Giant Cell Arteritis Presenting as Small Bowel Infarction

Giant cell arteritis predominantly affects cranial arteries and rarely involves other sites. We report a patient who presented with small bowel obstruction because of infarction from mesenteric giant cell arteritis. She had an unusual cause of her obstruction and a rare manifestation of giant cell arteritis. In spite of aggressive therapy with steroids, she died a month later because of multiple complications. We discuss the diagnosis and management of small bowel obstruction and differential diagnosis of vasculitis of the gastrointestinal tract. We were able to find 11 cases of bowel involvement with giant cell arteritis in the English literature. This case report illustrates that giant cell arteritis can be a cause of small bowel obstruction and bowel infarction. In the proper clinical setting, vasculitides need to be considered early in the differential diagnosis when therapy may be most effective

Genetic variation and exercise-induced muscle damage: implications for athletic performance, injury and ageing.

Prolonged unaccustomed exercise involving muscle lengthening (eccentric) actions can result in ultrastructural muscle disruption, impaired excitation-contraction coupling, inflammation and muscle protein degradation. This process is associated with delayed onset muscle soreness and is referred to as exercise-induced muscle damage. Although a certain amount of muscle damage may be necessary for adaptation to occur, excessive damage or inadequate recovery from exercise-induced muscle damage can increase injury risk, particularly in older individuals, who experience more damage and require longer to recover from muscle damaging exercise than younger adults. Furthermore, it is apparent that inter-individual variation exists in the response to exercise-induced muscle damage, and there is evidence that genetic variability may play a key role. Although this area of research is in its infancy, certain gene variations, or polymorphisms have been associated with exercise-induced muscle damage (i.e. individuals with certain genotypes experience greater muscle damage, and require longer recovery, following strenuous exercise). These polymorphisms include ACTN3 (R577X, rs1815739), TNF (-308 G>A, rs1800629), IL6 (-174 G>C, rs1800795), and IGF2 (ApaI, 17200 G>A, rs680). Knowing how someone is likely to respond to a particular type of exercise could help coaches/practitioners individualise the exercise training of their athletes/patients, thus maximising recovery and adaptation, while reducing overload-associated injury risk. The purpose of this review is to provide a critical analysis of the literature concerning gene polymorphisms associated with exercise-induced muscle damage, both in young and older individuals, and to highlight the potential mechanisms underpinning these associations, thus providing a better understanding of exercise-induced muscle damage

Pediatric acquired demyelinating syndromes: a nationwide validation study of the Danish National Patient Register

Magnus Spangsberg Boesen,1 Melinda Magyari,2,3 Alfred Peter Born,1 Lau Caspar Thygesen4 1Department of Pediatrics, Rigshospitalet, Copenhagen University Hospital, Copenhagen, Denmark; 2The Danish Multiple Sclerosis Registry, Department of Neurology, Rigshospitalet, University of Copenhagen, Denmark; 3Danish Multiple Sclerosis Center, Department of Neurology, Rigshospitalet, Copenhagen University Hospital, Copenhagen, Denmark; 4National Institute of Public Health, University of Southern Denmark, Copenhagen, Denmark Objective: To validate the Danish National Patient Register’s (NPR) diagnoses of pediatric acquired demyelinating syndromes (ADS) including multiple sclerosis (MS). Study design and setting: We identified ADS diagnostic groups using International Classification of Diseases (ICD) codes and reviewed medical records to validate the NPR diagnoses during 2008–2015. Results: Among 409 children in the study, 184 children had a validated and final ADS diagnosis after reviewing medical records as follows: optic neuritis (ON; n=46), transverse myelitis (TM; n=16), acute disseminated encephalomyelitis (ADEM; n=50), clinically isolated syndrome (CIS) including dissemination in space (CIS [DIS]) but not dissemination in time (n=6), neuromyelitis optica spectrum disorder (NMOsd; n=5), and MS (n=61). During the mean follow-up of 4.6 years, 33% of children initially diagnosed with monophasic ADS progressed to MS. Positive predictive value (PPV) was 0.71 (95% confidence interval [CI] =0.62–0.80) for ON, 0.64 (95% CI =0.43–0.82) for TM, 0.93 (95% CI =0.84–0.98) for MS, 0.27 (95% CI =0.19–0.35) for CIS, 0.43 (95% CI =0.10–0.82) for NMOsd, and 0.15 (95% CI =0.10–0.20) for ADEM. Assuming complete coverage for non-MS ADS, the sensitivity was 0.99 (95% CI =0.93–1.00) for ON, 0.83 (95% CI =0.36–1.00) for CIS (DIS), and 0.80 (95% CI =0.56–0.94) for TM, but only 0.58 (95% CI =0.43–0.72) for ADEM and 0.60 (95% CI =0.15–0.95) for NMOsd. Conclusion: PPV was high for MS and considered acceptable for ON and TM; therefore, these ICD revision 10 (ICD-10) codes from the NPR are useful for epidemiological studies. Conversely, PPV was low for CIS and ADEM; NMOsd was inconclusive. Keywords: pediatric MS, acquired demyelinating syndrome, ADEM, health registers, validation, ICD-1