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.

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.

[Hyponatremia - carbamazepine medication complications]. / Hyponatrémia - komplikácia liecby karbamazepínom.

Hyponatremia can be defined like the low sodium concentration, lower that 135 mmol/l. It becomes really serious when the concentration is lower than 120 mmol/l. The most frequent causes of hyponatremia are: the extrarenal loss (GIT, skin, bleeding, sequestration), the renal loss (diuretics, nephritis with the salt loss, osmotical diuresis, the Addison disease), hypothyroidism, the lack of glucocorticoids, emotional stress, pain, pseudohyponatremia (incorrect taking, dyslipoproteinemia). There is fatigue, exhaustion, headache and vertigoes dominating in the clinical record file. By the deficit increasing a patient becomes delirious, comatose even with the shock development. It is necessary to separate sufficient supply of sodium from much more often reason, which is loss of sodium which can be caused by: excessive sweating, vomitting with the metabolical alkalosis development, diarrhoea with the metabolical acidosis development, renal losses (a phase of renal failure). Treatment of hyponatremia: intensive treatment starts at the level of plasmatic concentration of sodium under 120 mmol/l or when neurological symptoms of brain oedema are present. In the therapy it is necessary to avoid fast infusions of hypertonic saline solutions (3-5% NaCl solutions) because of the danger of the development of serious CNS complications (intracranial bleeding, etc.). It is recommended to adjust the plasmatic concentration of sodium up to 120 mmol/l during the first four hours and a subsequent correction should not be higher than 2 mmol per an hour. Treatment of the basic illness is very important. We present 2 case histories: a 74-year old female patient and a 69-year old female patient both with the hyponatremia caused by taking of carbamazepine. We want to inform and warn about not only a well known side effect during long-term treatment but about hyponatremia that arose within 48 hours after the start of taking medicine as well.