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RESEARCH ARTICLEDOI: 10.4274/tjh.2015.0087Turk J Hematol 2016;33:293-298The Effect of Hyperparathyroid State on Platelet Functions andBone LossHiperparatiroidi Durumun Trombosit Fonksiyonları ve Kemik Kaybı Üzerine Olan EtkisiGöknur Yorulmaz 1 , Aysen Akalın 2 , Olga Meltem Akay 3 , Garip Şahin 4 , Cengiz Bal 51Eskişehir State Hospital, Clinic of Endocrinology, Eskişehir, Turkey2Eskişehir Osmangazi University Faculty of Medicine, Department of Endocrinology, Eskişehir, Turkey3Eskişehir Osmangazi University Faculty of Medicine, Department of Hematology, Eskişehir, Turkey4Eskişehir Osmangazi University Faculty of Medicine, Department of Nephrology, Eskişehir, Turkey5Eskişehir Osmangazi University Faculty of Medicine, Department of Biostatistics and Medical Informatics, Eskişehir, TurkeyAbstractObjective: Coagulation and fibrinolysis defects were reported inprimary hyperparathyroid patients. However, there are not enoughdata regarding platelet functions in this group of patients. Our aimwas to evaluate the platelet functions in primary and secondaryhyperparathyroid patients and to compare them with healthy subjects.Materials and Methods: In our study 25 subjects with primaryhyperparathyroidism (PHPT), 25 subjects with secondaryhyperparathyroidism (SHPT), and 25 healthy controls were included.Platelet functions of the subjects were evaluated by using plateletrichplasma and platelet aggregation tests induced with epinephrine,adenosine diphosphate (ADP), collagen, and ristocetin. Serum Pselectin levels, which indicate platelet activation level, were measuredin all subjects. Bone mineral densitometry was performed for allpatients.Results: There was no significant difference between the groupswith PHPT and SHPT and the control group regarding the plateletaggregation tests and serum P selectin levels. There was also nosignificant correlation between parathormone levels and aggregationparameters (ristocetin, epinephrine, collagen, and ADP: respectivelyp=0.446, 0.537, 0.346, and 0.302) and between P selectin (p=0.516)levels. When we separated the patients according to serum calciumlevels, there was also no significant difference between aggregationparameters and serum P selectin levels between the patients withhypercalcemia and the patients with normocalcemia. We could notfind any significant correlation between aggregation parameters, Pselectin levels, and serum calcium levels in this group of patients.Bone loss was greater in patients with PHPT.Conclusion: There is no significant effect of PHPT or SHPT and serumcalcium levels on platelet functions when evaluated by aggregationtests.Keywords: Hyperparathyroidism, Platelet function, P selectin,Calcium, Bone lossÖzAmaç: Koagülasyon ve fibrinoliz bozuklukları primer hiperparatiroidilihastalarda rapor edilmekle beraber bu hasta grubunda trombositişlevlerine ilişkin yeterli veri yoktur. Bu nedenle primer ve sekonderhiperparatiroidisi olan hastalarda ve sağlıklı kontrol grubundatrombosit fonksiyonlarını değerlendirmeyi ve gruplar arasında farkıkarşılaştırmayı amaçladık.Gereç ve Yöntemler: Çalışmamıza 25 primer hiperparatiroidisi(PHPT) olan hasta, 25 sekonder hiperparatiroidisi (SHPT) olan hastave 25 kontrol grubu dahil edildi. Trombosit fonksiyonları trombosittenzengin plazma ve epinefrin, adenozin difosfat (ADP), kollajen veristosetinle trombosit agregasyon testleri yapılarak değerlendirildi.Trombosit aktivasyon düzeyini gösteren serum P selektin düzeyleritüm hastalarda ölçüldü. Kemik mineral dansitometresi tüm hastalardadeğerlendirildi.Bulgular: PHPT ve SHPT’li hastalar ve kontrol grubunun trombositfonksiyon testleri ve serum P selektin düzeyleri arasında istatistikselaçıdan anlamlı bir fark saptanmadı. Parathormon düzeyi ile agregasyonparametreleri (ristosetin, epinefrin, kollajen, ve ADP: sırasıyla p=0,446,0,537, 0,346 ve 0,302) ve P selektin (p=0,516) düzeyi arasında daanlamlı bir korelasyon saptanmadı. Hastalar kalsiyum düzeylerinegöre hiperkalsemik ve normokalsemik olarak ayrıldıklarında daagregasyon parametreleri ve P selektin düzeyleri arasında anlamlı farksaptanmadı. Hasta gruplarımızda trombosit fonksiyonları, P selektindüzeyi, serum kalsiyum düzeyileri arasında istatistiksel açıdan anlamlıfark bulunmadı. Kemik kaybı PHPT’li olan grupta daha belirgindi.Sonuç: Agregasyon testleri ile değerlendirildiğinde PHPT veya SHPT veserum kalsiyum düzeylerinin trombosit fonksiyonları üzerine belirginetkisi yoktur.Anahtar Sözcükler: Hiperparatiroidism, Trombosit fonksiyonları, Pselektin, Kalsiyum, Kemik kaybıAddress for Correspondence/Yazışma Adresi: Göknur YORULMAZ, M.D.,Eskişehir State Hospital, Clinic of Endocrinology, Eskişehir, TurkeyPhone : +90 505 866 58 83E-mail : goknuryorulmaz@hotmail.comReceived/Geliş tarihi: February 20, 2015Accepted/Kabul tarihi: June 15, 2015293
Yorulmaz G, et al: Hyperparathyroidism and Platelet FunctionsTurk J Hematol 2016;33:293-298IntroductionHemostasis is regulated by a balance between stimulators andinhibitors of platelet functions. The deterioration of the balancebetween inhibitors and stimulators of platelet functions resultsin thrombosis or bleeding. Platelets are involved in primaryhemostasis, which includes the formation of a plug by theadhesion and activation of platelets in response to vasculardamage or the loss of integrity of the vascular wall. Manyphysiological stimuli can activate platelets both in vivo and invitro, such as collagen, proteolytic enzymes, and low-molecularweightcompounds. Clinically platelet functions are evaluatedby platelet aggregation and activation tests [1,2]. The use ofplatelet agonists such as collagen, adenosine diphosphate (ADP),epinephrine, and ristocetin triggers classical platelet responseand a great deal of information can be obtained from plateletaggregation. P selectin is a membrane glycoprotein withinplatelets and endothelial cells that is mobilized to the plasmamembrane following cell activation and it is used to evaluateplatelet activation [3,4].It is well known that primary hyperparathyroidism (PHPT) isassociated with a high risk of cardiovascular disease and increasedmortality and morbidity related to cardiovascular problems[5,6,7]. There are also studies that relate hyperparathyroidismwith a potential tendency toward hypercoagulation [8,9].There are some cases of thrombotic events seen in the courseof hyperparathyroidism [10]. However, knowledge aboutthe effects of hyperparathyroidism on platelet functions isunsatisfactory and conflicting. Whereas elevated parathormone(PTH) levels and hypercalcemia are significant features of PHPT,PTH elevation does not accompany hypercalcemia in secondaryhyperparathyroidism (SHPT). There are studies investigatingthe effect of serum calcium levels on platelet aggregation,coagulation, and thromboelastography in healthy people [11].However, it is not clear whether hyperparathyroidism disturbsplatelet function and if so whether it is related to the high PTHlevels per se or to the accompanying hypercalcemia.In this study we aimed to evaluate platelet functions in patientswith both PHPT and SHPT.Materials and MethodsTwenty-five subjects with PHPT, 25 subjects with SHPT, and25 healthy age-matched control subjects were included in thestudy. The diagnosis of PHPT was based on clinical assessmentand laboratory findings. Parathyroid adenomas were shown inall of the PHPT patients on both parathyroid ultrasound and99mtechnetium scans of the parathyroids. Elevated PTH levels in thecase of normal or low serum calcium level, vitamin D deficiency,and decreased urinary calcium excretion were regarded as signsof SHPT. Twenty-five healthy age- and sex-matched subjects withnormal values of biochemical parameters were used as controls.The purpose and the procedure of the tests were explained tothe subjects and written informed consent was obtained fromeach participant. The experimental protocol was designed andperformed according to the principles of the Declaration ofHelsinki and it was approved by the Ethics Committee of theEskişehir Osmangazi University Medical Faculty.Serum calcium, phosphorus, albumin, chloride, and creatininelevels were measured for each of the subjects. Serum intact PTHwas measured from venous blood samples at a central laboratoryusing a solid-phase two-site chemiluminescent enzyme-labeledimmunometric assay with a reference range of 15-65 pg/mL. Serum calcium, phosphorus, and creatinine levels weremeasured colorimetrically. Serum albumin levels were measuredby immunoturbidimetric assay and serum creatinine levels weremeasured by using an ion-selective electrode. Twenty-fourhour urine collections were used in order to calculate urinarycalcium excretion rates. Creatinine clearance (Ccr) levels werecalculated according to the Cockroft-Gault formula. Patientswith serum creatinine level above 1.2 mg/dL or Ccr level below70 mL/min were not included in the study in order to excludethe confounding effects of renal failure on platelet functions.Tubular reabsorption of phosphate was calculated as TRP=[1-(up/pp)x(pcr/ucr)]x100.Platelet functions of the subjects were evaluated by usingplatelet-rich plasma and platelet aggregation tests withepinephrine, ADP, collagen, and ristocetin. Serum P selectinlevels, which indicate platelet activation level, were alsomeasured in all subjects. Groups were matched with respect toage. Exclusion criteria included patients with known bleedingor other systemic disorders such as hepatic and endocrinediseases, acute infections, autoimmune disorders, or cancer, anda platelet count of less than 150x10 9 /L or more than 450x10 9 /Land a hemoglobin level of less than 10 g/dL. The patients didnot receive agents that could affect platelet functions such asacetylsalicylic acid, ticlopidine, dipyridamole, or nonsteroidalantiinflammatory drugs in the 10 days prior to the plateletaggregation studies.Sample Collection and Laboratory MethodsCitrated blood was collected under light tourniquet through19-gauge needles into 4.5-mL vacutainers (Becton Dickinson,USA) containing 3.2% trisodium citrate in a 9:1 blood/anticoagulant ratio. The collection was performed early in themorning after overnight fasting. Samples for blood countswere drawn into Becton Dickinson anticoagulated tubes andcomplete counts were made with a Beckman Coulter Gen-SSM (USA) automated blood counting device. Coagulationtests were performed with an ACL TOP Coagulation Analyzer(Instrumentation Laboratory, USA). Prothrombin time (PT) wasmeasured with a HemosIL RecombiPlasTin kit (Instrumentation294
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