RESUMO
Resumen Introducción: A pesar de que el carcinoma de paratiroides es uno de los cánceres menos frecuentes del mundo, es importante tenerlo en cuenta al plantear el diagnóstico diferencial del hiperparatiroidismo primario, ya que su diagnóstico temprano tiene repercusiones en el tratamiento y el pronóstico vital del paciente. Caso Clínico: A continuación, se expone un caso clínico de un paciente con sintomatología abigarrada de hiperfunción paratiroidea que, dada la sospecha clínica de carcinoma de paratiroides y la no infiltración de estructuras adyacentes, fue tratado con una paratiroidectomía. Conclusión: Esta cirugía supone una menor morbilidad, sin suponer un detrimento para la supervivencia global del paciente.
Introduction: Parathyroid carcinoma should be taken into consideration among the differential diagnosis of primary hyperparathyroidism, even though it is one of the less common malignant tumours in the world, because an early diagnosis is essential for the treatment and the prognosis of the patient. Case Report: We present the case of a patient whose symptoms were compatible with hyperfunction of parathyroid gland. Due to the malignant disease suspicion and the non-invasion of adjacent tissue, he was treated with a parathyroidectomy. Conclusión: This type of treatment supposes a lower morbidity without decrease in overall survival, according to bibliography.
Assuntos
Humanos , Masculino , Adulto , Hormônio Paratireóideo/metabolismo , Neoplasias das Paratireoides/metabolismo , Metástase Linfática , Neoplasias das Paratireoides/patologia , Tireoidectomia , Tomografia Computadorizada por Raios X , Paratireoidectomia , UltrassonografiaRESUMO
Both hypoparathyroidism (HypoPT), as well as its pathological counterpart, primary hyperparathyroidism (PHPT), can lead to skeletal abnormalities. Chronic deficiency of PTH in patients with HypoPT is associated with a profound reduction in bone remodeling, with consequent increases in bone density, and abnormalities in microarchitecture and bone strength. It is still not clear whether there is an increase in fracture risk in HypoPT. While standard therapy with calcium supplements and active vitamin D does not restore bone homeostasis, treatment of HypoPT with PTH appears to correct some of those abnormalities. In PHPT, the continuous exposure to high levels of PTH causes an increase in bone remodeling, in which bone resorption prevails. In the symptomatic form of PHPT, patients can present with fragility fractures, and/or the classical radiological features of osteitis fibrosa cystica. However, even in mild PHPT, catabolic skeletal actions of PTH are evident through reduced BMD, deterioration of bone microarchitecture and increased risk of fragility fractures. Successful parathyroidectomy improves skeletal abnormalities. Medical treatment, such as bisphosphonates and denosumab, can also increase bone density in patients with PHPT who do not undergo surgery. This article reviews skeletal involvement in HypoPT and in PHPT, as assessed by bone remodeling, DXA, trabecular bone score, and quantitative computed tomography, as well as data on bone strength and fracture risk. The effects of PTH replacement on the skeleton in subjects with HypoPT, and the outcome of parathyroidectomy in patients with PHPT, are also reviewed here.
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Hiperparatireoidismo Primário , Hipoparatireoidismo , Densidade Óssea , Remodelação Óssea , Osso e Ossos/metabolismo , Humanos , Hiperparatireoidismo Primário/complicações , Hipoparatireoidismo/complicações , Hormônio Paratireóideo/metabolismo , Hormônio Paratireóideo/uso terapêuticoRESUMO
Parathyroid hormone (PTH) has an important role in the maintenance of serum calcium levels. It activates renal 1α-hydroxylase and increases the synthesis of the active form of vitamin D (1,25[OH]2D3). PTH promotes calcium release from the bone and enhances tubular calcium resorption through direct action on these sites. Hallmarks of secondary hyperparathyroidism associated with chronic kidney disease (CKD) include increase in serum fibroblast growth factor 23 (FGF-23), reduction in renal 1,25[OH]2D3 production with a decline in its serum levels, decrease in intestinal calcium absorption, and, at later stages, hyperphosphatemia and high levels of PTH. In this paper, we aim to critically discuss severe CKD-related hyperparathyroidism, in which PTH, through calcium-dependent and -independent mechanisms, leads to harmful effects and manifestations of the uremic syndrome, such as bone loss, skin and soft tissue calcification, cardiomyopathy, immunodeficiency, impairment of erythropoiesis, increase of energy expenditure, and muscle weakness.
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Hiperparatireoidismo Secundário/etiologia , Hormônio Paratireóideo/metabolismo , Insuficiência Renal Crônica/complicações , Uremia/etiologia , Remodelação Óssea , Osso e Ossos/metabolismo , Cálcio/metabolismo , Metabolismo Energético , Fator de Crescimento de Fibroblastos 23 , Fatores de Crescimento de Fibroblastos/metabolismo , Humanos , Hiperparatireoidismo Secundário/metabolismo , Fósforo/sangue , Insuficiência Renal Crônica/metabolismo , Uremia/metabolismoRESUMO
We sought to evaluate the effects of magnesium (Mg) intake deficiency on bone metabolism in rats with induced periodontal disease (PD). Holtzman rats were randomly divided into two groups: Control - animals fed a standard diet and test - animals fed a diet with 90% Mg deficiency. After 60 days on the diets, all animals received ligature on the lower left first molars to induce PD. Animals were euthanized after 30 days following ligature placement. Blood and urine were collected for determination of serum concentrations of Mg, calcium, osteocalcin (OCN), alkaline phosphatase and parathyroid hormone (PTH) by enzyme-linked immunosorbent assay, and the urinary concentration of deoxypyridinoline (DPD). Systemic bone mineral density (BMD), bone volume and architectural bone parameters were evaluated by micro-CT in L4 lumbar vertebrae and mandible. Tartrate-resistant acid phosphatase staining and immunohistochemical (IHC) analysis of inducible nitric oxide synthase (iNOS), Runt-related transcription factor 2 (RUNX2), CD86, CD80, proliferating cell nuclear antigen, vascular endothelial growth factor, OCN and osteopontin were investigated. Reverse-transcription polymerase chain reaction was employed to assess mRNA expression of receptor-activator of nuclear factor-kB ligand, osteoprotegerin (OPG) and interleukin (IL)-6. Mg deficiency was associated with higher concentrations of PTH and DPD, and significant decrease on both systemic and mandibular BMD, as well as greater severity of alveolar and trabecular bone loss. Significant increase in osteoclasts was observed in the test group with PD. IHC analysis showed significant increase in the expression of iNOS and decreased expression of OCN and RUNX2. Increased IL-6 mRNA and decreased OPG mRNA expressions were evidenced in the test group with PD. Mg deficiency caused systemic effects indicative of altered bone metabolism in the vertebrae and affected both immune and stromal cells, aggravating inflammatory bone resorption in the ligature-induced model of periodontitis.
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Densidade Óssea , Reabsorção Óssea , Inflamação/metabolismo , Deficiência de Magnésio/metabolismo , Fosfatase Alcalina/metabolismo , Animais , Biomarcadores/metabolismo , Cálcio/metabolismo , Subunidade alfa 1 de Fator de Ligação ao Core/metabolismo , Interleucina-6/metabolismo , Magnésio/metabolismo , Osteocalcina/metabolismo , Osteoclastos/metabolismo , Hormônio Paratireóideo/metabolismo , Periodontite/metabolismo , RNA Mensageiro/metabolismo , Ratos , Microtomografia por Raio-XRESUMO
Vascular calcification (VC) is common in chronic kidney disease, increases in prevalence as patients progress to end-stage renal disease, and is significantly associated with mortality. VC is a complex and highly regulated process similar to bone formation whereby hydroxyapatite crystals deposit in the intimal or medial layer of arteries. Mineral bone abnormalities are common in chronic kidney disease; reduction in glomerular filtration rate and changes in vitamin D, parathyroid hormone, and fibroblast growth factor 23 result in the dysregulation of phosphorus and calcium metabolism. Cell culture studies, animal models, and observational and clinical studies all suggest this abnormal mineral metabolism plays a role in the initiation and progression of VC in kidney disease. This review will focus on these mineral bone abnormalities and how they may contribute to mechanisms that induce VC in kidney disease.
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Insuficiência Renal Crônica/metabolismo , Calcificação Vascular/metabolismo , Animais , Cálcio/metabolismo , Fator de Crescimento de Fibroblastos 23 , Fatores de Crescimento de Fibroblastos/metabolismo , Glucuronidase/metabolismo , Humanos , Proteínas Klotho , Hormônio Paratireóideo/metabolismo , Fósforo/metabolismo , Insuficiência Renal Crônica/complicações , Calcificação Vascular/etiologia , Vitamina D/metabolismoRESUMO
BACKGROUND AND AIM: Anorexia, which is a common condition in patients on hemodialysis (HD), is characterized by impaired appetite, a subjective condition that hinders anorexia diagnosis. Anorexia is frequently associated with protein energy wasting and inflammation, increasing morbidity and mortality risk. The aim of the study was to evaluate the association between appetite and nutritional, inflammatory, hormonal, and dietary intake parameters in patients on maintenance HD. METHODS: Cross-sectional study with clinical, laboratory, and anthropometric parameters, body composition, muscle function, and dietary intake assessment. To evaluate appetite, a three simple questions questionnaire previously validated was used. After appetite classification, the sample was dichotomized in "normal appetite" and "impaired appetite" and compared. Multiple logistic regression was used to identify association between variables and outcome. RESULTS: 125 patients on HD were included, aged 60.6 ± 14.12 years old, median HD vintage 35.5 months. In dichotomized sample, 78.4% patients showed "normal appetite", and 21.6% "impaired appetite". "Impaired appetite" was independently associated with increased serum PTH (OR 1.001; 95% CI 1.000-1.002; p = 0.03), low zinc intake (OR 0.860; 95% CI 0.746-0.991; p = 0.03) and lower urea serum (OR 0.982; 95% CI 0.965-0.999; p = 0.04). Both groups showed insufficient dietary intake. CONCLUSIONS: Appetite was independently associated with increased serum of PTH, low serum concentration of urea, and low zinc intake which may infer association of appetite with mineral bone disease, protein intake and zinc deficiency.
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Anorexia/metabolismo , Hormônio Paratireóideo/metabolismo , Diálise Renal/efeitos adversos , Adulto , Idoso , Idoso de 80 Anos ou mais , Anorexia/diagnóstico , Apetite , Composição Corporal , Estudos Transversais , Ingestão de Alimentos , Feminino , Humanos , Inflamação/complicações , Masculino , Pessoa de Meia-Idade , Avaliação Nutricional , Estado Nutricional , Inquéritos e Questionários , Síndrome de Emaciação/complicações , Síndrome de Emaciação/diagnóstico , ZincoRESUMO
INTRODUCTION AND OBJECTIVES: Vitamin D plays a role in the immune system, however studies regarding this are scarce. This study aimed to evaluate the nutritional status of vitamin D in patients with Common Variable Immunodeficiency (CVID) or Ataxia-Telangiectasia (A-T) and to relate it to body composition, inflammatory and bone metabolism markers. PATIENTS AND METHODS: This is a cross-sectional and controlled study involving 24 patients of both sexes (59.3% male), aged 8-56 years, with CVID (n=15) or A-T (n=9). The following variables were evaluated: body mass index (BMI), 25-hydroxyvitamin D (25 (OH) D), hepatic profile, parathormone, calcium, phosphorus, alkaline phosphatase, interleukin 6 and high-sensitivity C-reactive protein. RESULTS: The median age was 26.0 years. A deficiency of 25 (OH) D was found in four A-T patients (44%) and two CVID patients (13%). Nine patients with CVI (60%) and six with A-T (66.7%) were overweight and underweight, respectively. There was a negative correlation between vitamin D and fat mass in the CVID group, and vitamin D and BMI in the A-T group. Vitamin D was negatively associated with the percentage of total fat among the patients (ß - 0.842, 95% CI: -1.5-0.17, p=0.015), R2=0.21, after adjusting for sex and age. CONCLUSION: Vitamin D deficiency occurred in a quarter of the patients although there was no difference between the patient and the control group; without association with bone and inflammation biomarkers. The percentage of fat and BMI were negatively associated with the concentrations of 25 (OH) D.
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Ataxia Telangiectasia/metabolismo , Imunodeficiência de Variável Comum/metabolismo , Vitamina D/metabolismo , Adolescente , Adulto , Biomarcadores/metabolismo , Índice de Massa Corporal , Criança , Estudos Transversais , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Hormônio Paratireóideo/metabolismo , Adulto JovemRESUMO
There is increasing epidemiologic and animal evidence that a low calcium diet increases blood pressure. The aim of this review is to compile the information on the link between low calcium intake and blood pressure. Calcium intake may regulate blood pressure by modifying intracellular calcium in vascular smooth muscle cells and by varying vascular volume through the renin-angiotensin-aldosterone system. Low calcium intake produces a rise of parathyroid gland activity. The parathyroid hormone increases intracellular calcium in vascular smooth muscles resulting in vasoconstriction. Parathyroidectomized animals did not show an increase in blood pressure when fed a low calcium diet as did sham-operated animals. Low calcium intake also increases the synthesis of calcitriol in a direct manner or mediated by parathyroid hormone (PTH). Calcitriol increases intracellular calcium in vascular smooth muscle cells. Both low calcium intake and PTH may stimulate renin release and consequently angiotensin II and aldosterone synthesis. We are willing with this review to promote discussions and contributions to achieve a better understanding of these mechanisms, and if required, the design of future studies.
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Cálcio/administração & dosagem , Cálcio/farmacologia , Hipertensão/etiologia , Pressão Sanguínea/efeitos dos fármacos , Pressão Sanguínea/fisiologia , Humanos , Glândulas Paratireoides/efeitos dos fármacos , Glândulas Paratireoides/fisiologia , Hormônio Paratireóideo/metabolismoRESUMO
Chronic kidney disease mineral bone disorder (CKD-MBD) is common in end-stage renal disease and is associated with an increased risk of cardiovascular morbidity and mortality. Mainstays of treatment include decreasing serum phosphorus level toward the normal range with dietary interventions and phosphate binders and treating increased parathyroid hormone levels with activated vitamin D and/or calcimimetics. There is significant variation in serum levels of mineral metabolism markers, intestinal absorption of phosphorus, and therapeutic response among individual patients and subgroups of patients with end-stage renal disease. This variation may be partly explained by polymorphisms in genes associated with calcium and phosphorus homeostasis such as the calcium-sensing receptor gene, the vitamin D-binding receptor gene, and genes associated with vascular calcification. In this review, we discuss how personalized medicine may be used for the management of CKD-MBD and how it ultimately may lead to improved clinical outcomes. Although genetic variants may seem attractive targets to tailor CKD-MBD therapy, complete understanding of how these polymorphisms function and their clinical utility and applicability to personalized medicine need to be determined.
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Doenças Ósseas Metabólicas/terapia , Cálcio/metabolismo , Hiperparatireoidismo Secundário/terapia , Falência Renal Crônica/terapia , Fósforo/metabolismo , Doenças Ósseas Metabólicas/etiologia , Doenças Ósseas Metabólicas/genética , Doenças Ósseas Metabólicas/metabolismo , Doenças Cardiovasculares , Humanos , Hiperparatireoidismo Secundário/etiologia , Hiperparatireoidismo Secundário/metabolismo , Absorção Intestinal , Falência Renal Crônica/complicações , Falência Renal Crônica/metabolismo , Hormônio Paratireóideo/metabolismo , Polimorfismo Genético , Medicina de Precisão , Receptores de Detecção de Cálcio/genética , Calcificação Vascular/etiologia , Calcificação Vascular/metabolismo , Vitamina D/metabolismo , Proteína de Ligação a Vitamina D/genéticaRESUMO
Hyperphosphatemia is a common condition in patients with chronic kidney disease (CKD) and can lead to bone disease, vascular calcification, and increased risks of cardiovascular disease and mortality. Inorganic phosphate (Pi) is absorbed in the intestine, an important step in the maintenance of homeostasis. In CKD, it is not clear to what extent Pi absorption is modulated by dietary Pi. Thus, we investigated 5/6 nephrectomized (Nx) Wistar rats to test whether acute variations in dietary Pi concentration over 2 days would alter hormones involved in Pi metabolism, expression of sodium-phosphate cotransporters, apoptosis, and the expression of matrix extracellular phosphoglycoprotein (MEPE) in different segments of the small intestine. The animals were divided into groups receiving different levels of dietary phosphate: low (Nx/LPi), normal (Nx/NPi), and high (Nx/HPi). Serum phosphate, fractional excretion of phosphate, intact serum fibroblast growth factor 23 (FGF-23), and parathyroid hormone (PTH) were significantly higher and ionized calcium was significantly lower in the Nx/HPi group than in the Nx/LPi group. The expression levels of NaPi-IIb and PiT-1/2 were increased in the total jejunum mucosa of the Nx/LPi group compared with the Nx/HPi group. Modification of Pi concentration in the diet affected the apoptosis of enterocytes, particularly with Pi overload. MEPE expression was higher in the Nx/HPi group than in the Nx/NPi. These data reveal the importance of early control of Pi in uremia to prevent an increase in serum PTH and FGF-23. Uremia may be a determining factor that explains the expressional modulation of the cotransporters in the small intestine segments.