RESUMO
Fibroblast growth factor 23 (FGF23) has been casually linked to numerous hypophosphatemic bone diseases, however connection with bone loss or fragility fractures is still a matter of debate. The purpose of this review is to explore and summarise the known actions of FGF23 in various pathological bone conditions. Besides implication in bone mineralisation, elevated FGF23 showed a pathological effecton bone remodelling, primarily by inhibiting osteoblast function. Unlike the weak association with bone mineral density, high values of FGF23 have been connected with fragility fracture prevalence. This review shows that its effects on bone are concomitantly present on multiple levels, affecting both qualitative and quantitative part of bone strength, eventually leading to impaired bone strength and increased tendency of fractures. Recognising FGF23 as a risk factor for the development of bone diseases and correcting its levels could lead to the reduction of morbidity and mortality in specific groups of patients.
Assuntos
Doenças Ósseas Metabólicas , Hipofosfatemia , Humanos , Fatores de Crescimento de Fibroblastos/metabolismo , Fator de Crescimento de Fibroblastos 23 , Osso e Ossos/metabolismoRESUMO
We present eight cases of the homozygous MCPggaac haplotype, which is considered to increase the likelihood and severity of atypical hemolytic uremic syndrome (aHUS), especially in combination with additional risk aHUS mutations. Complement blockade (CBT) was applied at a median age of 92 months (IQR 36-252 months). The median number of relapses before CBT initiation (Eculizumab) was two. Relapses occurred within an average of 22.16 months (median 17.5, minimum 8 months, and maximum 48 months) from the first subsequent onset of the disease (6/8 patients). All cases were treated with PI/PEX, and rarely with renal replacement therapy (RRT). When complement blockade was applied, children had no further disease relapses. Children with MCPggaac haplotype with/without additional gene mutations can achieve remission through renal replacement therapy without an immediate need for complement blockade. If relapse of aHUS occurs soon after disease onset or relapses are repeated frequently, a permanent complement blockade is required. However, the duration of such a blockade remains uncertain. If complement inhibition is not applied within 4-5 relapses, proteinuria and chronic renal failure will eventually occur.
Assuntos
Síndrome Hemolítico-Urêmica Atípica , Falência Renal Crônica , Criança , Humanos , Síndrome Hemolítico-Urêmica Atípica/tratamento farmacológico , Síndrome Hemolítico-Urêmica Atípica/genética , Haplótipos , Cognição , Proteínas do Sistema ComplementoRESUMO
Fibroadenoma is the most prevalent benign breast tumor. It consists of epithelial and stromal components. In general, breast tumors are highly hormonally dependent and growth hormone by its physiology may have a possible oncogenic potential. Therefore, the aim of this study was to determine the expression of growth hormone and growth hormone receptor in epithelial and stromal components of fibroadenomas. Study group included 30 randomly chosen fibroadenomas from female patients aged between 18 and 69 years. The expression of growth hormone and growth hormone receptor was defined in both histologic components of fibroadenomas. Growth hormone was expressed in 96.7% of both epithelial and stromal components of fibroadenomas, with stronger expression in the stromal component. The same percentage of positive reaction (96.7%) was obtained in the epithelial component of fibroadenomas for growth hormone receptor expression. Only 6.7% of stromal components tested for growth hormone receptor were positive. The high expression of growth hormone and growth hormone receptor in fibroadenoma tissue indicates their possible role in the pathogenesis of this tumor. Follow up of patients with high expression of growth hormone and growth hormone receptor may be suggested.
Assuntos
Neoplasias da Mama/química , Fibroadenoma/química , Hormônio do Crescimento/análise , Receptores da Somatotropina/análise , Adolescente , Adulto , Idoso , Epitélio/química , Feminino , Humanos , Imuno-Histoquímica , Pessoa de Meia-Idade , Distribuição AleatóriaRESUMO
The real prevalence of resistant hypertension (RH) is unknown. Studies suggest that it affects 10%-15% of patients treated for hypertension by primary care physicians. RH is defined as blood pressure (BP) remaining above the goal despite the use of optimal doses of 3 or more medicines of different classes (including a diuretic). It means BP >140/90 mm Hg for the general population and >130/80 mm Hg for patients with diabetes or kidney disease. Prior to diagnosing a patient as having RH, it is important to document medication compliance and exclude white-coat hypertension, inaccurate BP measurement, and secondary causes. The role of aldosterone in RH has gained increasing recognition. There is strong evidence for the use of spironolactone as a highly effective antihypertensive agent. Aldosterone plays a significant role in RH pathogenesis, primarily due to its vasoconstrictive effects and the possibility of altering vascular compliance. In RH, there is a high prevalence of cardiac and extra-cardiac target organ damage. It is known that BP control in chronic kidney disease is the key factor for reducing cardiovascular risk and renal disease progression. The objective of the study was to evaluate the prevalence of RH in predialysis nondiabetic (CKD stage I-IV) patients.