[Since 1932, a number of animal studies have demonstrated the correlation of hypomagnesaemia and hypocalcaemia, and the variety of skeletal abnormalities resulting from low magnesium (Mg) intake. Several studies have shown that patients with osteoporosis have a decreased serum magnesium level, which is related to decreased bone mineral content and increased bone fragility. Mg has multiple physiological effects, thus it is not surprising that dozens of hypomagnesaemia-related diseases and symptoms have been reported. Adequate Mg concentration is necessary for the secretion of parathormone and its effect on target organs, activation of vitamin D in the kidney, the maintenance of calcium homeostasis, bone mineralisation and regeneration. Mild hypomagnesaemia is associated with general, atypical symptoms, whereas severe Mg deficiency is a life-threatening condition. Its concentration should be measured in serum and urine. Mg metabolism is determined by its absorption from the intestines and reabsorption in the kidneys. Recently revealed details of these processes give some insights into the mechanisms underlying a number of Mg deficient conditions related to genetic or medical reasons. Mg supplementation may be indicated for patient populations with the highest risk of hypomagnesaemia. For supplementation, the recommended total Mg dose is 350 mg, first in higher doses, several times per day for a longer period, complemented with Ca and K supplementation. Overdosing can only occur in patients with impaired renal function, which necessitates careful monitoring. Adequate Mg supplementation is an inexpensive, safe and effective preventive and therapeutic option for many diseases.]

[Osteoporosis is commonly associated with certain gastrointestinal diseases. Osteoporosis occurs most often in patients with coeliac disease, inflammatory bowel disease, chronic liver disease and following gastric surgery. Prevention, diagnosis and therapy are based on the experiences with elderly and postmenopausal patients with osteoporosis. In this review, we summarise the clinical data regarding bone loss associated with gastrointestinal diseases.]

[The effects of vitamin D in bone health have been known since the 1920s. Recently, it has been proven that its role in the body is much more complex. Activated vitamin D is a steroid hormone that regulates transcription of more than 200 human genes through its receptor that is detectable in almost all types of cells. In contrast to the former conceptions, it can be activated not only in the kidneys; moreover, local 1-α-hydroxylation plays a greater role in its extraskeletal effects. Vitamin D deficiency, currently defined as serum levels of <30 ng/ml, is caused by the lack of ‘effective’ sunlight exposition. Thus, vitamin D deficiency is one of the most frequent deficiencies in the developed world that plays a role not only in the development of skeletal conditions but many other diseases, as well. A low vitamin D level causes a reduced calcium absorption, a higher bone remodelling rate and increased bone loss. It also reduces muscle strength and increases the risk of falling. Normal vitamin D status is required for the effectiveness of drugs for osteoporosis treatment; however vitamin D treatment in itself is not effective in osteoporosis. An increasing number of studies show the benefits of vitamin D supplementation and treatment in extraskeletal conditions. Vitamin D plays an important role in the prevention of several auto-immune diseases, infections, cardiovascular diseases, and cancers. Therefore, all UV-B radiation-deprived adults require an intake of vitamin D to maintain a level of >30 ng/ml. Vitamin D3 treatment is safe. The necessary dose can be reliably approximated by the calculation that an incremental consumption of 100 IU/day raises serum vitamin levels by 1,0 ng/ml. Clinical trials suggest that for the vast majority of individuals, a prolonged intake of 10,000 IU/day does not pose any risk.]

[INTRODUCTION - Children with pituitary insufficiency normally receive growth hormone and thyroid hormone substitution, but glucocorticoid treatment is rarely necessary. Sex hormone replacement is introduced in puberty, which, at the same time, promotes growth and bone maturation. In this study the effect of testosterone replacement on bone mineral content was examined. PATIENTS AND METHODS - Nine boys (16.3±1.3 years) with hypopituitarism were involved in the study who had been receiving growth hormone and thyroid hormone replacement for several years by the beginning of the study.Androgen was substituted by the intramuscular administration of 50 mg testosterone biweekly.The children's height,weight, the rate of pubescence, and bone age were checked, and bone mineral density was measured by single photon absorptiometry every six month. During the substitution treatment serum thyroxin and testosterone levels remained in the normal ranges. RESULTS - A significant increase in bone mineral density was observed during the testosterone treatment, with Z-scores -1.80, -0.91 and +0.14 at baseline, 12 and 24 months, respectively (p<0,001). Z-scores adjusted for bone age remained in the normal range throughout the study (-0.904 at baseline and -0.946 at one year). CONCLUSION - The increase rate of bone mineral density (0.16 g/cm/year) was significantly higher compared both to the normal reference in this age group (0.07 g/cm/yr, p=0.0015) and to the normal reference relative to their bone age (p<0.0006). The increase in bone mineral density suggests that testosterone replacement has an important role both in the quantitative and qualitative development of bones.]

[Stroke is the third leading cause of death and a leading cause of major adult disability in developed countries. The annual incidence of hospitalized stroke varies between 400-500 per 100 000 inhabitants every year in Hungary. In the past decade, cholesterol lowering with 3- hydroxy-3-methylglutaryl-coenzyme A (HMGCoA) reductase inhibitors (statins) has proved to reduce risk of stroke in patients with and without coronary disease (CAD). In patients with CAD, statin therapy reduces the risk of first stroke by 25% to 35% versus placebo and, moreover, intensive statin therapy to LDL-C targets below 2.6 mmol/L (100 mg/dL) appears to reduce the risk further. More recently it has also been shown that intensive statin therapy can reduce risk of recurrent stroke in nondiabetic as well as diabetic patients with recent stroke or transient ischaemic attack but no CAD. The overall reduction of stroke and TIA was 23%. Evidence from retrospective studies suggests that in addition to risk reduction statin pretreatment may improve stroke outcome. It may due to their pleiotropic effects that include improvement of endothelium function, anti-inflammatory, antithrombotic, and immunomodulatory effects. As statins have both an excellent safety profile and simple administration, physicians should consider using statins, at dosages shown to have efficacy in clinical trials, in all patients whose cardiovascular risk profile puts them at high risk of stroke.]