Search

The concentration of calcium is carefully maintained under physiological conditions with parathormone, calcitonin and 1,25-dihydroxyvitamin D at appropriate levels. There are multiple causes that may bring about increased concentrations of calcium which exceed physiological values. Increased production of parathormone in parathyroid glands is only one of the possible causes. Malignant diseases are a very frequent cause of hypercalcemia, due to their creating mediators which stimulate osteoclasts and thereby osteolysis. A less frequent cause is represented by granulomatous processes, a typical example of which is sarcoidosis, whose cells increasingly (independently of parathormone) hydroxylate 25-hydroxyvitamin D to 1,25-dihydroxyvitamin D. However there are also hereditary forms of hypercalcemia. One of the causes of the hereditary form of hypercalcemia is mutations of the calcium sensing receptor. In order to locate the adenoma of parathyroid glands, essential apart from sonographic imaging is scintigraphy 99mTc-methoxyisobutylisonitrile (MIBI) and even more exact is PET-CT examination with a radio-pharmaceutical 18F-fluorocholine. PET-CT examinations are beneficial with regard to detecting a malignant cause of hypercalcemia in until then undetected malignancy or an undetected granulomatous process. The essential treatment procedures for malignant hypercalcemia include appropriate hydratation of ionic solutions without calcium, administering of bisphosphonates or denosumab. The text describes in detail the symptoms of hypercalcemia and diagnostics of causes of hypercalcemia.bisphosphonates - cinacalcet - denosumab - granulomatous diseases - hereditary hypercalcemia - hypercalcemia - hypercalciuria - hyperparathyreosis - calcimimetics - calcitonin - multiple myeloma - malignant hypercalcemia - parathormone - sarcoidosis - 1,25-dihydroxyvitamin D.

Introduction: Procalcitonin (PCT) is a 13 kD protein with a chain of 116 amino acids. It consists of parafollicularcells of the thyroid gland. Inflammatory procalcitonin is made up of 114 amino acids. Procalcitonin from plasma in the course of inflammatory process, does not consistof C-cells of the thyroid gland but it is generatedin the liver, and, to a lesser extent, in the lungs, kidneys, testes, prostate and small intestine. Objectives: 1. To compare the levels and the dynamics of C-reactive protein (CRP) and procalcitonin in the inflammatory process. in three patients with different diagnoses. To compare the number of examined PCT according to indicated VFN (General University Hospital) departments in the years 2009, 2012 and 2015. 3. To study the dynamics of the number of examined PCT in the years 2001- 2016. Methods: The levels of CRP and PCT were measured in the ÚLBLD laboratory of the General University Hospital in Prague in the period from May 20to June 17, 2016. The CRP was measured by immunoturbidimetricanalyzerUnicelDxC 880i. The PCT was measured by theCobas analyser using the electrochemiluminescence technology. In order to evaluate the data, graphs were processed with levels of bothanalytesfor 3 patients. Further, data needed for the evaluation of the above mentioned objectives no. 2...

Inflammation plays an important role in the pathophysiology of acute coronary syndrome as well as in the process of atherosclerosis in general. At the moment of myocardial ischaemia, local and systemic inflammatory reaction is amplified; in ischaemic myocardium there is increased expression of proinflammatory cytokines, particularly interleukin-6, which mediates C reactive protein (CRP) production by hepatocytes. CRP activates the complement cascade and thereby contributes to the lysis and removal of damaged cardiomyocytes. Whereas in a healthy population CRP levels range from 1.2 to 2.0 mg / l, in patients with ACS the levels of CRP significantly increase with the peak of 2nd to 4th day from the onset of myocardial infarction. Peak CRP levels ranged from 20 to 250 mg / l in patients with STEMI treated conservatively, the median of peak of CRP levels was 79 mg/ l in patients with anterior wall STEMI treated with primary PCI. There is a recommendation of CRP evaluation within the early risk stratification of patients with ACS according to the current ESC guidelines. In patients with NSTEMI, CRP levels10 mg/ l are associated with increased longterm mortality. In patients with STEMI treated with primary PCI, CRP levels79 mg/ l could predict negative left ventricle remodelation. The predictive value of GRACE risk score was improved using CRP, levels22 mg/ l predicted worse prognosis in patients with either STEMI or NSTEMI treated invasively. However, if also cardiac troponin and natriuretic peptides in addition to GRACE risk score were used, CRP levels were useless in further risk stratification improvement. In clinical practice, in terms of coinciding infection, problems with CRP levels interpretation can occur as well. Several patients either in cardiogenic shock or after cardiopulmonary resuscitation have signs of systemic inflammatory response, and sometimes it is very difficult to decide whether there is a necessity to iniciate the antibio-tic therapy because of infectious cause. In patients after cardiopulmonary resuscitation, CRP levels180 mg/ l indicate highly probable infection, but with the poor sensitivity. For patients in cardiogenic shock, procalcitonin appears to be more useful for the detection of infection; in this group of patients, procalcitonin levels2 ng/ ml are common, and levels10 ng/ ml indicate infection undoubtedly.

Fever and elevated C-reactive protein are frequently found in hematooncological patients. It is sometimes difficult to distinguish between infectious fever and drug-related or tumour-associated fever. Tumour-related fever is not very common in multiple myeloma (unlike malignant lymphomas). C-reactive protein (CRP) is usually elevated simultaneously with fever and so it cannot be used in differential diagnosis of febrile states. There is another marker that provides information about the origins of the fever--rocalcitonin. We present cases of three patients that illustrate the significance of procalcitonin in patients with multiple myeloma.

Calcitonin is 32 amino acids polypeptide whose primary function is to inhibit osteoclasts activated bone resorption. In mammals calcitonin is secreted in the thyroid gland by specialized cells called C cells which have embryonic origin in ultimobranchial bodies. C cells are about 0.1% of the mass of thyroid gland. To achieve hypocalcemic effect all 32 amino acids are necessary. From thyroid gland calcitonin is released namely by calcium and magnesium. Calcitonin decreases bone resorption which can be demonstrated in vivo and in vitro. Calcitonin is used to treat osteoporosis and algodystrophic syndrome. In the PROOF study was given salmon calcitonin at a dose 200 units daily for 5 years. In this dose spine bone density increased about 1.5%, however; there was no significant increase of bone density in the hip. Administration of nasal spray of calcitonin in a study PROOF reduced the risk of new fracture by 36% compared to placebo. Intracranially calcitonin acts as a neurotransmitter. According to the predominant view, calcitonin protects the skeleton under conditions of increased calcium demand during growth, pregnancy and lactation. Calcitonin is also important tumor marker of thyroid carcinoma.

The review is aimed at the importance of determining procalcitonin serum levels (S-PCT) in numerous infectious and non-infectious diseases. Detecting increased S-PCT is particularly important for differential diagnosis of systemic bacterial as well as fungal infections. High S-PCT concentrations are also of predictive value in severe sepsis and septic shock. S-PCT kinetics may be used for monitoring the effect of antibiotic therapy. When compared to the other routinely used markers of bacterial infection (i.e. C-reactive protein, white blood cell count and neutrophil percentage), S-PCT has higher sensitivity and specificity in predicting bacterial infection.

In the group of 450 patients operated in the Cardiosurgical Department of the Faculty Hospital in Plzen during the period from III/2003 till XI/2003, 1451 samples were collected to examine the following-procalcitonin levels (PCT), white blood cell counts (Leu) and C-reactive protein levels (CRP). The findings were assessed with respect to the respective patient's clinical status, and any correlation between procedures with extracorporeal circulation (MO), signs of inflammation, septic and non-septic serious complications and between the above mentioned markers levels, was searched. It was detected, that the PCT levels correlated well with the clinical signs of inflammation and sepsis, as well as with the non-inflammatory complications. The CRP and Leu changes were not statistically significant and their levels are commonly increased by the surgical procedure itself.

Systemic inflammatory response syndrome and the resulting complications continue to be important causes of morbidity in surgical patients. A favourable prognosis of patients with postoperative inflammatory intraabdominal complications is limited by forwardness if diagnosis of this severe complication. Cytokines play a significant role not only in regulating pathogenic mechanisms, during the rising of SIRS, but can themselves directly lead to tissue damage. Increased concentrations of inflammatory cytokines observed in the initial phase of postoperative complications have great significance in the early diagnosis of systemic complications. Procalcitonin, alongside to cytokines, appears as a significant parameter. Despite lots of its pathophysiological points are unclear it is a highly selective and specific indicator of systemic bacterial inflammation. Leptin is not only a hormone of adipocytes but also a member of inflammatory network of cytokines and acute phase reactants. Leptin is possibly a necessary factor for adequate course of acute phase reaction. Proinflammatory cytokines as interleukin-1 or tumour necrosis factor-alpha are the main regulatory factors of leptin in this period.

It is known that in cases of increased bone remodelation rate, i.e. after castration, local bone blood flow is also increased. But in case of adequate hormonal substitution, bone blood flow, similarly as the remodelation rate, return to normal ranges. Until now, there is no knowledge, if other drug can influence enhanced bone blood flow in oophorectomized animals. In this study authors treated oophorectomized female rats with calcitonin and followed bone blood flow, together with biochemical parameters of bone remodelation activity (osteocalcine), IGF-I levels, weight of bone ash and bone density. The female rats were divided in four groups: controls, oophorectomized, with calcitonin and oophorectomized with calcitonin. The bone blood flow was determined by method of body dispersion of radioactive strontium labelled microspheres. The results of this study show, that, in comparison with controls, the bone remodelation rate (documented with increased osteocalcine levels) and radioactive strontium labelled microspheres capture in bone in increased after oophorectomy (p0.05). Ash weight and bone density were decreased (p0.05). Simultaneously, the blood IGF-I levels were increased (p0.05). After oophorectomized animals were treated with calcitonin, all parameters mentioned above headed towards normal ranges in comparison with group of oophorectomized female rats without calcitonin (p0.05). Changes of serum IGF-I levels follow changes of microspheres capture in each group of animals. Authors support the hypothesis, that blood levels of IGF-I could influence local bone blood flow. Calcitonin treatment of oophorectomized animals diminishes also decrement of ash weight and bone density. Results of this work show, that similarly as hormonal substitution therapy after oophorectomy, calcitonin also diminishes increased bone blood flow and bone remodelation parameters. The degree of bone blood flow is probably connected with activity of bone remodelling.

Incidence of bacterial infections in hospitalised patients with liver disease is high. Due to a liver dysfunction immune reactivity is significantly impaired and bacterial infections are more frequent. Also incidence of nosocomial infections is higher in patients with liver disease compared to patients hospitalised for other conditions. To make a differential diagnosis of infectious and non-infectious aetiology of an inflammation is very difficult. Characteristic laboratory tests for bacterial infection include test of a number of leucocytes in peripheral blood, differential count of leucocytes, erythrocyte sedimentation, procalcitonin, C-reactive protein, tumor necrosis factor alpha, interleukin-1, interleukin-6, interleukin-8, and complement fragment C3a. Clinically the most significant are C-reactive protein test and procalcitonin test. Procalcitonin is a protein, a calcitonin precursor, which is in healthy individuals produced by cells of thyroid gland. A half-life of procalcitonin in serum is 20-24 hours which makes it suitable for daily monitoring and enables to control a course of treatment and to distinguish bacterial infection from other types of inflammations. Procalcitonin levels rise in bacterial, parasite, and yeast infections. Elevated procalcitonin levels appear only in inflammations of an infectious etiology with systemic signs. In patients with liver cirrhosis bacterial infections are more frequent. They usually include spontaneous bacterial peritonitis, infection of the respiratory system, urinary infections, and bacteremia. A timely proof of a bacterial infection and an appropriate and effective antibiotic therapy lead to an improvement of the general state of a patient and to his/her better prognosis. Procalcitonin determination is appropriate for diagnosing infections and control of treatment.

One of the most difficult tasks in differential diagnosis of patients with septic syndrome at the Intensive Care Units is to differentiate between infection and non-infection etiology of this syndrome. In the last years, new parameters have played an important role in this area--C-reactive protein, Interleukin-6 and procalcitonin.Of the investigation was to compare these three parameters in differential diagnosis of the septic syndrome. THE COHORT AND METHODS: The authors examined 56 patients (17 women and 39 men, mean age being 43 and 51 years, respectively) hospitalized at the Intensive Care Units who corresponded to the criteria of the syndrome of inflammatory response, sepsis or septic shock. A total of 99 examinations were done. The samples were taken up to 24 hours after the beginning of clinical symptomatology and submitted to the laboratory within four hours. Immediately afterwards the determination of concentrations of all three parameters--C-reactive protein, interlaukin-6 and procalcitonin, were done. The results of the examinations were compared to each other as well as to the diagnosis of sepsis--the confirmed infection etiology.In all the evaluated parameters the authors detected significant differences between the values of entry examination and all measurements between the patients with the syndrome of systemic inflammatory response and septic shock as well as among patients with sepsis and the septic shock. Likewise, the authors confirmed significant differences between concentrations of all three parameters in comparing the patients with sepsis and those with the septic shock. Only in the case of procalcitonin there was a significant difference in concentration between patients with the syndrome of systemic inflammatory response of non-infectious etiology and those with sepsis. The concentration of procalcitonin was the only predictive marker of diagnosis with the correlation coefficient r = 0.7263, r2 = 0.5275, P0.00005.Calcitonin proved to be the most specific parameter in demonstrating infection etiology in patients with the septic syndrome, its predictive value being higher than that of C-reactive protein and Interleukin-6. Monitoring of calcitonin dynamism provides important information on efficiency of the applied antibiotic treatment. In patients with diagnostic uncertainties as far as the etiology of the septic syndrome is concerned; procalcitonin is the parameter of choice, while it may be supplemented with the examination of C-reactive protein.

The dynamic changes in levels of procalcitonin (PCT), as well as other cytokines and acute phase proteins (APP) in post-operative stages reflect the systemic immune response, integrating perioperative infectious and non-infectious stimuli. This study evaluates PCT in context of 16 other inflammatory parameters in patients with different types of infectious post-operative complications. It analyses the specificity and sensitivity of PCT, cytokines and APP and their relationships during systemic inflammatory response.The study involved the following groups of patients: those with confirmed bacterial sepsis, fulfilling the SIRS criteria (N = 28), those with limited infectious site at the wound (N = 16), those with post-operative pneumonia (N = 15) and a control group of N = 25. In 24-hour interval we assessed plasma levels of: PCT, TNF-alpha, IL-1 beta, IL-1ra, IL-6, IL-8, sIL-2R and a spectrum of APP.PCT in patients with wound infection (1.4 +/- 0.31 ng/ml) and in those with pneumonia (0.7 +/- 0.30 ng/ml) does not rise above levels expected in uncomplicated post-op course (1.7 +/- 0.04 ng/ml), but it differs significantly in comparison to healthy controls (0.2 +/- 0.07 ng/ml). Initial levels of PCT as well as their maximum levels were significantly different in septic patients compared to other groups (p0.001). According to specificity and sensitivity tests PCT is the most significant marker for diagnosis of sepsis as opposed to uncomplicated post-operative course (AUC 0.91, CI 0.82-1.0).Individual inflammatory parameters vary in sensitivity and specificity to causative stimulus. PCT when compared to major cytokines and APP reacts sensitively mainly to systemic stimuli accompanying bacterial infection, notably endotoxin. It is characterized by markedly lower sensitivity to non-bacterial stimuli (trauma of surgery) or localized bacterial inflammations. It is this behaviour that makes it a useful diagnostic tool in post-op courses. Unlike other parameters, PCT allows with sufficient sensitivity and specificity single-test diagnosis of initial sepsis.

Early diagnosis of peritoneal inflammation in the initial stage with equivocal clinical manifestations is not always simple. At present there are in the literature many new laboratory indicators which to a different extent describe the inflammatory process. In the present paper the authors focused attention on the practical importance of the use of cytokines in the diagnosis of peritoneal inflammations. They compare the diagnostic impact of clinical examination as compared with assessed plasma concentrations of inflammation promoting cytokines. The authors maintain that the diagnosis of secondary peritonitis is based on the clinical examination of the patient. Elevated values of PCT or IL-6 can support this clinical conclusion. In postoperative peritonitis dynamic investigation of cytokines is important. The diagnosis of tertiary peritonitis is based on laboratory findings.

Procalcitonin (PCT) is a new early indicator of developing systemic bacterial infection. As compared with other anti-inflammatory markers (cytokines, acute stage proteins), the attained plasma levels during extensive but uncomplicated surgery are by orders lower than maximal levels during sepsis. The authors assume that PCT will be used in surgical practice as an early indicator of developing systemic bacterial infection (in multiple injuries, after surgery) and for subsequent evaluation of the effectiveness of treatment of septic conditions.

The objective of this study was to compare effects of 17 beta-estradiol and intranasal salmon calcitonin on bone mass and biochemical markers of bone turnover in postmenopausal women with an accelerated bone loss and osteopenia or osteoporosis.72 women with significantly increased bone resorption were evaluated (urinary hydroxyproline/creatinineor = 21.9 mmol/mol, mean age, 53.7 +/- 6.3 years, time since menopause 6.1 +/- 2.6 years). All patients received daily 500 mg Ca2+ and 400 IU vitamin D supplement. 48 patients with osteopenia and 24 patients with osteoporosis were randomly allocated to treatment with open-label 17 beta-estradiol (50 micrograms transdermally or 2 mg orally) or calcitonin (200 IU every other day). Bone mass was measured by dual-energy x-ray absorptiometry (DPX-L, Lunar, C.V., 1.10 +/- 0.55% and 1.41 +/- 0.55%, lumbar spine and femoral neck, respectively) every six month for 2.5 year, bone stiffness was measured by ultrasound (Achilles, Lunar, C.V., 3.88 +/- 1.95%). Biochemical markers of bone turnover (plasma osteocalcin and tartrate-resistant acid phosphatase, serum bone specific alkaline phosphatase and urinary hydroxyproline) were measured before and after 6, 12 and 24 month of treatment. Patients who received 17 beta-estradiol experienced significant increases (p0.05) in bone mass on the first and second year (by 2.6% and 2.1% at lumbar spine, 1.1% and 1.0%, at femoral neck, and 2.3% and 2% at the heel). A significant positive correlation was found between rates of bone mass change in all sites (p0.001). No statistically significant bone changes were found in calcitonin treated patients. In 17 beta-estradiol treated patients, biochemical markers of bone turnover decreased by 40-50% to the mean values in premenopausal women. In calcitonin treated patients, biochemical markers reached the upper normal limit.Estrogen replacement therapy increases bone mass in lumbar spine as well as in femoral neck. It is efficient for both prevention and treatment of postmenopausal osteoporosis. Salmon calcitonin effectively prevents bone loss. Efficacy of both the treatment can be assessed after 6 months using a biochemical marker of bone resorption and after 2 years using dual-energy x-ray densitometry.

Basic indicators of calcium and bone metabolism and the calcium tolerance test were investigated in patients with untreated hyperthyroidism, Hashimoto's thyroiditis, after total thyroidectomy and in controls. In florid hyperthyroidism elevated values of indicators of bone new formation (osteocalcin and bone fraction of alkaline phosphatases) and of bone resorption (urinary pyridinoline and deoxypyridinoline) were found and a protracted return of the serum calcium level to baseline values (during the 120th minute after completed infusion containing calcium). The calcitonin serum levels were significantly reduced after completion of the infusion up to the 120th minute. These results suggest a reduced calcitonin activity in hyperthyroidism, caused probably by exhaustion of C cells during the prolonged tendency of hypercalcaemia associated with untreated hyperthyroidism. In patients with autoimmune Hashimoto's thyroiditis no significant deviations in basal indicators of the calcium and bone metabolism were found nor deviations of the serum calcium and calcitonin levels during the calcium tolerance test. After total thyroidectomy the basal values of calcitoninaemia are significantly reduced and during the calcium tolerance test the elevated serum calcium level persists from the end of the calcium containing infusion up to the 120th minute. The calcitonin values are at all time intervals significantly low or cannot be detected (during the 120th and 240th minute). Changes of the serum calcium and calcitonin level are due to the surgical removal of the calcitonin source, thyroid C cells. The investigation confirmed the impaired calcium and bone metabolism and impaired calcium tolerance test in hyperthyroidism and in particular after total thyroidectomy. Reduced calcitonin values in these patients can act as a factor promoting the development of osteoporosis.

In a group of 94 patients with a histologically verified medullary thyroid carcinoma were 59 patients with the sporadic form and 35 patients with the familial form. After radical surgery and subsequent actinotherapy in all patients the values of immunoreactive calcitonin were monitored along with the sonographic examination. In all with calcified thyroid residues confirmed on sonography, or when metastases were detected in the liver, elevated or high levels of immunoreactive calcitonin were found. The authors emphasize the importance of this examination for the early detection of relapses of medullary thyroid carcinoma.

A radioimmunoanalytical determination of the immunoreactive calcitonine in the humen serum was worked out using the authors' own specific antiserum, the preparation and properties of which are reported in the present paper. The precision and reliability of the analytical procedure is within the usual limits (the intraserial variation coefficient was 8.6%, the calculated sensitivity was 6 pg/ml). The reported procedure was employed to determine calcitonine in a larger number of patients who were examined because of suspected medullar carcinoma of the thyroid gland and in patients suffering from other thyropathies. The results are discussed from the viewpoint of heterogeneity of calcitonine in the circulation.

The author describes the excellent effect of two-years therapy of a female patient suffering from multiple myeloma, using the calcitonin preparation Miacalcic Sandoz. During the two and a half year follow up of the patient only a small progression of the bone affection occurred. The patient who on account of pain was treated with opiates was unable to walk unaided, now walks does not take analgesics.

The review concentrates on calcitropic hormones (parathormone, calcitonin and the active metabolite of vitamin D-1,25-dihydroxyvitamin D3) and their action on bone remodeling. Attention is drawn to mechanisms of their action on the bone cell, on their manifestations in histology of osseous tissue and clinical symptomatology in pathological conditions. Attention is also drawn to the possible therapeutic application of calcitropic hormones.