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1.
Transplant Proc ; 51(10): 3369-3374, 2019 Dec.
Article in English | MEDLINE | ID: mdl-31739988

ABSTRACT

INTRODUCTION: Post-transplant diabetes mellitus (PTDM) is a serious and frequent metabolic complication after the transplantation of solid organs. PTDM incidence 12 months after the transplantation is 2.5%-25%. MATERIALS AND METHODS: It is a retrospective analysis with 6-month follow-up of patients after liver transplantation without diabetes mellitus type 1 or 2 at the time of transplantation. We recorded all known risk factors for PTDM; however, only patients with tacrolimus in standard immunosuppression protocol were included in the analysis. RESULTS: The PTDM incidence in the group of 102 patients was 18.6%. We identified following independent risk factors for PTDM: alcohol-related liver disease (Hazard Ratio 1.8261 [1.2246-2.723], P = .0031) and average level of tacrolimus ≥ 10 ng/mL (2.5482 [1.1592-5.6019], P = .0199). PTDM was diagnosed in average 2.5 months after the liver transplantation. CONCLUSION: PTDM leads to infections, cardiovascular disease, and decreased survival. The mechanism by which alcohol-related liver disease influences the development of PTDM remains unclear.


Subject(s)
Diabetes Mellitus, Type 2/etiology , Liver Diseases, Alcoholic/complications , Liver Transplantation/adverse effects , Postoperative Complications/etiology , Adult , Female , Humans , Immunosuppression Therapy/methods , Immunosuppressive Agents/therapeutic use , Incidence , Liver Diseases, Alcoholic/surgery , Male , Middle Aged , Retrospective Studies , Risk Factors , Tacrolimus/therapeutic use
2.
Vnitr Lek ; 64(4): 432-436, 2018.
Article in Czech | MEDLINE | ID: mdl-29791178

ABSTRACT

Combination of Turner syndrome (TS) and classic congenital adrenal hyperplasia (CAH) is rare. Globally, the incidence of CAH, autosomal recessive disorder caused by enzyme defect of steroidogenic pathway, is very low (1 : 10 000-16 000). 90 % of CAH cases are caused by 21-hydroxylase gene mutation (CYP21A2). Globally, the incidencie of Turner syndrome reaches 1 : 2 500. Phenotypically, females with TS may render wide spectrum of clinical features. Dominant symptoms are lowered terminal height and gonadal dysgenesia, ultimately leading to absence of puberty and infertility. Virilisation may be evident among TS women with chromosome Y 45, X/46, XY. We present a 57 year old woman suffering from both TS 45, X/46, XX and 21-hydroxylase deficiency. Based on the intersex, she was misdiagnosed as a male after the birth. Dominant signs were intrauterine growth retardation and Prader 5 virilisation of the external genitalia. Testes were not palpable. Laparoscopy at the age of 6 showed uterus and ovaries. After this examination, clitoroplasty and vaginoplasty was performed. Karyotyping revealed a 45, X/46, XX pattern. The presence of virilising features at the time of puberty however could not be explained with the diagnosis of Turner syndrome. Laboratory tests revealed elevated level of 17-hydroxyprogesterone, dehydroepiandrosterone with low cortisol concentration and elevated ACTH. With the genomic analysis CYP21A2 gene, namely IN2G (IVS 2-13 A/C>G), large deletion/conversion was detected. Glucocorticoid treatment was initiated. Due to increased plasma renin concentration, fludrocortisone therapy was also initiated. Within this therapy, patient´s state improved significantly.Key words: congenital adrenal hyperplasia - CYP21A2 - Turner syndrome - 21-hydroxylase deficiency.


Subject(s)
Adrenal Hyperplasia, Congenital , Turner Syndrome , Adrenal Hyperplasia, Congenital/complications , Adrenal Hyperplasia, Congenital/diagnosis , Adrenal Hyperplasia, Congenital/genetics , Female , Glucocorticoids , Humans , Middle Aged , Steroid 21-Hydroxylase/genetics , Turner Syndrome/complications , Turner Syndrome/genetics
3.
BMC Cardiovasc Disord ; 17(1): 117, 2017 05 08.
Article in English | MEDLINE | ID: mdl-28482816

ABSTRACT

BACKGROUND: The role of vaspin in the pathogenesis of stable coronary artery disease (SCAD) have been repeatedly addressed in clinical studies. However, from the point of view of clinical practice, the results of earlier studies are still inconclusive. METHODS: The data of 106 SCAD patients who received coronary angiography and 85 coronary artery disease-free controls were collected and analysed. The patients were divided into subgroups according to their pre-test probability (PTP) and according to the result of coronary angiography. Fasting vaspin concentrations were compared between subgroups of SCAD patients and between target group and controls. The effect of age and smoking on the result of coronary angiography was compared to the effect of vaspin using the binomial regression. RESULTS: We did not find significant difference in vaspin level between target group and controls. Unless the pre-test probability was taken into account, we did not find vaspin difference in the target group, when dividing patients on the basis of presence/absence of significant coronary stenosis. In the subgroup of SCAD patients with PTP between 15% - 65%, those with significant coronary stenoses had higher mean vaspin concentration (0,579 ± 0,898 ng/ml) than patients without significant stenoses. (0,379 ± 0,732 ng/ml) (t = -2595; p = 0,012; d = 0,658; 1-ß = 0,850). Age, smoking status and vaspin significantly contributed to the HSCS prediction in binomial regression model in patients with low PTP (OR: 1.1, 4.9, 8.7, respectively). CONCLUSION: According to our results, vaspin cannot be used as an independent marker for the presence of CAD in general population. However, our results indicate that measuring vaspin in SCAD patients might be clinically useful in patients with PTP below 66%.


Subject(s)
Coronary Angiography , Coronary Artery Disease/blood , Coronary Artery Disease/diagnostic imaging , Coronary Stenosis/blood , Coronary Stenosis/diagnostic imaging , Serpins/blood , Aged , Biomarkers/blood , Case-Control Studies , Chi-Square Distribution , Fasting/blood , Female , Humans , Linear Models , Male , Middle Aged , Predictive Value of Tests , Prognosis , Severity of Illness Index
4.
Vnitr Lek ; 63(2): 139-144, 2017.
Article in Czech | MEDLINE | ID: mdl-28334546

ABSTRACT

Parathyroid cancer is a rare endocrine malignancy, representing less than 1 % of all cases of primary hyperparathyroidism. The exact etiology of the disease remains unknown. Known risk factors include neck irradiation, end stage renal failure, genetic factors, particularly the the HPRT2/CDCT73 gene mutation. The clinical picture is often indolent, yet progressive with a trend of local invasion and metastasis formation in advanced disease. The clinical picture includes symptoms of severe and resistant hypercalcemia, requiring intensive therapy often with the need of dialysis. Radical surgery is the mainstay of the parathyroid cancer treatment. Chemotherapy and radiotherapy are generally ineffective. An early and correct diagnosis of parathyroid carcinoma significantly influences both morbidity and mortality.Key words: diagnosis - hyperparathyroidism - parathyroid cancer - treatment.


Subject(s)
Carcinoma/epidemiology , Kidney Failure, Chronic/epidemiology , Parathyroid Neoplasms/epidemiology , Radiotherapy/statistics & numerical data , Carcinoma/complications , Carcinoma/genetics , Carcinoma/surgery , Humans , Hypercalcemia/etiology , Hyperparathyroidism/etiology , Hypoxanthine Phosphoribosyltransferase/genetics , Mutation , Neck , Parathyroid Neoplasms/complications , Parathyroid Neoplasms/genetics , Parathyroid Neoplasms/surgery , Risk Factors
5.
Int J Endocrinol ; 2015: 967698, 2015.
Article in English | MEDLINE | ID: mdl-26783391

ABSTRACT

Cerebrovascular disorders, particularly ischemic stroke, are one of the most common neurological disorders. High rates of overweight and obesity support an interest in the role of adipose tissue and adipose tissue releasing cytokines in inducing associated comorbidities. Adipokines can serve as a key messenger to central energy homeostasis and metabolic homeostasis. They can contribute to the crosstalk between adipose tissue and brain. However recent research has offered ambiguous data on the network of adipose tissue, adipokines, and vascular disorders. In our paper we provide a critical insight into the role of adipokines in evolution of ischemic stroke.

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