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Severe hypocalcemia due to osteoblastic metastasis of prostate cancer
Hipocalcemia intensa por metástasis osteoblásticas de adenocarcinoma de próstata
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Hypocalcemia usually manifests itself in mild forms associated with vitamin D deficiency, hypomagnesemia, renal failure or induced by bisphosphonates.<a class="elsevierStyleCrossRef" href="#bib0030"><span class="elsevierStyleSup">1</span></a> Severe hypocalcemia is very rare, being usually associated with the presence of osteoblastic metastases of breast and, especially, prostate cancer.</p><p id="par0010" class="elsevierStylePara elsevierViewall">We report the case of an 84-year-old patient with a history of hypertension, prostatic hypertrophy and heart failure of valvular aetiology with severe systolic dysfunction. The patient received regular treatment with torasemide 5<span class="elsevierStyleHsp" style=""></span>mg, ramipril 2.5<span class="elsevierStyleHsp" style=""></span>mg, acetylsalicylic acid 100<span class="elsevierStyleHsp" style=""></span>mg, carvedilol 6.25<span class="elsevierStyleHsp" style=""></span>mg and dutasteride<span class="elsevierStyleHsp" style=""></span>+<span class="elsevierStyleHsp" style=""></span>tamsulosin. Admitted in Internal Medicine due to a heart failure exacerbation, initiating treatment with intravenous furosemide. Systematic lab tests showed a significant hypocalcemia (corrected calcium 5.2<span class="elsevierStyleHsp" style=""></span>mg/dl; NV 8.1–10.4) with high phosphorus (8.6<span class="elsevierStyleHsp" style=""></span>mg/dl; NV 2–5) normal magnesium (2<span class="elsevierStyleHsp" style=""></span>mg/dl; NV 1.6–2.6), along with a marked elevation of alkaline phosphatase (AP 8.050<span class="elsevierStyleHsp" style=""></span>U/l; NV 40–117 and <span class="elsevierStyleItalic">prostate specific antigen</span> (PSA) 526<span class="elsevierStyleHsp" style=""></span>ng/ml; NV less than 4); normocytic anaemia was also evident (Hb 9.1<span class="elsevierStyleHsp" style=""></span>g/dl, MCV 89<span class="elsevierStyleHsp" style=""></span>fl), low albumin (26<span class="elsevierStyleHsp" style=""></span>g/l, NV 34–48) and impaired renal function (creatinine 1.26<span class="elsevierStyleHsp" style=""></span>mg/dl, estimated glomerular filtration rate 52<span class="elsevierStyleHsp" style=""></span>ml/min/1.73<span class="elsevierStyleHsp" style=""></span>m<span class="elsevierStyleSup">2</span>). The complementary lab study showed high levels of parathyroid hormone (PTH 91.2<span class="elsevierStyleHsp" style=""></span>pg/ml; NV 14–72), 25-hydroxyvitamin D deficiency (19.1<span class="elsevierStyleHsp" style=""></span>ng/ml; NV 30–100) with normal values of 1,25-dihydroxyvitamin D (76.4<span class="elsevierStyleHsp" style=""></span>pg/ml; NV 26.1–86.5). Venous blood gases and levels of ferritin, folate and vitamin B<span class="elsevierStyleInf">12</span> were normal, and negative for transglutaminase antibodies.</p><p id="par0015" class="elsevierStylePara elsevierViewall">The patient reported a general syndrome with loss of 8<span class="elsevierStyleHsp" style=""></span>kg plus lumbago, muscle weakness, and paresthesias in acral areas. Trousseau and Chvostek signs were negative. The ECG showed a prolonged QTc interval (549<span class="elsevierStyleHsp" style=""></span>ms). Thoracoabdominal CT showed extensive infiltration of the whole skeleton at the expense of many blastic metastases, and a heterogeneous prostate gland. Bone scintigraphy showed radiotracer hyperfixation throughout the whole skeleton. Oral intake of calcium was initiated (calcium carbonate 3<span class="elsevierStyleHsp" style=""></span>g/day), intravenous calcium infusion (calcium gluconate 736<span class="elsevierStyleHsp" style=""></span>mg/day) and calcitriol (1<span class="elsevierStyleHsp" style=""></span>μg/day). After evaluation by Urology and with the clinical diagnosis of metastatic prostate adenocarcinoma, treatment was initiated with bicalutamide and leuprolide. Within 20 days from the start of treatment, lab results showed persistence of hypocalcemia (calcium corrected 7.7<span class="elsevierStyleHsp" style=""></span>mg/dl), normalization of phosphorus values (3.8<span class="elsevierStyleHsp" style=""></span>mg/dl), PTH close to normal (74<span class="elsevierStyleHsp" style=""></span>pg/ml), with marked decrease of AP (5.086<span class="elsevierStyleHsp" style=""></span>mg/dl) and PSA (281<span class="elsevierStyleHsp" style=""></span>mg/dl). Given the hypocalcemia treatment resistance, the dose of calcium and calcitriol was progressively increased up to 6<span class="elsevierStyleHsp" style=""></span>g of oral calcium, 1472<span class="elsevierStyleHsp" style=""></span>mg of intravenous calcium (1<span class="elsevierStyleHsp" style=""></span>mg/kg/h) and 2.5<span class="elsevierStyleHsp" style=""></span>μg of calcitriol, achieving normal calcium levels after 25 days of treatment. During hospitalization, the patient had an episode of atrial flutter and another of atrial fibrillation. He died a month after admission from respiratory failure in relation to a worsening of his congestive heart failure.</p><p id="par0020" class="elsevierStylePara elsevierViewall">Hypocalcemia associated with malignancy is caused by an imbalance between bone formation and resorption, with stimulus of the first one. Excessive osteoclast activity produces a massive deposition of calcium in the newly formed bone; low levels of calcium stimulate PTH secretion, generating a secondary hyperparathyroidism.<a class="elsevierStyleCrossRef" href="#bib0035"><span class="elsevierStyleSup">2</span></a> The usual lab test profile is low calcium in blood and urine, hyperparathyroidism and elevated bone resorption markers, such as AP.<a class="elsevierStyleCrossRefs" href="#bib0040"><span class="elsevierStyleSup">3–5</span></a> The treatment consists of high doses of oral calcium (1–2<span class="elsevierStyleHsp" style=""></span>g/day), intravenous calcium (0.5–1.5<span class="elsevierStyleHsp" style=""></span>mg/kg/h) and oral calcitriol (0.5–3<span class="elsevierStyleHsp" style=""></span>μg/day) plus antitumor treatment.<a class="elsevierStyleCrossRefs" href="#bib0040"><span class="elsevierStyleSup">3,5</span></a> The androgen deprivation therapy helps to reduce disease activity, inducing a decrease of calcium deposition in the bone, which contributes to the correction of hypocalcemia.</p><p id="par0025" class="elsevierStylePara elsevierViewall">The case reported corresponds to severe hypocalcemia associated with secondary hyperparathyroidism, in a patient with multiple osteoblastic metastases due to prostate adenocarcinoma. High doses of calcium and calcitriol were required for its correction in addition to hormone-blocking treatment for almost a month.</p></span>" "pdfFichero" => "main.pdf" "tienePdf" => true "NotaPie" => array:1 [ 0 => array:2 [ "etiqueta" => "☆" "nota" => "<p class="elsevierStyleNotepara" id="npar0005">Please cite this article as: Diéguez Felechosa M, Noval Menéndez J, Manjón Miguelez L. Hipocalcemia intensa por metástasis osteoblásticas de adenocarcinoma de próstata. Med Clin (Barc). 2017;148:287–288.</p>" ] ] "bibliografia" => array:2 [ "titulo" => "References" "seccion" => array:1 [ 0 => array:2 [ "identificador" => "bibs0005" "bibliografiaReferencia" => array:5 [ 0 => array:3 [ "identificador" => "bib0030" "etiqueta" => "1" "referencia" => array:1 [ 0 => array:2 [ "contribucion" => array:1 [ 0 => array:2 [ "titulo" => "Hypocalcemia in malignancy – unexpected but common" "autores" => array:1 [ 0 => array:2 [ "etal" => false "autores" => array:5 [ 0 => "B. Diniotis" 1 => "E. 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