Different Therapeutic Approaches (different + therapeutic_approach)

Distribution by Scientific Domains


Selected Abstracts


Crohn's-like ileo-colitis in patients affected by glycogen storage disease Ib: two years'follow-up of patients with a wide spectrum of gastrointestinal signs

ACTA PAEDIATRICA, Issue 12 2003
D Melis
Aim: To investigate the presence of inflammatory bowel disease (IBD) and to evaluate the progression of bowel involvement after two years'follow-up in seven patients affected by glycogen storage disease type Ib (GSDIb). Methods: Seven patients (5F, 2M, aged 4.5,20.6 y) entered the study. Bowel involvement was evaluated by ileocolonoscopy and specific IBD serologic markers. To evaluate disease activity, Paediatric Crohn's Disease Activity Index (PCDAI), terminal ileum wall thickness detected at ultrasonography (US), 99mTechnetium labelled autologous White Cell Scan (Tc-WCS) and barium meal with follow-through were investigated. Results: Ileocolonoscopy and histology examination revealed variable degrees of bowel involvement in all patients. The results of serologic markers were indicative of a Crohn's-like ileocolitis. US and Tc-WCS, could clearly define patients with severe inflammatory involvement, but failed to identify all patients with mild to moderate disease. For the most severely affected patients, anti-inflammatory agents and steroids were prescribed, whereas nutritional therapy with polymeric formula and antibiotics were assumed by two other patients and antibiotics only by one patient. Granulocyte colony-stimulating factor (G-CSF) was prescribed to all patients. Ileocolonoscopy and histology data improved in all patients. The assumption of G-CSF and/or gastric drip feeding (g.d.f.) was inversely associated with the PCDAI results (p < 0.05). Conclusion: IBD is common in patients affected by GSDIb independently of the severity of gastrointestinal signs and symptoms. Different therapeutic approaches can be used according to the severity of IBD. G-CSF treatment and g.d.f. can be protective factors for IBD. [source]


Hemifacial spasm or somatoform disorder , postexcitatory inhibition after transcranial magnetic cortical stimulation asa diagnostic tool

ACTA NEUROLOGICA SCANDINAVICA, Issue 5 2000
S. Kotterba
Hemifacial spasm (HFS) presents a frequent movement disorder. It is thought to have an organic origin. It therefore has to be distinguished from other facial involuntary movements, especially psychogenic tics, because the therapeutic approach differs. The present study opted to evaluate the diagnostic value of the postexcitatory inhibition (pI) after transcranial magnetic stimulation (TMS). After stimulating the contralateral hemisphere with the conventional flat coil and recording from the mentalis muscle, in 10 healthy controls and 10 patients postexcitatory inhibition was determined. PI showed no side to side difference in healthy controls (96.9±12.7 ms right, 87.9±10.8 ms left side, interhemispheric difference 6.4±3.8 ms). In 8 patients with hemifacial spasm, the duration of pI on the non-affected side did not differ from the healthy controls (87.9±43.5 ms). During spasm, pI on the affected side shortened increasingly until no inhibition could be induced. Afterwards the spasm pI was prolonged significantly (up to 140 ms longer than opposite side) before returning to normal values. Two patients presented no side differences of pI during the "spasm". An emotional conflict situation could be evaluated, supporting the diagnosis of somatoform disorder. As postexcitatory inhibition is mainly due to cerebral mechanisms, the electrophysiological results of the study pointed to a cortical influence on the hemifacial spasm. TMS seems to be an electrophysiological tool which allows a differentiation between organic and psychogenic spasm and enables a different therapeutic approach. [source]


Functional Differences Between Growth Plate Apoptotic Bodies and Matrix Vesicles,

JOURNAL OF BONE AND MINERAL RESEARCH, Issue 10 2003
Thorsten Kirsch
Abstract Mineralization often occurs in areas of apoptotic changes. Our findings indicate that physiological mineralization is mediated by matrix vesicles. These matrix vesicles use mechanisms to induce mineralization that are different from the mechanisms used by apoptotic bodies released from apoptotic cells. Therefore, different therapeutic approaches must be chosen to inhibit pathological mineralization depending on the mechanism of mineralization (matrix vesicles versus apoptotic bodies). Introduction: Physiological mineralization in growth plate cartilage is restricted to regions of terminally differentiated and apoptotic chondrocytes. Pathological mineralization of tissues also often occurs in areas of apoptosis. We addressed the question of whether apoptotic changes control mineralization events or whether both events are regulated independently. Methods: To induce mineralization, we treated growth plate chondrocytes with retinoic acid (RA); apoptosis in these cells was induced by treatment with staurosporine, anti-Fas, or TNF,. The degrees of mineralization and apoptosis were determined, and the structure and function of matrix vesicles and apoptotic bodies were compared. Results: Release of matrix vesicles and mineralization in vivo in the growth plate occurs earlier than do apoptotic changes. To determine the functional relationship between apoptotic bodies and matrix vesicles, growth plate chondrocytes were treated with RA to induce matrix vesicle release and with staurosporine to induce release of apoptotic bodies. After 3 days, approximately 90% of staurosporine-treated chondrocytes were apoptotic, whereas only 2,4 % of RA-treated cells showed apoptotic changes. RA- and staurosporine-treated chondrocyte cultures were mineralized after 3 days. Matrix vesicles isolated from RA-treated cultures and apoptotic bodies isolated from staurosporine-treated cultures were associated with calcium and phosphate. However, matrix vesicles were bigger than apoptotic bodies. Furthermore, matrix vesicles but not apoptotic bodies contained alkaline phosphatase and Ca2+ channel-forming annexins II, V, and VI. Consequently, matrix vesicles but not apoptotic bodies were able to take up Ca2+ and form the first mineral phase inside their lumen. Mineralization of RA-treated cultures was inhibited by antibodies specific for annexin V but not mineralization of staurosporine-treated cultures. Conclusion: Physiological mineralization of growth plate chondrocytes is initiated by specialized matrix vesicles and requires alkaline phosphatase and annexins. In contrast, mineral formation mediated by apoptotic bodies occurs by a default mechanism and does not require alkaline phosphatase and annexins. [source]


Advances in the understanding and future therapy of COPD

CLINICAL & EXPERIMENTAL ALLERGY REVIEWS, Issue 4 2002
L. Fabbri
Summary Chronic obstructive pulmonary disease (COPD) is an enormous public health problem, which currently causes about 5% of all deaths worldwide. The main feature of COPD is a progressive loss of lung function as a result of structural changes in the airways and lung parenchyma. It is predominantly a disease of smokers, although only about 15% of smokers are thought to develop severe enough disease to be symptomatic. The reasons why some smokers are more susceptible to the disease than others are not clear, and are the subject of extensive research. Characteristically, inflammation is central to the pathophysiology of COPD, and it is clear that the inflammation of COPD differs from that seen in asthma. The most important treatment for COPD is smoking cessation, as other current treatments do not alter the course of the disease. Recent research into the cellular and molecular mechanisms underlying chronic obstructive pulmonary disease has provided potential new avenues for the development of rationally designed drugs, which may improve the outlook for patients with this debilitating condition. It is likely that different therapeutic approaches will be needed in different patients, because of the heterogeneity of the disease. [source]