Influence of Disease Activity and Body Composition Parameters on Cross-Sectional Area of the Median Nerve in Acromegalic Patients.

Carpal tunnel syndrome (CTS) is neuropathy that occurs due to compression of the median nerve in the carpal tunnel. Acromegaly is one of the important causes of CTS. The aim of this study was to examine median nerve with ultrasound in acromegalic patients and to assess the relationship with activity, duration of disease and body composition parameters. We prospectively examined the cross-sectional area (CSA) of the median nerve with high-resolution ultrasound in 107 acromegalic patients (70 females and 37 males) and 107 healthy controls (70 females and 37 males) matched for age, gender, and BMI. Body composition parameters were assessed by dual-energy X-ray absorptiometry (DXA). The Student t-tests and Pearson correlation were used for data analysis. The cross sectional area of the median nerve was increased in acromegalic patients compared to controls (11.9 ± 4.8 mm2 vs. 7.7 ± 2.4 mm2, P < 0.001). Positive correlation was found between IGF-1 levels and CSA in the acromegalic group (R = 0.400, P < 0.001). Relationship between CSA and duration of acromegaly was not confirmed. In acromegalic patients, BMI correlated with the CSA (R = 0.294, P = 0.002). There was no significant difference in BMI, fat mass between the acromegalic and control group, but lean mass was higher in acromegalic patients compared with controls (54.8 ± 13.3 vs. 51 ± 11.6, P = 0.047). Lean mass and LMI (total body lean mass/height) positively correlated with CSA in acromegalic patients (R = 0.340, P < 0.001; R = 0.424, P < 0.001). No correlation was observed between fat mass and CSA of median nerve in all groups. We confirmed the enlargement of the median nerve in acromegalic patients. This enlargement is proportional to the degree of IGF-1 levels and is not dependent on the duration of the disease. The enlargement of the median nerve in acromegalic patients also depends on lean body mass and is not dependent on fat body mass.

The role of proteinuria, paricalcitol and vitamin D in the development of post-transplant diabetes mellitus.

INTRODUCTION: Post-transplant diabetes mellitus (PTDM) occurs most frequently during the first year after transplantation. We focused on parameters of calcium-phosphate metabolism and proteinuria as possible new risk factors for PTDM after kidney transplantation. MATERIALS AND METHODS: We have prospectively identified risk factors for post-transplant diabetes mellitus with follow-up of 12 months in a set of 167 patients after kidney transplantation. Patients with diabetes mellitus type 1 and type 2 as well as patients using ciclosporin A or mTOR inhibitor have been excluded from the monitoring. From the perspective of immunosuppression it was a homogeneous set of patients. RESULTS: We identified the following independent risk factors for PTDM in our set: average proteinuria > 0.300 g/24 h (HR 3.0785, (95 % CI 1.6946-5.5927), p=0.0002), level of vitamin D<20 ng/ml (HR 5.4517, (95 % CI 2.3167-11.8209), p1.45 mmol/l (HR0.0821, (95 % CI0.0042-1.5920), p=0.0439). The lowest occurrence of PTDM and proteinuria was recorded in patients whose treatment included paricalcitol (p<0.0001) and these patients had at the same time the highest level of vitamin D (p<0.0001). CONCLUSION: Deficit of vitamin D, proteinuria and hyperphosphatemia have been independent risk factors for the development of PTDM in our set. We identified the usage of paricalcitol as protective factor with regard to the PTDM development (Tab. 6, Fig. 4, Ref. 29).

The effect of adenoidectomy on cough reflex sensitivity in atopic children.

The aim of this study was to determine whether cough sensitivity is changed after adenoidectomy in atopic children with chronic cough. 21 Children having symptoms of chronic cough and adenoid hypertrophy verified by nasal fiberoptic endoscopy were submitted to cough sensitivity measurement before and after adenoidectomy. Their pulmonary function was within normal range. Concentrations of capsaicin causing two (C2) and five coughs (C5) were reported. Children' (14 boys and 7 girls, mean age 6,52 yrs) cough sensitivity (geometric mean, with 95% CI) for C2 was preoperatively (before adenoidectomy) 19.95 (9.95-39.98) micromol/l vs. children' C2 postoperatively 14.04 (7.16-27.55) (P = .083 for Wilcoxon paired two sample test). Children' C5 was preoperatively 86.26 (39.25-189.57) micromol/l vs. C5 postoperatively 95.23 (46.33-195.75) micromol/l (P = .794 for Wilcoxon paired two sample test). We conclude that cough sensitivity for C2 and C5 was not significantly changed after adenoidectomy in atopic children with chronic cough.

Correlation between CMV Infection and Post-transplantation New-onset Diabetes Mellitus.

BACKGROUND: New-onset diabetes mellitus after transplantation (NODAT) is a well-known complication of transplantation. OBJECTIVE: To determine the correlation between CMV infection and NODAT. METHODS: Retrospectively, we detected CMV replication (PCR) in every month after renal transplantation in the first 12 months of the procedure in a homogenous group of patients from the immunosuppression point of view. RESULTS: In 167 patients (64 with NODAT and 103 in the control group), the average amount of CMV viremia was not significantly different between the NODAT and the control group (p=0.929). In the 10th month of transplantation, we recorded a significantly higher CMV viremia in the NODAT group (p<0.0001), however, in the multivariant analysis, the observed statistical difference vanished. The survival of patients and grafts was 12 months after kidney transplantation without any statistically significant difference between the studied groups (p=0.611 and p=0.538, respectively). CONCLUSION: CMV is not a risk factor for NODAT.

Hypoglycemia associated with non-islet cell tumors.

UNLABELLED: Tumor hypoglycemia is rare but life-threatening medical condition which may be associated with insulinoma and non-islet cell tumors (mainly of mesenchymal origin). The pathogenesis is connected with abnormal processing of insulin-like growth factor-2 (IGF-2) precursor and production of pathognomic "big" IGF-2 - incompletely processed posttranslational precursor of IGF-2, which is responsible for hypoglycemia. Other typical laboratory features include low level of fasting glucose and C-peptide, low IGF-1 and increased IGF-2 : IGF-1 ratio. Although paraneoplastic hypoglycemia is often present in patients with already diagnosed malignancy, it is necessary to consider this possibility in patients having unclear and inexplicable hypoglycemia. The adequate treatment can significantly reduce the symptoms and improve the quality of life.    KEYWORDS: tumor hypoglycemia, non-islet cell tumor, insulin-like growth factor.

[Genetic and molecular background in autoimmune diabetes mellitus]. / Genetický a molekulový podklad vývoja autoimunitného diabetes mellitus.

Type 1 diabetes mellitus (T1 DM) is caused by autoimmune-mediated and idiopathic beta-cell destruction of the pancreatic islets of Langerhans resulting in absolute insulin deficiency. Susceptibility to T1 DM is influenced by both genetic and environmental factors. It is generally believed that in genetically susceptible individuals, the disease is triggered by environmental agents, such as viral infections, dietary factors in early infancy, or climatic influences. Many candidate genes for diabetes have been reported; those within the Major Histocompatibility Complex being among the most important. The most common autoantigens are insulin, glutamic acid decarboxylase 65, insuloma-associated antigen 2, and zinc transporter ZnT8. The destruction of beta-cells is mediated mainly by cellular mechanisms; antibodies only seem to reflect the ongoing autoimmune processes and are not directly involved in the tissue damage. They, however, appear prior to the onset of insulin deficiency which makes them suitable for use in the prevention of the disease.

[Paraneoplastic hypoglyacemia]. / Paraneoplastická hypoglykémia -  popis prípadu a prehlad problematiky.

Paraneoplastic hypoglyacemia (PH) is a relatively rare phenomenon, which may be caused by insulinomas or nonislet cell tumours (NICT). Both types are among the major "fasting" hypoglyacemia as opposed to reactive postprandial hypoglyacemia. The most common group of nonislet cell tumours causing hypoaglycemia are large mesenchymal tumours, which account for over 50 % of all neoplasms associated with hypoglyacemia. Neuroglycopenic symptoms in patients with NICT may be present for months or years before the actual diagnosis of the underlying disease. Differentiation and correct diagnosis of this type of disease leads to significant improvement in the quality of life of these patients.

Genetic susceptibility to type 1 diabetes mellitus in humans.

Type 1 diabetes mellitus (DM 1A) is an autoimmune disease belonging to the most frequent chronic diseases of the childhood and young adults. DM 1A results from immune-mediated destruction of the insulin-producing beta cells of the pancreas. It is a genetically determined disease and many genes or genetic regions were found to be associated with its induction. In addition to the insulin-dependent diabetes mellitus 1 (IDDM1) gene, which marks the HLA region, and IDDM2 which marks the insulin gene, significant associations of DM 1A to other IDMM genes or genetic regions we reported. We shortly review recent achievements in the field, and the state of current knowledge.

Association of HLA-DPB1 alleles with type I diabetes mellitus in Slovak population.

BACKGROUND: Genes of HLA complex on chromosome 6p21 principally contribute to the genetic risk of insulin-dependent diabetes mellitus type I (T1 DM). Associations of HLA class II loci allelic variants with T1 DM are well established. Another prime candidate, particularly the polymorphic DPB1 gene, has been reported as probably contributing to the disorder, but its relative contribution to the predisposition to the disease is difficult to assess due to strong linkage disequilibrium of HLA alleles. DPB1*0301 and DPB1*0202 have been reported as positively and DPB1*0402 as negatively associated alleles in different Caucasoid populations (predisposing versus protective alleles, respectively). OBJECTIVES: The aim of this study was to establish the occurrence rates of HLA-DPB1 alleles in patients suffering from T1 DM and to compare them with those in healthy subjects. METHODS: A PCR-SSP method was performed to identify HLA-DPB1 alleles in 61 patients and 160 healthy controls. The exact Fisher's test was used to determine the statistical significance of allele frequency differences between patients and control subjects. RESULTS: The analysis of obtained results has shown a significantly decreased frequency of DPB1*0402 and slightly increased occurrence rates of DPB1*0101 and DPB1*1301, respectively in the investigated group of patients. Neither DPB1*0301 nor DPB1*0202 were observed to be over-represented. CONCLUSIONS: The expected significant decrease in the frequency of DPB1*0402 was confirmed, whereas positive associations with DPB1*0301 and DPB1*0202, did not prove to be true, respectively (Tab. 1, Ref: 19).