Pub Date : 2016-09-22DOI: 10.1024/0040-5930/a000811
T. Roos
Zusammenfassung. Die Fruhgeburtlichkeit ist unverandert eines der grossten Probleme in der Geburtshilfe. Sie betrifft in den westlichen Industrienationen 5 % bis 11 % der Neugeborenen. Fur die Betroffenen konnen die Folgen eines zu kurzen Gestationsalters insbesondere bei Hirnschaden die lebenslange Gesundheit schwer beeintrachtigen. Die Fruhgeburtlichkeit lasst sich nicht auf einen einzelnen auslosenden Faktor reduzieren, sondern im Gegenteil liegen der Genese verschiedenste und auch interagierende Faktoren zu Grunde, so dass zu Recht von einem Fruhgeburtsyndrom gesprochen wird. Wenige auslosende Faktoren wie Infektionen sind bekannt und viele Mechanismen bislang unklar. Vorzeitige Wehentatigkeit oder Blasensprung verursachen die spontane Fruhgeburtlichkeit, deren Anteil an der Gesamtrate 75 % betragt. Das restliche Viertel (iatrogene Fruhgeburten) hat in wesentlichen Anteilen maternale Ursachen, die auf Grund eines schlechten Zustandes der Mutter und/oder des Feten zur vorzeitigen Schwangerschaftsbeendi...
{"title":"Prädiktion und Prävention der Frühgeburt","authors":"T. Roos","doi":"10.1024/0040-5930/a000811","DOIUrl":"https://doi.org/10.1024/0040-5930/a000811","url":null,"abstract":"Zusammenfassung. Die Fruhgeburtlichkeit ist unverandert eines der grossten Probleme in der Geburtshilfe. Sie betrifft in den westlichen Industrienationen 5 % bis 11 % der Neugeborenen. Fur die Betroffenen konnen die Folgen eines zu kurzen Gestationsalters insbesondere bei Hirnschaden die lebenslange Gesundheit schwer beeintrachtigen. Die Fruhgeburtlichkeit lasst sich nicht auf einen einzelnen auslosenden Faktor reduzieren, sondern im Gegenteil liegen der Genese verschiedenste und auch interagierende Faktoren zu Grunde, so dass zu Recht von einem Fruhgeburtsyndrom gesprochen wird. Wenige auslosende Faktoren wie Infektionen sind bekannt und viele Mechanismen bislang unklar. Vorzeitige Wehentatigkeit oder Blasensprung verursachen die spontane Fruhgeburtlichkeit, deren Anteil an der Gesamtrate 75 % betragt. Das restliche Viertel (iatrogene Fruhgeburten) hat in wesentlichen Anteilen maternale Ursachen, die auf Grund eines schlechten Zustandes der Mutter und/oder des Feten zur vorzeitigen Schwangerschaftsbeendi...","PeriodicalId":87030,"journal":{"name":"Therapeutische Umschau und medizinische Bibliographie. Revue therapeutique et bibliographie medicale","volume":"28 1","pages":"404-420"},"PeriodicalIF":0.0,"publicationDate":"2016-09-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"76231450","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2016-03-23DOI: 10.1024/0040-5930/a000766
Barbara Ankli, S. Krähenbühl
Gout is the most frequent arthritis worldwide. Despite progress in therapeutic options the majority of gout patients are still insufficiently treated. International guidelines (ACR, EULAR, 3e initiative) clearly specify treatment targets: keep the patient flare-free and maintain a low urate serum level (< 360 µmol/l). The treat to target strategy includes therapy of flares, urate lowering treatment (ULT) and prophylaxis of flares. Evolution of gout guidelines over several years shows a broader indication for ULT, mandatory prophylaxis of flares during the initiation of ULT over several months and an earlier start of ULT in patients with flares as soon as symptoms have diminished. Colchicine is the preferred specific flare treatment, Caution has to be taken especially in patients with kidney disease, patients with hepatic dysfunction or in patients with interacting comedication. Low dose oral colchicine is nowadays the standard flare treatment. NSAIDs and prednisone are valuable alternatives. Interleukin-1 blockers offer a quick resolution of flares and may be an option in patients with chronic gout and severe kidney disease. Xanthinoxidase inhibitors (XOI) are the mainstay of ULT, with allopurinol still being the preferred XOI. The recently approved XOI febuxostat is eliminated mostly by the liver and can induce a faster lowering of urate. Uricosuric drugs such as probenecid are recommended in patients with sufficient renal function in whom the treatment goals cannot be reached with XOI. In Switzerland, only the two gout-lowering drugs allopurinol and probenecid are available, which reduces the therapeutic possibilities. Treatment success is often hampered by malcompliance. Recent guidelines stress the importance of patient education to ameliorate compliance. Comorbidities such as metabolic syndrome, cardiovascular and kidney disease are often found in gout patients. Patients with severe kidney disease are the most difficult to treat: the choice of antiinflammatory treatment is narrowed, ULT has to be uptitrated very carefully and patients often suffer from repeated flares. Another factor associated with treatment failure is the low physician’s adherence towards the guidelines. Therapeutic failure can lead to chronic and refractory gout (polyarticular gout, uncontrolled flare activity, chronic synovitis, destructive tophi) which makes the further management very difficult. Most gout patients are treated in primary care settings. Patients with chronic gout or at high risk for development of chronic gout (in particular patients with severe kidney disease or patients transplanted) should be additionally treated by a rheumatologist.
{"title":"[Gout management: an update].","authors":"Barbara Ankli, S. Krähenbühl","doi":"10.1024/0040-5930/a000766","DOIUrl":"https://doi.org/10.1024/0040-5930/a000766","url":null,"abstract":"Gout is the most frequent arthritis worldwide. Despite progress in therapeutic options the majority of gout patients are still insufficiently treated. International guidelines (ACR, EULAR, 3e initiative) clearly specify treatment targets: keep the patient flare-free and maintain a low urate serum level (< 360 µmol/l). The treat to target strategy includes therapy of flares, urate lowering treatment (ULT) and prophylaxis of flares. Evolution of gout guidelines over several years shows a broader indication for ULT, mandatory prophylaxis of flares during the initiation of ULT over several months and an earlier start of ULT in patients with flares as soon as symptoms have diminished. Colchicine is the preferred specific flare treatment, Caution has to be taken especially in patients with kidney disease, patients with hepatic dysfunction or in patients with interacting comedication. Low dose oral colchicine is nowadays the standard flare treatment. NSAIDs and prednisone are valuable alternatives. Interleukin-1 blockers offer a quick resolution of flares and may be an option in patients with chronic gout and severe kidney disease. Xanthinoxidase inhibitors (XOI) are the mainstay of ULT, with allopurinol still being the preferred XOI. The recently approved XOI febuxostat is eliminated mostly by the liver and can induce a faster lowering of urate. Uricosuric drugs such as probenecid are recommended in patients with sufficient renal function in whom the treatment goals cannot be reached with XOI. In Switzerland, only the two gout-lowering drugs allopurinol and probenecid are available, which reduces the therapeutic possibilities. Treatment success is often hampered by malcompliance. Recent guidelines stress the importance of patient education to ameliorate compliance. Comorbidities such as metabolic syndrome, cardiovascular and kidney disease are often found in gout patients. Patients with severe kidney disease are the most difficult to treat: the choice of antiinflammatory treatment is narrowed, ULT has to be uptitrated very carefully and patients often suffer from repeated flares. Another factor associated with treatment failure is the low physician’s adherence towards the guidelines. Therapeutic failure can lead to chronic and refractory gout (polyarticular gout, uncontrolled flare activity, chronic synovitis, destructive tophi) which makes the further management very difficult. Most gout patients are treated in primary care settings. Patients with chronic gout or at high risk for development of chronic gout (in particular patients with severe kidney disease or patients transplanted) should be additionally treated by a rheumatologist.","PeriodicalId":87030,"journal":{"name":"Therapeutische Umschau und medizinische Bibliographie. Revue therapeutique et bibliographie medicale","volume":"73 3 1","pages":"115-24"},"PeriodicalIF":0.0,"publicationDate":"2016-03-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"85311345","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2016-03-23DOI: 10.1024/0040-5930/a000771
T. Manigold
Gout is the most frequent arthritis worldwide with increasing prevalence in industrialized countries and massive socioeconomic consequences. The knowledge regarding the pathomechanisms which lead to arthritis has substantially increased during the last decade. Consistently, new therapeutic approaches and substances appear at the horizon. This review covers aspects of clinical presentation, diagnosis and current treatment. The pathomechanisms leading to NLRP3 inflammasome activation and IL-1beta secretion are reviewed in detail. Finally, selected new therapeutic targets and substances are discussed.
{"title":"[Causes, mechanisms and possible therapeutic targets of gout].","authors":"T. Manigold","doi":"10.1024/0040-5930/a000771","DOIUrl":"https://doi.org/10.1024/0040-5930/a000771","url":null,"abstract":"Gout is the most frequent arthritis worldwide with increasing prevalence in industrialized countries and massive socioeconomic consequences. The knowledge regarding the pathomechanisms which lead to arthritis has substantially increased during the last decade. Consistently, new therapeutic approaches and substances appear at the horizon. This review covers aspects of clinical presentation, diagnosis and current treatment. The pathomechanisms leading to NLRP3 inflammasome activation and IL-1beta secretion are reviewed in detail. Finally, selected new therapeutic targets and substances are discussed.","PeriodicalId":87030,"journal":{"name":"Therapeutische Umschau und medizinische Bibliographie. Revue therapeutique et bibliographie medicale","volume":"1 1","pages":"147-52"},"PeriodicalIF":0.0,"publicationDate":"2016-03-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"89166896","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2016-03-23DOI: 10.1024/0040-5930/a000773
Min jeong Kim, H. Hopfer, M. Mayr
Different types of kidney disease are known to be associated with hyperuricemia. The underlying pathophysiologic mechanisms strongly vary, and different ways of therapeutic approach are therefore required. In tumor lysis syndrome, a rapid, excessive increase of serum uric acid level can cause an acute renal failure. For chronic urate nephropathy, on the other hand, constantly elevated serum uric acid level for a longer period seems to be important. Being still controversial as a disease entity however, the aetiology for putative chronic urate nephropathy might be in fact chronic lead intoxication, as suggested by quite an amount of association data. In terms of uric acid nephrolithiasis, the major risk factor is a urinary acidification defect with persistently acidic urine pH, and not necessarily hyperuricemia or hyperuricosuria. Evidence suggests that metabolic diseases with increased insulin resistance are strongly associated with urinary acidification defect. Patients with uric acid kidney stones should therefore be thoroughly evaluated for such metabolic diseases and in a positive case adequately treated.
{"title":"[Uric acid, kidney disease and nephrolithiasis].","authors":"Min jeong Kim, H. Hopfer, M. Mayr","doi":"10.1024/0040-5930/a000773","DOIUrl":"https://doi.org/10.1024/0040-5930/a000773","url":null,"abstract":"Different types of kidney disease are known to be associated with hyperuricemia. The underlying pathophysiologic mechanisms strongly vary, and different ways of therapeutic approach are therefore required. In tumor lysis syndrome, a rapid, excessive increase of serum uric acid level can cause an acute renal failure. For chronic urate nephropathy, on the other hand, constantly elevated serum uric acid level for a longer period seems to be important. Being still controversial as a disease entity however, the aetiology for putative chronic urate nephropathy might be in fact chronic lead intoxication, as suggested by quite an amount of association data. In terms of uric acid nephrolithiasis, the major risk factor is a urinary acidification defect with persistently acidic urine pH, and not necessarily hyperuricemia or hyperuricosuria. Evidence suggests that metabolic diseases with increased insulin resistance are strongly associated with urinary acidification defect. Patients with uric acid kidney stones should therefore be thoroughly evaluated for such metabolic diseases and in a positive case adequately treated.","PeriodicalId":87030,"journal":{"name":"Therapeutische Umschau und medizinische Bibliographie. Revue therapeutique et bibliographie medicale","volume":"3 1","pages":"159-65"},"PeriodicalIF":0.0,"publicationDate":"2016-03-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"79835746","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2016-03-23DOI: 10.1024/0040-5930/a000772
Beate Nickolai, C. Kiss
Nutrition and nutritional behaviours have been found to play a major role in the development of gout. Studies show that body mass index (BMI), as well as excessive intake of alcoholic beverages, meat, soft drinks and fruit juices increase the risk of developing gout. Similarly, dairy products and coffee have been seen to decrease the risk of hyperuricemia and gout, as they increase the excretion of uric acid. Flares of gout are often caused by large meals and high alcohol consumption. Each additional intake of meat portion per day increases the risk of gout by 21 %. Taking total alcohol consumption into account, the risk of gout increases after one to two standard drinks. In contrast to previous assumptions purine-rich plant foods like legumes and vegetables do not increase the risk of gout. The current dietary guidelines take into account nutritional factors, which not only consider purine intake, but also their endogenous production and their influence on renal excretion. A balanced diet based on the Swiss healthy eating guideline pyramid as well as the Mediterranean diet is appropriate for this patient population. The treatment of gout is multi-faceted, since this patient population presents other comorbidities such as obesity, diabetes mellitus, dyslipidemia and hypertension. Collectively, these risk factors are diet dependent and require a treatment strategy that is centered on modifying one's nutrition and nutritional behaviours. The aim of such therapy is to educate the patient as well as treat the accompanying comorbidities with the goal of decreasing serum uric acid values. Motivated patients require consultation and follow-up care in order to be able to actively decrease the serum uric acid.
{"title":"[Nutritional therapy of gout].","authors":"Beate Nickolai, C. Kiss","doi":"10.1024/0040-5930/a000772","DOIUrl":"https://doi.org/10.1024/0040-5930/a000772","url":null,"abstract":"Nutrition and nutritional behaviours have been found to play a major role in the development of gout. Studies show that body mass index (BMI), as well as excessive intake of alcoholic beverages, meat, soft drinks and fruit juices increase the risk of developing gout. Similarly, dairy products and coffee have been seen to decrease the risk of hyperuricemia and gout, as they increase the excretion of uric acid. Flares of gout are often caused by large meals and high alcohol consumption. Each additional intake of meat portion per day increases the risk of gout by 21 %. Taking total alcohol consumption into account, the risk of gout increases after one to two standard drinks. In contrast to previous assumptions purine-rich plant foods like legumes and vegetables do not increase the risk of gout. The current dietary guidelines take into account nutritional factors, which not only consider purine intake, but also their endogenous production and their influence on renal excretion. A balanced diet based on the Swiss healthy eating guideline pyramid as well as the Mediterranean diet is appropriate for this patient population. The treatment of gout is multi-faceted, since this patient population presents other comorbidities such as obesity, diabetes mellitus, dyslipidemia and hypertension. Collectively, these risk factors are diet dependent and require a treatment strategy that is centered on modifying one's nutrition and nutritional behaviours. The aim of such therapy is to educate the patient as well as treat the accompanying comorbidities with the goal of decreasing serum uric acid values. Motivated patients require consultation and follow-up care in order to be able to actively decrease the serum uric acid.","PeriodicalId":87030,"journal":{"name":"Therapeutische Umschau und medizinische Bibliographie. Revue therapeutique et bibliographie medicale","volume":"56 1","pages":"153-8"},"PeriodicalIF":0.0,"publicationDate":"2016-03-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"74616149","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2016-03-23DOI: 10.1024/0040-5930/a000770
Ka Murray, T. Burkard
Hyperuricemia, gout as well as arterial hypertension and metabolic syndrom are highly prevalent and clinicians are frequently confronted with both conditions in the same patient. Hyperuricemia and gout are associated with cardiovascular comorbidities and a high cardiovascular risk. Despite coherent pathophysiological concepts, it remains to be determined, if this association is independent and causal. In daily clinical practice, cardiovascular risk factors should be thoroughly identified and consequently treated in all patients with hyperuricemia and gout. If preventive treatment of asymptomatic hyperuricemia with urate-lowering agents may improve cardiovascular risk and outcomes remains to be determined and is recommended only in special situations like young patients with severe hyperuricemia.
{"title":"[Hyperuricemia, gout and cardiovascular diseases].","authors":"Ka Murray, T. Burkard","doi":"10.1024/0040-5930/a000770","DOIUrl":"https://doi.org/10.1024/0040-5930/a000770","url":null,"abstract":"Hyperuricemia, gout as well as arterial hypertension and metabolic syndrom are highly prevalent and clinicians are frequently confronted with both conditions in the same patient. Hyperuricemia and gout are associated with cardiovascular comorbidities and a high cardiovascular risk. Despite coherent pathophysiological concepts, it remains to be determined, if this association is independent and causal. In daily clinical practice, cardiovascular risk factors should be thoroughly identified and consequently treated in all patients with hyperuricemia and gout. If preventive treatment of asymptomatic hyperuricemia with urate-lowering agents may improve cardiovascular risk and outcomes remains to be determined and is recommended only in special situations like young patients with severe hyperuricemia.","PeriodicalId":87030,"journal":{"name":"Therapeutische Umschau und medizinische Bibliographie. Revue therapeutique et bibliographie medicale","volume":"14 1","pages":"141-6"},"PeriodicalIF":0.0,"publicationDate":"2016-03-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"85218145","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2016-03-23DOI: 10.1024/0040-5930/a000769
T. Hügle, V. Krenn
Despite being a frequent cause of arthritis and bone erosions, the underlying cellular and subcellular reaction in gout is insufficiently understood. The inflammasome as intracellular sensor for crystals plays an important role, notably resulting in interleukin (IL)-1 production. Morphologically, hyperplasia of the synovial membrane with joint effusion, along with fibrinogen deposition and influx of neutrophils and lymphocytes are observed. Extracellular NET formation by neutrophils is involved in the regulation of inflammatory tissue reaction. Furthermore, the release of IL-10 and tumor necrosis factor (TNF)-receptors along with lymphocyte proliferation induce the natural resolution of acute gouty arthritis which typically occurs after several days. In contrast to acute gout, tophi consisting of urate crystals are surrounded by histiocytes and multinucleated cells, resembling a foreign body reaction. The deposition of extracellular matrix by fibrocytes is usually observed around tophi. This fibrotic reaction is likely enhanced by Th2-lymphocytes. Bone erosions in gout occur around tophi and are triggered by osteoclast activation through RANK-ligand expression by lymphocytes. In conclusion, understanding the orchestration of inflammation in gout might help to identify new therapeutic targets.
{"title":"[Histopathophysiology of Gout].","authors":"T. Hügle, V. Krenn","doi":"10.1024/0040-5930/a000769","DOIUrl":"https://doi.org/10.1024/0040-5930/a000769","url":null,"abstract":"Despite being a frequent cause of arthritis and bone erosions, the underlying cellular and subcellular reaction in gout is insufficiently understood. The inflammasome as intracellular sensor for crystals plays an important role, notably resulting in interleukin (IL)-1 production. Morphologically, hyperplasia of the synovial membrane with joint effusion, along with fibrinogen deposition and influx of neutrophils and lymphocytes are observed. Extracellular NET formation by neutrophils is involved in the regulation of inflammatory tissue reaction. Furthermore, the release of IL-10 and tumor necrosis factor (TNF)-receptors along with lymphocyte proliferation induce the natural resolution of acute gouty arthritis which typically occurs after several days. In contrast to acute gout, tophi consisting of urate crystals are surrounded by histiocytes and multinucleated cells, resembling a foreign body reaction. The deposition of extracellular matrix by fibrocytes is usually observed around tophi. This fibrotic reaction is likely enhanced by Th2-lymphocytes. Bone erosions in gout occur around tophi and are triggered by osteoclast activation through RANK-ligand expression by lymphocytes. In conclusion, understanding the orchestration of inflammation in gout might help to identify new therapeutic targets.","PeriodicalId":87030,"journal":{"name":"Therapeutische Umschau und medizinische Bibliographie. Revue therapeutique et bibliographie medicale","volume":"72 6 1","pages":"137-40"},"PeriodicalIF":0.0,"publicationDate":"2016-03-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"77254789","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2016-03-23DOI: 10.1024/0040-5930/a000768
A. Hirschmann, U. Studler
Cristal deposit disorders are characterised by cristal deposits in hyaline and fibrocartilage, in synovium, capsule, ligaments and tendons and periarticular soft tissue. Calciumpyrophosphatedihydrate (CPPD), hydroxyapatite (calcific tendinitis) and uric acid arthropathies are the most common cristal deposit diseases. Radiography is still the number one image modality for initial imaging and the identification of cristal-induced inflammatory arthropathies. Differentiation between the entities of cristal deposit arthropathies can be challenging. Clincial and radiological findings may overlap in different cristal deposit arthropathies, owing a certain diagnosis difficult.
{"title":"[Imaging findings of cristal deposit disorders].","authors":"A. Hirschmann, U. Studler","doi":"10.1024/0040-5930/a000768","DOIUrl":"https://doi.org/10.1024/0040-5930/a000768","url":null,"abstract":"Cristal deposit disorders are characterised by cristal deposits in hyaline and fibrocartilage, in synovium, capsule, ligaments and tendons and periarticular soft tissue. Calciumpyrophosphatedihydrate (CPPD), hydroxyapatite (calcific tendinitis) and uric acid arthropathies are the most common cristal deposit diseases. Radiography is still the number one image modality for initial imaging and the identification of cristal-induced inflammatory arthropathies. Differentiation between the entities of cristal deposit arthropathies can be challenging. Clincial and radiological findings may overlap in different cristal deposit arthropathies, owing a certain diagnosis difficult.","PeriodicalId":87030,"journal":{"name":"Therapeutische Umschau und medizinische Bibliographie. Revue therapeutique et bibliographie medicale","volume":"1 1","pages":"131-6"},"PeriodicalIF":0.0,"publicationDate":"2016-03-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"83230543","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2016-03-16DOI: 10.1024/0040-5930/a000763
F. Meier-Gibbons
Glaucoma is a progressive disease of the optic nerve potentially leading to a destruction of the nerve and therefore to blindness. It is a multifactorial disease and patients of all age groups can be affected. Different risk factors influence the course of the disease. The quality of life of the patients is already reduced when the patients show moderate changes of their visual field. The patients experience more falls and may be forced to stop driving. With an early and adequate treatment the progression of the disease can be slowed down. The early recognition of the disease is important and belongs into the hands of ophthalmologists. The treatment for glaucoma is a difficult task and needs an intense collaboration of the ophthalmologist with the patient and the treating primary care physician.
{"title":"[Early recognition and management of the disease].","authors":"F. Meier-Gibbons","doi":"10.1024/0040-5930/a000763","DOIUrl":"https://doi.org/10.1024/0040-5930/a000763","url":null,"abstract":"Glaucoma is a progressive disease of the optic nerve potentially leading to a destruction of the nerve and therefore to blindness. It is a multifactorial disease and patients of all age groups can be affected. Different risk factors influence the course of the disease. The quality of life of the patients is already reduced when the patients show moderate changes of their visual field. The patients experience more falls and may be forced to stop driving. With an early and adequate treatment the progression of the disease can be slowed down. The early recognition of the disease is important and belongs into the hands of ophthalmologists. The treatment for glaucoma is a difficult task and needs an intense collaboration of the ophthalmologist with the patient and the treating primary care physician.","PeriodicalId":87030,"journal":{"name":"Therapeutische Umschau und medizinische Bibliographie. Revue therapeutique et bibliographie medicale","volume":"1 1","pages":"99-101"},"PeriodicalIF":0.0,"publicationDate":"2016-03-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"84732323","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2016-03-16DOI: 10.1024/0040-5930/a000759
M. Abegg, Eveline Gentile
The visual system has a pivotal role in most human activities. Many health disorders and psychomotor deficits involve the visual system at some level. From this some therapists infer a causal relation and apply a variety of visual therapies and trainings to cure a variety of deficits. The most prominent example is dyslexia, a disorder not caused by a defect in the primary visual system. Worldwide various non-evidence based therapies are used to treat dyslexia. The great number of exercises and visual trainings is contrasted by scientific evidence, which shows that exercises are useful in only few and selected disorders. The human visual system seems to be optimized such that no improvement can be achieved with training.
{"title":"[Visual training in children].","authors":"M. Abegg, Eveline Gentile","doi":"10.1024/0040-5930/a000759","DOIUrl":"https://doi.org/10.1024/0040-5930/a000759","url":null,"abstract":"The visual system has a pivotal role in most human activities. Many health disorders and psychomotor deficits involve the visual system at some level. From this some therapists infer a causal relation and apply a variety of visual therapies and trainings to cure a variety of deficits. The most prominent example is dyslexia, a disorder not caused by a defect in the primary visual system. Worldwide various non-evidence based therapies are used to treat dyslexia. The great number of exercises and visual trainings is contrasted by scientific evidence, which shows that exercises are useful in only few and selected disorders. The human visual system seems to be optimized such that no improvement can be achieved with training.","PeriodicalId":87030,"journal":{"name":"Therapeutische Umschau und medizinische Bibliographie. Revue therapeutique et bibliographie medicale","volume":"55 1","pages":"73-7"},"PeriodicalIF":0.0,"publicationDate":"2016-03-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"83104137","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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