocalcemia Due to Various Causes. The diagnosis of a serious mineral disorder is usually clear, as illustrated by the nonoverlapping domains in the figure, but in the early stages of these disorders, the values for either serum calcium or parathyroid hormone may overlap with the normal ranges. The following diagnoses are not shown: familial hypocalciuric hypercalcemia (midpoint of the range for serum calcium, 11.5 mg per deciliter, and for serum parathyroid hormone, 30 pg per milliliter); neonatal severe primary hyperparathyroidism (midpoint for serum calcium, 18 mg per deciliter, and for serum parathyroid hormone, 500 pg per milliliter); hypercalciuric hypocalcemia (midpoint for serum calcium, 7 mg per deciliter, and for serum parathyroid hormone, 10 pg per milliliter); tertiary uremic hyperparathyroidism (midpoint for serum calcium, 11 mg per deciliter, and for serum parathyroid hormone, 2000 pg per milliliter); tertiary hyperparathyroidism after renal transplantation that corrected uremia (midpoint for serum calcium, 12 mg per deciliter, and for serum parathyroid hormone, 200 pg per milliliter); and adynamic bone disease with uremia (midpoint for serum calcium, 9 mg per deciliter, and for serum parathyroid hormone, 50 pg per milliliter). To convert values for serum calcium to millimoles per liter, multiply by 0.25, and to convert values for serum parathyroid hormone to picomoles per liter, multiply by 0.11.
- Fig. 1. Relationship between intact parathyroid hormone ( iPTH ) and ionized calcium in normal physiologic state and hyperparathyroidism. Shaded area = normal range for ionized calcium.
- INCIDENCIA ANNUAL 20/100000 PREVALENCIA EN MUJERES POSMENOPASICAS The annual incidence of PHPT was estimated to be approximately 20 per 100 000,with a prevalence in postmenopausal women of 21 in 1000, which is equivalent to 3 in 1000 in the general population. Although in the USA PHPT might be present in more than 1·5% of people aged 65 years or older, representing several million people,surgery for PHPT is only performed on approximately 12 000 patients per year. It appears, therefore, that the majority of patients remain undiagnosed or untreated(5) during a 10-year follow-up of 121 patients with PHPT,14 of 52 asymptomatic patients who were not offered surgery had progression of disease and developed at least one new indication for parathyroidectomy (5)
- Different patterns of presentation of primary hyperparathyroidism in three different time periods. The latest survey shows that 80 percent of patients are asymptomatic and discovered incidentally on routine blood screening; bone disease, on the other hand, has virtually disappeared as a presenting symptom. Bone disease was assessed by x-rays and bone scans; patients with skeletal involvement by bone density measurement were not included. Data from Cope, O, N Engl J Med 1966; 274:1174; Heath, H III, et al, N Engl J Med 1980; 302:189; and Silverberg, SJ, et al, Am J Med 1990; 89:327.
- Biochemical screening tests that include measurements of serum calcium currently account for the identification of at least 80 percent of patients with primary hyperparathyroidism in western countries (show figure 1) [4]. These patients are usually asymptomatic and have mild and often intermittent hypercalcemia [5,6]. In most asymptomatic patients, the mean serum calcium concentration is less than 1.0 mg/dL (0.25 mmol/L) above the upper limit of the normal range [5]. Occasionally, patients are normocalcemic, and elevated parathyroid hormone levels are detected through a work-up of low bone density [7]. This entity, termed normocalcemic hyperparathyroidism, is discussed elsewhere. (See &quot;Diagnosis and differential diagnosis of primary hyperparathyroidism&quot; section on Normocalcemic primary hyperparathyroidism versus secondary hyperparathyroidism). Some patients with presumed asymptomatic hyperparathyroidism, when carefully questioned, have nonspecific symptoms, such as fatigue, weakness, anorexia, mild depression, and mild cognitive or neuromuscular dysfunction, and others simply miss work often [8-11]. With time, patients with true asymptomatic hyperparathyroidism may develop clinical manifestations of hyperparathyroidism, including skeletal manifestations, nephrocalcinosis, or kidney stones. Thus, the differentiation between symptomatic and asymptomatic primary hyperparathyroidism is not always clear-cut
- Patients without an apparent secondary cause may have a &quot;forme fruste&quot; of primary hyperparathyroidism. in the natural history of primary hyperparathyroidism, elevated PTH levels would precede the development of overt hypercalcemia In one prospective study of 37 patients with normocalcemic hyperparathyroidism, 41 percent developed evidence for progressive hyperparathyroid disease during a median of three years(3)
- — Secondary hyperparathyroidism occurs when the parathyroid gland appropriately responds to a reduced level of extracellular calcium. PTH concentrations rise, and calcium is mobilized by increasing intestinal absorption (via increase in calcitriol) and by increasing bone resorption. Thus, it is characterized biochemically by elevated PTH and normal or low serum calcium concentrations Secondary hyperparathyroidism may occur in patients with renal failure and impaired calcitriol (1,25 dihydroxyvitamin D) production, as well as in individuals with inadequate calcium intake or absorption, as can occur with vitamin D deficiency or with gastrointestinal diseases causing malabsorption (show table 3). Assessment of renal function (serum creatinine), vitamin D status (25-hydroxyvitamin D, 25OHD), and calcium sufficiency (urinary calcium excretion) may help differentiate normocalcemic primary and secondary hyperparathyroidism
- — Secondary hyperparathyroidism occurs when the parathyroid gland appropriately responds to a reduced level of extracellular calcium. PTH concentrations rise, and calcium is mobilized by increasing intestinal absorption (via increase in calcitriol) and by increasing bone resorption. Thus, it is characterized biochemically by elevated PTH and normal or low serum calcium concentrations Secondary hyperparathyroidism may occur in patients with renal failure and impaired calcitriol (1,25 dihydroxyvitamin D) production, as well as in individuals with inadequate calcium intake or absorption, as can occur with vitamin D deficiency or with gastrointestinal diseases causing malabsorption (show table 3). Assessment of renal function (serum creatinine), vitamin D status (25-hydroxyvitamin D, 25OHD), and calcium sufficiency (urinary calcium excretion) may help differentiate normocalcemic primary and secondary hyperparathyroidism
- Measurement of serum calcium — A single elevated serum calcium concentration should be repeated to confirm the presence of hypercalcemia. The total serum calcium concentration should be used for both the initial and the repeat serum calcium measurements. If a laboratory known to measure ionized calcium reliably is available, some authorities prefer to measure the ionized calcium, although this usually adds little in patients with normal serum albumin concentrations and no abnormalities in acid base balance Diagnosis is made by documenting hypercalcaemia in the presence of an elevated or inappropriately ‘normal’ serum PTH level, and a fractional urinary excretion of calcium >0.02.3 The fractional excretion of calcium is calculated as (urine calcium x serum creatinine) ÷ (serum calcium x urine creatinine).
- Preventive measures — A number of measures should be recommended to patients who do not undergo surgery, including the following: Avoid factors that can aggravate hypercalcemia, including thiazide diuretic and lithium carbonate therapy, volume depletion, prolonged bed rest or inactivity, and a high calcium diet (>1000 mg/day). Encourage physical activity to minimize bone resorption. Encourage adequate hydration (at least six to eight glasses of water per day) to minimize the risk of nephrolithiasis. Maintain a moderate calcium intake (1000 mg/day) A low calcium diet may lead to further increases in PTH secretion and could aggravate bone disease Maintain moderate vitamin D intake (400 to 600 int. units daily). (Vitamin D deficiency stimulates PTH secretion and bone resorption, and therefore is deleterious in patients with primary HPPT) (4) Preventive measures — A number of measures should be recommended to patients who do not undergo surgery, including the following: Avoid factors that can aggravate hypercalcemia, including thiazide diuretic and lithium carbonate therapy, volume depletion, prolonged bed rest or inactivity, and a high calcium diet (>1000 mg/day). Encourage physical activity to minimize bone resorption. Encourage adequate hydration (at least six to eight glasses of water per day) to minimize the risk of nephrolithiasis. Maintain a moderate calcium intake (1000 mg/day) A low calcium diet may lead to further increases in PTH secretion and could aggravate bone disease Maintain moderate vitamin D intake (400 to 600 int. units daily). (Vitamin D deficiency stimulates PTH secretion and bone resorption, and therefore is deleterious in patients with primary HPPT) (4)
- Estrogen-progestin therapy — Estrogen-progestin therapy is beneficial in postmenopausal women with primary hyperparathyroidism because of its ability to reduce bone resorption. In two trials, serum calcium concentrations decreased by 0.5 to 1.0 mg/dL and bone density increased slightly However, there are significant risks associated with estrogen-progestin therapy, including increased risks of breast cancer, stroke, and coronary heart disease. Therefore, estrogen or estrogen-progestin therapy should not be a first-line therapy for women with primary hyperparathyroidism(4) bisphosphonates are recommended for the treatment of low bone mass in patients with hyperparathyroidism who are not candidates for surgery Raloxifene — Raloxifene, a selective estrogen receptor modulator is available in many countries for the prevention and treatment of osteoporosis. In a short-term study of 18 postmenopausal women with asymptomatic PHPT, raloxifene (60 mg/day for eight weeks) reduced mean serum calcium concentration by 0.4 mg/dL at a single time point (8 weeks) [67]. Further data are needed before recommending raloxifene for this indication(4) Calcimimetics — Calcimimetic agents activate the calcium-sensing receptor in the parathyroid gland, thereby inhibiting PTH secretion. One calcimimetic drug, cinacalcet, is now available in some countries for the treatment of secondary hyperparathyroidism associated with renal failure and for hypercalcemia in parathyroid cancer. Although not currently approved for use in primary hyperparathyroidism (PHPT), cinacalcet may normalize serum calcium in these patients. In a one-year trial of 78 patients with PHPT randomly assigned to cinacalcet or placebo , cinacalcet therapy normalized serum calcium in 73 percent of subjects compared with only 5 percent in the placebo group. Serum PTH concentrations decreased by 7.5 percent with cinacalcet, but increased in the placebo group. Thus, cinacalcet is not the medical equivalent of parathyroidectomy, because there is no improvement in BMD.