[Specificities of the Diagnostics and Therapy of Exocrine Pancreatic Insufficiency].

[Specificities of the diagnostics and therapy of exocrine pancreatic insufficiency].

Vnitr Lek. 2013 Jan; 59(1): 65-70
Díté P, Novotny I, Kocna P, Bojková M, Kupka T, Nechutová H, Kianicka B

Exocrine pancreatic insufficiency develops steadily; however, the initial reduction in secretion is practically not diagnosable. More advanced stages, which usually replicate morphological changes, can be determined with tests which asses the exocrine pancreatic capacity. Substantial damage of the pancreas and replacement of viable parenchyma with connective tissue is accompanied by the occurrence of steatorrhoea. This corresponds to a reduction in exocrine pancreatic secretion below 10% of physiological secretion. Exocrine pancreatic secretion tests are still not sufficiently sensitive for diagnosing early stages of pancreas defects and thus are not suitable for diagnostics. Furthermore, detecting reduced exocrine secretion does not provide any information about the aetiology of the disease, e.g. inflammation/tumor. The most precise test is a costly examination, including a stimulation of the gland with enterohormones; however, breath tests are usually recommended for the assessment of exocrine insufficiency therapy. Exocrine pancreatic insufficiency therapy consists of administering drugs containing pancreatin (amylase, lipase, and peptidase) to patients diagnosed with steatorrhoea, manifest pancreatic insufficiency. As standard, capsules containing microparticles of 1-2mm are recommended. They have a protective coating that prevents inactivation in the microparticles of the contained enzymes by gastric hydrochloric acid. The drug should be administered during each meal, i.e. several times a day. The most common mistake during pancreatic enzyme therapy is under dosage. The following rule applies to patients with digestive insufficiency: 40,000-50,000 UNT of lipase are to be administered during “main meals” and 25,000 UNT of lipase during morning or afternoon snacks. The drug should be taken during the meal; insufficient treatment and dosage are associated with insufficient digestion and absorption ofa number of substances and also with pancreatic malabsorption. HubMed – drug


[Drug induced osteoporosis].

Vnitr Lek. 2013 Jan; 59(1): 59-63
Zofková I

Loss of bone mass resulting from the treatment of chronic diseases is not unusual. However, osteoporosis in such patients is typically diagnosed too late, usually after a fracture appears. Particular attention should be given to glucocorticoids, which are commonly used in internal medicine. These hormones delay bone formation (via inhibition of osteoblast differentiation and osteoblast function) and activate bone resorption (through RANKL). Moreover, glucocorticoids inhibit calcium absorption from the intestines, which results in hypocalcemia. Following hyperparathyroidism further accelerates bone resorption. Severe damage to bone microstructure and its mechanical characteristics leads to atraumatic fractures. Bone loss sustained during glucocorticoid treatment occurs very early (3-5 % of bone mass in the first year and up to 1 % each year thereafter). Fortunately, most skeletal damage is reversible with early supplementation of vitamin D and calcium. Osteopenia (osteoporosis) complicates long-term treatment with supressive doses of thyroid hormone most often in females with hypoestrinism. L-thyroxine administered in doses > 0.093 mg/day leads to bone resorption, which is in part due to suppressed (low) levels ofTSH. Medications which pose a high risk of fracture are those which induce hypoestrinism (aromatase inhibitors) and antiandrogens (GnRH agonists). Similarly, some oral antidiabetics (such as thiazolindiones) promote adipogenesis to the detriment of osteogenesis, which increases bone loss. Fractures are also frequently observed in patients treated with selective serotonin reuptake inhibitors, anti-epileptics, diuretics, anticoagulation drugs and proton pump inhibitors. This review discusses the mechanisms of bone damage induced by the abovementioned pharmaceuticals. HubMed – drug


Neuropeptide Y in the noradrenergic neurons induces the development of cardiometabolic diseases in a transgenic mouse model.

Indian J Endocrinol Metab. 2012 Dec; 16(Suppl 3): S569-76
Ruohonen ST, Pesonen U, Savontaus E

Neuropeptide Y (NPY) is a neuropeptide widely expressed in the brain and a peptide transmitter of sympathetic nervous system (SNS) co-released with noradrenaline (NA) in prolonged stress. Association of a gain-of-function polymorphism in the human NPY gene with dyslipideamia, diabetes and vascular diseases suggests that increased NPY plays a role in the pathogenesis of the metabolic syndrome in humans. In the hypothalamus, NPY plays an established role in the regulation of body energy homeostasis. However, the effects of NPY elsewhere in the brain and in the SNS are less explored. In order to understand the role of NPY co-expressed with NA in the sympathetic nerves and brain noradrenergic neurons, a novel mouse model overexpressing NPY in noradrenergic neurons was generated. The mouse displays metabolic defects such as increased adiposity, hepatosteatosis, and impaired glucose tolerance as well as stress-related hypertension and increased susceptibility to vascular wall hypertrophy. The mouse phenotype closely reflects the findings of the several association studies with human NPY gene polymorphisms, and fits with the previous work on the effects of stress-induced NPY release on metabolism and vasculature. Thus, in addition of promoting feeding and obesity in the hypothalamus, NPY expressed in the noradrenergic neurons in the brain and in the SNS induces the development of cardiometabolic diseases. HubMed – drug