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It has multiple etiologies, with a wide range of differential diagnoses taking into account endocrinological, neoplastic, pharmacological diseases or, less frequently, granulomatous diseases.</p><p id="par0010" class="elsevierStylePara elsevierViewall">This is the case report of a patient who consulted for disorientation and asterixis, being diagnosed with tumor hypercalcemia induced by prostate adenocarcinoma recurrence.</p><p id="par0015" class="elsevierStylePara elsevierViewall">The patient is an 86-year-old man with a history of hypertension, chronic renal failure and a prostate adenocarcinoma diagnosed 10 years earlier, treated with radiotherapy and GnRH analogues.</p><p id="par0020" class="elsevierStylePara elsevierViewall">He went to the emergency room due to a 1-week-disorientation, 2 days earlier having involuntary and sporadic limb movements and progressively decreased consciousness. Physical examination showed normal vital signs, highlighting a score 9 on the Glasgow scale and asterixis.</p><p id="par0025" class="elsevierStylePara elsevierViewall">The lab tests showed metabolic acidosis with acute-on-chronic kidney failure (pH 7.28, bicarbonate 20<span class="elsevierStyleHsp" style=""></span>mmol/l, creatinine 1.96<span class="elsevierStyleHsp" style=""></span>mg/dl) and hypercalcemia (ionized calcium 1.45<span class="elsevierStyleHsp" style=""></span>mmol/l, corrected plasma calcium 10.54<span class="elsevierStyleHsp" style=""></span>mg/dl). The patient underwent a cranial computed tomography and a lumbar puncture that were normal. Brain nuclear magnetic resonance was normal and the electroencephalogram confirmed findings of diffuse encephalopathy without epileptiform activity.</p><p id="par0030" class="elsevierStylePara elsevierViewall">The patient was diagnosed with metabolic encephalopathy with asterixis secondary to hypercalcemia and acute renal failure due to dehydration. The patient underwent intensive fluid therapy with saline.</p><p id="par0035" class="elsevierStylePara elsevierViewall">The patient clearly showed neurological improvement along with normalization of calcemia, recovering an optimal level of consciousness and full recovery from asterixis. Both, electrolyte imbalance and kidney failure were considered responsible for the neurological symptoms and signs. However, once the deterioration of renal function and acidemia had been resolved, the altered state of consciousness and asterixis had reappeared with the recovery of calcemia, which was considered mainly responsible for it. Therefore treatment with calcitonin was added depending on it. Hypercapnia and hepatic encephalopathy, common causes of asterixis, were ruled out by clinical context, arterial blood gas test and the absence of ultrasound signs of chronic liver disease.</p><p id="par0040" class="elsevierStylePara elsevierViewall">As part of the etiological study, we noted slightly high PTH levels (99<span class="elsevierStyleHsp" style=""></span>pg/ml), low 1,25-hydroxy-vitamin D3 levels (11<span class="elsevierStyleHsp" style=""></span>pg/ml), low 25-hydroxy-vitamin D3 levels (13.2<span class="elsevierStyleHsp" style=""></span>pg/ml) and normal phosphorus, consistent with hyperparathyroidism secondary to chronic renal failure, without explaining hypercalcemia.</p><p id="par0045" class="elsevierStylePara elsevierViewall">Based on the history of prostate adenocarcinoma, a prostate-specific antigen was found that was strikingly high (388<span class="elsevierStyleHsp" style=""></span>ng/ml). The ultrasound showed a small prostate after radiotherapy and multiple retroperitoneal adenopathies, with normal bone scintigraphy. A positron emission tomography showed focal hypermetabolic lesion of the prostate and multiple retroperitoneal and pelvic adenopathies. The patient died of an uncontrollable hypercalcemia. Therefore, histological confirmation of the diagnosis could not be obtained, which eventually was diffuse encephalopathy with asterixis as an expression of tumor hypercalcemia secondary to recurrence of prostate adenocarcinoma.</p><p id="par0050" class="elsevierStylePara elsevierViewall">Given the patient's chronic renal failure, we might have thought of hypocalcemia with secondary hyperparathyroidism instead of hypercalcemia with slightly high PTH. Hypercalcemia was probably the result of ectopic secretion of PTH-like peptide (PTHrp), without completely inhibiting high parathormone levels due to secondary hyperparathyroidism.</p><p id="par0055" class="elsevierStylePara elsevierViewall">Neoplasms are the leading cause of hypercalcemia in the hospitalized patient, with a prevalence up to 44%.<a class="elsevierStyleCrossRef" href="#bib0030"><span class="elsevierStyleSup">1</span></a> There are different physiopathological mechanisms of tumor hypercalcemia, the most frequent being the secretion of PTHrP (80%), followed by osteolytic bone metastases and ectopic secretion of vitamin D.<a class="elsevierStyleCrossRef" href="#bib0035"><span class="elsevierStyleSup">2</span></a></p><p id="par0060" class="elsevierStylePara elsevierViewall">The symptomatology depends on the degree of hypercalcemia and the speed of onset. The most frequent neurological manifestations are altered behavior, decreased level of consciousness, headache and seizures.<a class="elsevierStyleCrossRef" href="#bib0040"><span class="elsevierStyleSup">3</span></a> Asterixis is an unusual clinical sign poorly described in the literature.<a class="elsevierStyleCrossRefs" href="#bib0045"><span class="elsevierStyleSup">4,5</span></a></p><p id="par0065" class="elsevierStylePara elsevierViewall">It is important to differentiate between PTH-dependent and independent hypercalcemia and measure vitamin D and phosphorus.<a class="elsevierStyleCrossRef" href="#bib0030"><span class="elsevierStyleSup">1</span></a> If hypercalcemia <12<span class="elsevierStyleHsp" style=""></span>mg/dl or asymptomatic, oral hydration should be indicated and the cause can be treated. On the other hand, if symptomatic or >12<span class="elsevierStyleHsp" style=""></span>mg/dl, in addition to the etiological treatment, intensive fluid therapy should be first indicated with 0.9% saline (200<span class="elsevierStyleHsp" style=""></span>ml/h, and then decrease it depending on its development). The use of loop diuretics is not recommended because it causes volume depletion. If insufficient, the use of calcitonin or bisphosphonates is recommended. Tumor hypercalcemia is usually associated with advanced neoplasms and has a bad prognosis.</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: Grafia I, Marco-Hernández J. Asterixis como forma de presentación atípica de hipercalcemia. 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