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© Borgis - Postępy Nauk Medycznych 12/2014, s. 838-842
*Waldemar Misiorowski, Magdalena Kochman
Ostra niewydolność nerek w przebiegu przełomu hiperkalcemicznego u chorego z rakiem przytarczyc – opis przypadku
Acute renal failure in the course of hypercalcemic crisis due to parathyroid carcinoma – the case study
Department of Endocrinology, Centre of Postgraduate Medical Education, Bielański Hospital, Warszawa
Head of Department: prof. Wojciech Zgliczyński, MD, PhD
Streszczenie
Rak przytarczyc stanowi rzadką przyczynę pierwotnej nadczynności przytarczyc. Manifestuje się przede wszystkim objawami nadmiernej produkcji parathormonu, a w obrazie klinicznym choroby dominują konsekwencje hiperkalcemii. Dlatego podstawowym wyzwaniem terapeutycznym jest jej objawowe zwalczanie.
Przedstawiono przypadek 56-letniego mężczyzny, przyjętego do szpitala z objawami ostrej niewydolności nerek w przebiegu przełomu hiperkalcemicznego. Intensywne nawodnienie dożylne i furosemid spowodowały poprawę czynności nerek, bez istotnego wpływu na stężenie wapnia w surowicy. Wybitnie podwyższone stężenie PTH w surowicy potwierdziło rozpoznanie pierwotnej nadczynności przytarczyc, zaś ostry przebieg kliniczny wraz ze skrajnie wysokimi stężeniami wapnia i PTH wskazały na możliwość raka przytarczyc. Ponieważ niewydolność nerek uniemożliwiła zastosowanie bisfosfonianów, standardowego objawowego leczenia ostrej hiperkalcemii, zdecydowano podać choremu kalcimimetyk – cynakalcet (Mimpara®). Po uzyskaniu zadowalającej redukcji kalcemii stan chorego znacznie się polepszył, co umożliwiło ukończenie niezbędnych badań diagnostycznych i skierowanie chorego do leczenia operacyjnego. Badanie histopatologiczne potwierdziło wstępne rozpoznanie raka przytarczyc.
Cynakalcet wydaje się lekiem wysoce skutecznym w objawowym zwalczaniu ostrej hiperkalcemii w przebiegu pierwotnej nadczynności przytarczyc.
Summary
Parathyroid carcinoma is an uncommon cause of PTH-dependent hypercalcemia. The clinical features of parathyroid carcinoma are due primarily to the effects of hypercalcemia due to excessive secretion of PTH. Thus, signs and symptoms of hypercalcemia often dominate the clinical picture. The therapeutic goal at this point is to control the hypercalcemia.
A history of the 56-years man admitted to the hospital with acute renal failure in course of the hypercalcemic crisis is described. He was treated with saline hydration and furosemide, with improvement of renal function, however of very little effect on serum calcium levels. Extremely elevated serum PTH-intact of 1789 pg/ml confirmed the diagnosis of primary hyperparathyroidism and a possibility of parathyroid carcinoma had been considered. Since renal failure prevented the use of bisphosphonates, eventually a calcimimetic cinacalcet (Mimpara®), has been used to treat. Satisfactory reduction of serum calcium and PTH enabled to complete the necessery diagnostic procedures and refer the patient for surgery. Histopathological diagnosis of the parathyroid carcinoma had been confirmed.
Cinacalcet appears to have been highly effective at controlling acute hypercalcemia in patients with primary hyperparathyroidism.



Parathyroid carcinoma is an uncommon cause of primary hyperparathyroidism. Approximately only 400 cases of this disease were reported in the English since 1930 (1-28). The clinical features of parathyroid carcinoma are due primarily to the effects of hypercalcaemia due to excessive PTH secretion and do not consist the typical features of advanced neoplastic disease (1-6, 9-10, 12, 18, 27-28). Thus, unlike in the majority of present-day benign primary hyperparathyroidism cases, signs and symptoms of acute hypercalcemia often dominate the clinical picture in parathyroid carcinoma, the controlling of which becomes, in consequence, the primary goal of the therapy. The critical, life-threatening hypercalcemia (hypercalcemic crisis) of parathyroid carcinoma is treated in the same way as hypercalcemia due to any other case (28-30). Due to the persistently excessive PTH secretion, saline hydration and loop diuretics rarely suffice to control the hypercalcemia, and addition of agents that interfere with osteoclast-mediated bone resorption is always necessary. However, in the case described here, the classic inhibitors of osteoclastic bone resorption, i.e. bisphosphonates, could not be used because of acute renal failure. Upon application the cinacalcet (Mimpara®, Amgen) – a calcimimetic, a drug of a new therapeutic class, a satisfactory reduction of calcemia was achieved.
Case study
A 56-year-old male was admitted to the hospital lethargic and fell asleep during examination. He also experienced intermittent nausea, vomiting, and watery diarrhea, however he denied having any fever, chills, or any other associated symptoms. He also noted excessive thirst and increased in urination but denied dysuria or hematuria. His past medical history was only significant for nephrolithiasis. He was not taking any medications regularly. However, he complained of worsening pain in the spine and pelvis and noted a painful deformation of the right knee and the lower leg. Physical examination revealed blood pressure of 160/80 mmHg, heart rate 96/min regular. His cardiopulmonary exam was unremarkable. Abdominal exam revealed mild tenderness in the epigastrium area and left lower quadrant without any signs of guarding or rigidity. Bowel sounds were active. Acute abdominal series X-ray did not show any acute process. Bedside glucose reading was 115 mg/dl. Laboratory investigation showed normal CBC and urine analysis. Serum creatinine level was 5.4 mg/dL (0.5-1.4 mg/dL). Serum calcium was 14.5 mg/dL (reference range 8-10.5 mg/dL), and ionized calcium was elevated at 1.78 mmol/L (reference range 1.10-1.30 mmol/L) and the acute renal failure in the course of hypercalcemic crisis was diagnosed.
Patient was treated with intravenous fluid hydration and loop diuretic while the etiology of hypercalcemia was being sought. Extremely elevated serum PTH-intact level of 1789 pg/ml confirmed the diagnosis of primary hyperparathyroidism and a possibility of parathyroid carcinoma had been considered. Left knee and lower leg X-ray and CT revealed a typical picture of osteitis fibrosa cystica (fig. 1). Renal failure excluded the possibility of using the standard symptomatic treatment of hypercalcemia, which are bisphosphonates. Hydratation and furosemide treatment improved significantly renal function, however had a very little effect on serum calcium level. Eventually, it was decided to treat patient with calcimimetic – cinacalcet (Mimpara®), recently registered for symptomatic control of hypercalcemia due to primary hyperparathyroidism. After the administration of the drug at the smallest recommended dose of 30 mg twice a day, the serum calcium began to reduce at a quick rate, dropped to 12.24 mg/dL after the third day of the treatment, and after increase of total daily dose to 90 mg/d, subsequently deceased above 12.00 mg/dL. Consequently, the saline hydration was stopped, which in turn did not affect the serum calcium values. After two weeks of cinacalcet treatment the PTH levels also decreased from 1789 pg/ml before the start of the treatment to 785 pg/ml, respectively. Improving the general condition of the patient allowed to perform the parathyroid imagining studies. Technetium 99mTc-MIBI scan as well as computed tomography indicated the enlarged left inferior parathyroid gland (fig. 2). The patient underwent surgery. Enlarged parathyroid tumor (3.0 x 3.0 cm) had been removed with left thyroid lobe and isthmus, and with surrounding, not enlarged and macroscopically unaffected lymph nodes. The left reccurent laryngeal nerves was preserved with neuromonitoring use. Twenty-four hours after surgery, serum calcium was 6.8 mg/dL, phosphorus was 1.6 mg/dL, and PTH was 24 pg/ml, with subtetany symptoms and positive Chvostek’s sign. Patient had been treated with calcium gluconate iv and then with oral calcium carbonate (3.0 g daily) and alphacalcidiol up to 3.0 μg/daily. He was discharged two week later. Histopathological diagnosis of the parathyroid carcinoma had been established.
Fig. 1. Left lower leg x-ray (A) and CT scan (B) revealing osteitis fibrosa cystica features.
Fig. 2. Anterior 99MTc – MIBI SPECT image show the intense uptake and delayed washout in a large left inferior parathyroid gland.
Discussion

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otrzymano: 2014-10-15
zaakceptowano do druku: 2014-11-07

Adres do korespondencji:
*Waldemar Misiorowski
Department of Endocrinology Centre of Postgraduate Medical Education Bielański Hospital
ul. Cegłowska 80, 01-809 Warszawa
tel. +48 (22) 569-01-05
w_misiorowski@wp.pl

Postępy Nauk Medycznych 12/2014
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