COVID-19 vaccine
In March 2021, the European Medicines Agency (EMA) announced that out of the around 20 million people who had received the Oxford–AstraZeneca COVID-19 vaccine, general blood clotting rates were normal, but that it had identified seven cases of disseminated intravascular coagulation, and eighteen cases of cerebral venous sinus thrombosis. It had been proposed that inadvertent injection of COVID-19 vaccine into deltoid muscle vasculature may result in vaccine distribution to distant tissues that may be causing these rare adverse reactions. A causal link with the vaccine, however, had not been proven, but the EMA decided to conduct further analysis and to inform recipients of the remote possibility of such rare syndromes. EMA confirmed that the vaccines benefits still outweigh the risks and later released updated product information. and issued warnings to patients and healthcare professionals. The British Medicines and Healthcare products Regulatory Agency (MHRA) confirmed 79 cases of thrombosis, including 19 fatalities, within the first 20 million vaccinations in Great Britain. Guidelines on management of suspected cases was issued by the British Society for Haematology; it discouraged the use of heparin until it was clearer that heparin would not aggravate the thrombosis. On 13 April 2021 the Centers for Disease Control and Prevention paused the use of the Janssen COVID-19 vaccine in the United States due to six cases of CVST that occurred 6 to 13 days after administration. The recommended pause was lifted on 23 April 2021 following a safety review.
Pathophysiology
There are multiple theories proposed to explain the mechanisms of muscle changes of sarcopenia including changes in satellite cell recruitment, changes in anabolic signalling, protein oxidation, inflammation, and developmental factors. The pathologic changes of sarcopenia include a reduction in muscle tissue quality as reflected in the replacement of muscle fibers with fat, an increase in fibrosis, changes in muscle metabolism, oxidative stress, and degeneration of the neuromuscular junction.The distribution of muscle fibers types also changes in sarcopenic muscle causing a decrease in type II muscle fibers, or "fast twitch," with little to no decrease in type I muscle fibers, or "slow-twitch" muscle fibers. Deinervated type II fibers are often converted to type I fibers by reinnervation by slow type I fiber motor nerves.The failure to activate satellite cells upon injury or exercise is also thought to contribute to the pathophysiology of sarcopenia. Additionally, oxidized proteins can lead to a buildup of lipofuscin and cross-linked proteins causing an accumulation of non-contractile material in the skeletal muscle and contribute to sarcopenic muscle.An apparent protective factor is sufficient levels of the protein BNIP3, which prevents cells buildup of damaged mitochondria. Deficiency of BNIP3 leads to muscle inflammation and atrophy. Diagnosis
Multiple diagnostic criteria have been proposed by various expert groups and continues to be an area of research and debate.