Lege Artis Medicinae

[PREVALENCE OF OSTEOPOROSIS IN PATIENTS WITH COLLES’ FRACTURE]

NAGY József, BÁLINT Géza, TAKÁCS Katalin, WINKLER Valéria, RATKÓ István, BÁLINT Péter

JANUARY 20, 2007

Lege Artis Medicinae - 2007;17(01)

[INTRODUCTION - Studies suggest that Colles’ fracture is the earliest of the osteoporotic fractures, and thus may be the first indication of the disease. PATIENTS AND METHODS - Fifty-seven consecutive patients with Colles’ fracture who presented between 1st of October 2003 and 1st of February 2004 at the traumatology out-patient clinic of Semmelweis Hospital, Kiskunhalas were screened for osteoporosis. RESULTS - Of the 43 postmenopausal women, 41 was found to have osteoporosis by DEXA scan, but only one was aware of her disease and received treatment. Out of these 41 patients 15 had fractures previously, 9 of whom had more than one. None of the four premenopausal women had osteoporotic DEXA measurement values. All of the 10 male patients had osteoporosis, 6 had previous fractures, 5 of them more then once. One patient required surgery, there was a prolonged fracture healing in 10 cases, and reflex sympathetic dystrophy developed in 3 patients. CONCLUSION - Since in this study more than 95% of postmenopausal women with Colles’ fracture had underlying osteoporosis, the authors conclude that DEXA scanning of these patients is recommended. Based on the results, it seems that screening for osteoporosis is indicated for both men and women after radius fracture.]

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[PATHOLOGICAL FEATURES OF SYSTEMIC SCLEROSIS]

VARJÚ Cecília, KUMÁNOVICS Gábor, CZIRJÁK László

[Systemic sclerosis is characterized by fibrosis and subsequent atrophy of the skin and several internal organs as well as by generalized obliterative vasculopathy. The ethiology of systemic sclerosis is not quite clear yet, but the role of certain environmental factors, genetic properties and microchimaerism has been proven. Vasculopathy is a key feature that includes both functional changes (Raynaud's phenomenon) and morphological alterations (lesion of the endothel). The triggering event is the activation of endothelial cells. This is followed by an autoimmune inflammatory process causing vascular lesion, which will eventually lead to progressive pathologic fibrosis with increased deposition of collagen and intercellular matrix proteins. Normal tissues of vital internal organs will gradually loose structure, become atrophic and irreversibly damaged. In the treatment of systemic sclerosis the most significant achievements of the past decade have been made in the therapy and prevention of scleroderma renal crisis, pulmonary arterial hypertension and other vascular complications, resulting in higher survival rates and better quality of life. In pulmonary fibrosis the beneficial effect of cyclophosphamide therapy has been proven. Today, research focuses on new therapeutic approaches based on the recently clarified molecular pathological processes, as well as on laboratory and clinical markers that predict the activity of the disease or the efficiency of therapy. The aim of the present paper is to review current knowledge on the pathology of systemic sclerosis and provide help in the diagnosis, therapy and follow-up of the disease.]

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SZALKA András

[Glycylcyclines are a new class of antimicrobial agents, of which tigecycline is the first to have reached the final stage of clinical trials. It is the 9-t-butylglycylamido derivative of minocycline. The addition of a side-chain into position 9 overcomes the problem of the development of resistance typical to tetracyclines. Tigecycline inhibits translation of bacterial proteins through its effect on the 30S ribosomal subunit. The efficacy of tigecycline is impressive against multiresistant Gram-positive bacteria, including methicillin- resistant Staphylococcus aureus, penicillin- resistant Streptococcus pneumoniae, and vancomycin-resistant enterococci, against most genera of Enterobacteriaceae, including extended- spectrum β-lactamase-producing strains, and against most strains of Bacteroides fragilis, as well as atypical pathogens. Clinical studies showed good results in parenteral treatment for complicated skin, soft tissue and intraabdominal infections. Tigecycline will be most useful as empirical monotherapy in infections with suspected polymicrobial etiology and/or multidrugresistant agents.]

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[OUR EXPERIENCE WITH BORTEZOMIB-BASED THERAPY OF MULTIPLE MYELOMA BASED ON THE FIRST 60 PATIENTS]

MIKALA Gábor, BÁTAI Árpád, CEGLÉDI Andrea, CSUKLY Zoltán, DOLGOS János, HALM Gabriella, JÁNOSI Judit, KAPÁS Balázs, LOVAS Nóra, LUEFF Sándor, PETŐ Mónika, REMÉNYI Péter, SIPOS Andrea, TÓTH Zsuzsanna

[INTRODUCTION - Bortezomib, a first-in-itsclass proteasome-inhibitor drug was registered in 2004 for the salvage treatment of relapsed and/or refractory multiple myeloma. We have been using this drug in our department for the treatment of myeloma patients since 2005. PATIENTS AND METHODS - In this retrospective study, treatment results (response rate, response duration, survival) as well as the complications and side effects were analysed based on 60 myeloma patients treated over a period of 18 months. The patients received at least one full cycle of non-first-line bortezomib-based (predominantly combinational) therapy. RESULTS - At least minimal laboratory and/or clinical response was observed in 47 of the 56 patients who could be analysed. Clinically meaningful (at least partial remission) response was seen in 41 of 56 patients. Immune-fixation negative complete remission was achieved in six patients. Median progression-free survival of our patient population was 13 months (10.8-14.8 months, n=49, adjusted for patients lost in the first 6 weeks and for those with less than 6 weeks of follow-up). As for overall survival, the median has not been reached, while treated patients had an 80.3% probability of survival at one year. CONCLUSIONS - Based on the treatment results of 60 myeloma patients, bortezomibbased therapy is clearly effective in relapsed and/or refractory myeloma.]

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TÕKE Judit, TAMÁS GYULA, STELLA Péter, NAGY Erzsébet, NÁDASDI Ágnes, VARGA Piroska, KERÉNYI ZSUZSA

[INTRODUCTION - Data on bone mineral density (BMD) in diabetes mellitus are contradictory in the literature. Early studies described a decreased bone mineral density in type 1 diabetes mellitus (T1DM), but recent studies report no osteopenia in T1DM.The BMD may depend on the quality of treatment for diabetes mellitus and on the presence of chronic complications. In type 2 diabetes mellitus (T2DM) the BMD is not decreased, occasionally it can even be increased. PATIENTS AND METHODS - Bone mineral density was measured in 122 regularly controlled diabetic patients (T1DM: n=73, mean age: 43.6±11.1 years,T2DM: n=49, mean age: 61.8±9.8 years) by dual energy X-ray absorptiometry at the lumbar spine and at the femur. Results were compared to those of 40 metabolically healthy control persons with a mean age of 47.5±11.9 years.The patients’ carbohydrate metabolism was assessed by the average HbA1c level of the last three years.These values were 7.9±1.4 % in T1DM, and 7.5±1.7 % in T2DM. BMDs were classified based on the T-score and Z-score using the WHO criteria. RESULTS - There was no significant difference in T1DM or in T2DM compared to the reference group in the prevalence of either osteoporosis or of osteoporosis and osteopenia combined. CONCLUSION - BMD was not found to be decreased in patients with well-controlled metabolism compared to healthy controls.]

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[Studies in the last couple of years found more and more convincing evidence about the fact that impaired glucose metabolism leads to structural changes in the skeletal system leading toward osteoporosis. While patients with type 1 diabetes mellitus have decreased bone density, measurement showed increased bone mineral density in patients with type 2 diabetes mellitus. Despite these differences, risk of vertebral and nonvertebral fractures is increased in both groups of diabetic patients. Decreased pancreatic beta cell function is accompanied by several hormonal disturbances leading to decreased bone formation even in the early stage of diabetes. Peak bone mass of diabetic children is lower than found in nondiabetic children. Late complications of diabetes, vascular and neuronal impairments, impaired renal function, and secondary hormonal disturbances are added to this process. IGF-1 may have a crucial role in the pathogenesis of osteoporosis in diabetes. The structure of the molecule is similar to insulin. IGF-1 has effect on normal bone formation, inhibits the apoptosis and interferes with several other metabolic pathways. IGF-1 mediates the effect of growth hormone to the muscular and skeletal system. IGF-1 level decreases with age, and lower level of IGF-1 is found in diabetic patients. Long term complications of diabetes can also occur, which may enhance the process of bone resorption. Although the evidence is growing that fracture risk is higher in diabetic patiens, there are still scientists who question the association between the two disorders.]

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[The risk factors of osteoporosis and osteoporotic fractures in Hungarian women: the results of the NOKK study]

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[From the Palaeolithic age to the twentieth century, nutritional habits as well as the quality and composition of nutritients changed dramatically. The protein-based calorie intake of former Homo species had been replaced by a carbohydrate-based nutrition since the Neolithic revolution (the transition to agriculture). The start of food production also changed the range of nutrients and the start of sedentary lifestyle. At the same time, approximately five thousand years ago osteoporosis appeared. In this paper, the authors give a short review of eating habits and foods of early Homo species in the Palaeolithic Age and of Homo sapiens in Neolithic Age, Antiquity, Middle Ages and Modern Age, and discuss the possible relationship of nutrition and osteoporosis.]