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Query: UMLS:C0028754 (obesity)
 124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Ideally, treatment is based on etiology, if possible on pathophysiology, and in practice on anatomical and clinical findings. A systematic search for the etiological factors of osteoarthritis (OA) shows that the various mechanisms are frequently associated. Etiological treatments are rare. We may mention acetabular tectoplasty in hip dysplasia with minimal joint space narrowing. Valgus osteotomy would also be indicated for early medial tibiofemoral OA in genu varum if we had definite proof that, if left untreated, this deformity inevitably leads to clinically severe OA. This is not the case. One of the limitations of this etiological treatment lies in the fact that we do not know which patients are at risk of developing painful OA. Instead, certain risk factors for OA are known, so that primary and secondary prevention of the disease is possible. While age, sex and genetic predisposition are not amenable to preventive action, the same does not apply to the following factors: obesity, sports, and occupational activity. Thanks to in vitro studies of cultured normal and osteoarthritic chondrocytes and to experimental models of OA in animals, the pathophysiological mechanisms of OA are beginning to be better known. The prospect thus arises of "therapeutic manipulations" of precise pharmacological targets, even if it is still too soon to speak of true pathophysiological treatment of this disease. For instance, various interventions along the IL-1 pathway can be envisaged and have all been tested in animals. In practice, treating OA means taking into consideration its various signs: pain which appears to be mechanical and more or less chronic, joint stiffness, instability, effusion, and--the consequence of these symptoms--the professional, social and personal handicap of the patient. The treatment of OA must be approached from a global perspective, associating whenever possible symptomatic treatment, disease-modifying treatment, education and rehabilitation. In other words, the treatment of OA requires an overall approach, associating pharmacological and non-pharmacological modalities.
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PMID:The therapeutic approach to osteoarthritis. 1470 6

Total hip arthroplasty (THA) usually involves an incision of approximately 20 to 25 cm long. Surgeons recently have begun to question the need for such a long incision and are developing less invasive approaches to THA. A mini-incision approach to THA promotes shorter hospital stays, faster rehabilitation, and an increase in patient satisfaction without a detrimental effect on outcome. The surgical technique is based on the classic Moore approach to the hip. The incisions measure 6 to 10 cm in length, and the surgery involves significantly less deep soft-tissue disruption. All the basic tenets of THA are respected and visualization is maintained throughout the procedure for proper placement of the components. Mini-incision THA offers a safe and effective alternative to THA performed through a larger incision. Obese patients typically are not good candidates. Patients with severe hip dysplasia or those undergoing revision surgery require a wider exposure to perform the arthroplasty to ensure the best possible result. In properly selected patients, however, THA can be performed through an abridged mini-incision without compromising the results or exposing the patient to additional risk.
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PMID:The mini-incision approach to total hip arthroplasty. 1511 8

Snoring and obstructive sleep apnea are a frequent problem not only in adults, but also in children and adolescents, as can be seen from current epidemiological data. The epidemiology, etiology, diagnosis, and management of obstructive sleep apnea syndrome (OSAS) in adults have been adequately established on the basis of evidential data. As a result of this, both physicians and the public are increasingly aware of OSAS in adults. Although there are numerous parallels between pediatric and adult OSAS, the situation in children differs that in adults. There is a greater variety of symptoms in children with OSAS, diagnosis is often more difficult with serious consequences for growth and development of children. Treatment of OSAS in children is also different from that of the adult patient. There are many possible causes for the development of obstructive sleep apnea in children. These include hypertrophy of the tonsils and syndromes such as Down syndrome, Pickwickian syndrome, Prader-Willi syndrome or Marfan syndrome. OSAS can, however, also be the result of obesity, midfacial dysplasia, retro- or micrognathia, allergic rhinitis or muscular dystrophy. Epidemiological data presented in the literature concerning the incidence of OSAS in children is extremely varied. This wide range is probably due to the fact that snoring may be misdiagnosed as OSAS. The diagnosis of OSAS in children may only be made by considering clinical history (such as rate of growth, tendency to fall asleep during the day, sleep disturbances, susceptibility to infection, etc.), polysomnography (if possible during several nights) and accompanying instrumental diagnosis including cephalometry or laryngoscopy. One of the problems of polysomnography in childhood is that performance and interpretation of the results have not yet been standardized or evaluated for different age groups. Treatment depends on the cause of OSAS and require multidisciplinary management involving the pediatrician, pediatric or adolescent psychiatrist, ear, nose, and throat specialist, maxillofacial surgeons, and neurosurgeons. Adenotonsillectomy (ATE) is the therapy generally chosen if the child has adenoidal vegetations and/or tonsillar hypertrophy. Corrective surgery is possible for rare malformation syndromes. Nocturnal masks for continuous positive airway nasal pressure or procedures for mask respiration are effective in children, but are only used in exceptional cases, such as when ATE is contraindicated or when symptoms of OSAS remain after surgery. The success of pharmacological treatment of OSAS in children has not been evaluated in controlled clinical trials.
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PMID:Obstructive sleep apnea syndrome in children: a state-of-the-art review. 1518 12

Patients with diastrophic dysplasia have walking difficulties of obscure etiology; some are even wheelchair-bound. To explore the problem, physical examination, treadmill, magnetic resonance imaging (MRI), and electroneurophysiologic studies were performed on 87 patients (56 females, 31 males) with an average age of 31 (range 3-56) years. Mobility of the spine, hips, knees, and feet was diminished. Some of the patients were obese (mean body mass index 27.0 kg/m). In the treadmill study, patients were able to walk an average of 638 m (range 0-1,618 m). On MRI, five patients showed compression of neural structures; one of them also had clinical symptoms. Somatosensory evoked potentials and electroneuromyography revealed evidence of compression of neural structure in three (3%) and two (3%) patients, respectively. The walking difficulties seem to have a multifactorial etiology: flexion contractures of the knees, early and rapid osteoarthrosis, equinus or equinovarus foot deformities, and obesity, but only rarely spinal stenosis.
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PMID:Walking ability in patients with diastrophic dysplasia: a clinical, electroneurophysiological, treadmill, and MRI analysis. 1530 6

Prader-Willi syndrome (PWS) is characterized by hypotonia, obesity, hypogonadism, small hands and feet, and mental deficiency. Obesity and hypogonadism are also frequently associated with slipped capital femoral epiphysis (SCFE), suggesting that children with PWS might be at increased risk of developing SCFE. Members of the Prader-Willi Syndrome Association (U.S.A.) were surveyed regarding the history of orthopaedic problems in general and of SCFE in particular. A total of 565 (63%) responses were received. The prevalence of orthopaedic conditions included 47% with flat feet, 41% with scoliosis, 19% with knock knees, 10% with hip dysplasia, 9% with osteoporosis, 7% with patellofemoral instability, 3% with bowlegs, 2% each with clubfeet, nursemaid's elbow, or leg-length inequality, and one patient (0.2%) with SCFE. The results of the survey indicate that SCFE is uncommon in patients with PWS, but the prevalence of hip dysplasia is increased approximately 10-fold compared with the general population.
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PMID:High incidence of hip dysplasia but not slipped capital femoral epiphysis in patients with Prader-Willi syndrome. 1530 8

A description of the clinical features of Majewski osteodysplastic primordial dwarfism type II (MOPD II) is presented based on 58 affected individuals (27 from the literature and 31 previously unreported cases). The remarkable features of MOPD II are: severe intrauterine growth retardation (IUGR), severe postnatal growth retardation; relatively proportionate head size at birth which progresses to true and disproportionate microcephaly; progressive disproportion of the short stature secondary to shortening of the distal and middle segments of the limbs; a progressive bony dysplasia with metaphyseal changes in the limbs; epiphyseal delay; progressive loose-jointedness with occasional dislocation or subluxation of the knees, radial heads, and hips; unusual facial features including a prominent nose, eyes which appear prominent in infancy and early childhood, ears which are proportionate, mildly dysplastic and usually missing the lobule; a high squeaky voice; abnormally, small, and often dysplastic or missing dentition; a pleasant, outgoing, sociable personality; and autosomal recessive inheritance. Far-sightedness, scoliosis, unusual pigmentation, and truncal obesity often develop with time. Some individuals seem to have increased susceptibility to infections. A number of affected individuals have developed dilation of the CNS arteries variously described as aneurysms and Moya Moya disease. These vascular changes can be life threatening, even in early years because of rupture, CNS hemorrhage, and strokes. There is variability between affected individuals even within the same family.
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PMID:Majewski osteodysplastic primordial dwarfism type II (MOPD II): natural history and clinical findings. 1536 97

The incidence of esophageal cancer has increased dramatically in the Western population in the last 2 decades. In 1975, about three fourths of the esophageal neoplasms were squamous cell carcinomas and the remainder were adenocarcinomas. During the last 2 to 3 decades, this pattern has changed dramatically and the incidence of squamous cell carcinomas has declined while the incidence of adenocarcinomas has increased. The reason for this dramatic increase is not clear, but gastro esophageal reflux disease, obesity and Barrett's esophagus have been identified as risk factors. High grade dysplasia in Barrett's esophagus is a premalignant condition which can progress to invasive adenocarcinoma. In this article, we discuss the natural history of high grade dysplasia (HGD), difficulties in the diagnosis, the incidence of adenocarcinoma in resected specimens and the surgical aspects in the treatment of HGD, including minimally invasive esophagectomy.
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PMID:Surgical aspects of the patient with high-grade dysplasia. 1642 39

ADP-ribosylation factor-like 3 (Arl3) is a member of a small subfamily of G-proteins involved in membrane-associated vesicular and intracellular trafficking processes. Genetic studies in Leishmania have shown that the Arl3 homolog is essential for flagellum biogenesis. Mutations in a related human family member, Arl6, result in Bardet-Biedl syndrome in humans, which is characterized by genital, renal, and retinal abnormalities, obesity, and learning deficits. As part of our large-scale phenotypic screen, mice deficient for the Arl3 gene were generated and analyzed. Arl3 (-/-) mice were born at a sub-Mendelian ratio, were small and sickly, and had markedly swollen abdomens. These mutants failed to thrive, and all died by 3 weeks of age. The (-/-) mice exhibited abnormal development of renal, hepatic, and pancreatic epithelial tubule structures, which is characteristic of the renal-hepatic-pancreatic dysplasia found in autosomal recessive polycystic kidney disease. Absence of Arl3 was associated with abnormal epithelial cell proliferation and cyst formation. Moreover, mice lacking Arl3 exhibited photoreceptor degeneration as early as postnatal day 14. These results are the first to implicate Arl3 in a ciliary disease affecting the kidney, biliary tract, pancreas, and retina.
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PMID:ADP-ribosylation factor-like 3 is involved in kidney and photoreceptor development. 1656 2

This review highlights areas of clinical research in gastroenterology and hepatology that were published predominantly in the journal Clinical Gastroenterology and Hepatology during the last year and were summarized during the American Gastroenterological Association Presidential Plenary Session in May 2006. The topics included eosinophilic esophagitis in children, detecting high-grade dysplasia or carcinoma in Barrett's esophagus, advances in management of celiac disease with elemental diet or gluten predigestion, the safety of NSAIDs in inflammatory bowel disease, the role of steroids in development of abscesses, prognosis of colorectal cancer associated with inflammatory bowel disease, screening for familial colorectal cancer in apparently sporadic disease, a new syndrome of familial colorectal cancer, new drugs in the treatment of chronic constipation and obesity, hepatoma risk factors and underserved racial/ethnic groups, and the application of new imaging and biology in diagnosis of gastroenterological disorders.
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PMID:Gastroenterology and hepatology clinical research update: 2005-2006. 1694 47

A relatively young patient with chronic gastroesophageal reflux disease (GERD), obesity, smoking, and alcohol intake presented with widespread metastatic disease in lymph nodes, liver and lungs from a lower esophageal adenocarcinoma extending into the gastroesophageal junction associated with Barrett's mucosa and dysplasia.A complete response was achieved with six cycles of chemotherapy that sustained for more than 4 years without further recurrence. Unfortunately, there was presence of esophageal metaplasia after complete response which eventually converted to low to high grade dysplasia and ultimately to a second primary localized lower esophageal adenocarcinoma that was treated with thoracoabdominal esophagectomy and lymphadenectomy. No evidence of disease recurrence was seen 2 years later. The pathogenesis of a recent increase in the incidence of GERD, Barrett's esophagus and lower esophageal adenocarcinoma are discussed. Surgery, radiotherapy and combination chemotherapy are effective in the early stages leading to tumor shrinkage and prolongation of life and even cure in some cases. Lower esophageal adenocarcinoma is frequently associated with Barrett's high-grade dysplasia. Since there has been a dramatic increase in the incidence of Barrett's dysplasia, appropriate surveillance with upper gastrointestinal endoscopy and preventive strategies, such as the use of aspirin, cyclo-oxygenase II inhibitors and other nonsteroidal antiinflammatory drugs known to be chemopreventive agents against colon, esophagus, gastric and bladder cancers, need to be studied.
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PMID:Esophageal adenocarcinoma arising from Barrett's dysplasia: a case report of double occurrence and prolonged survival after chemotherapy. 1698 98


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