Re: 132 flu patients hit with brain disorders since July
From SnowyOwl's find:
"Fatal neuropsychiatric adverse reactions to oseltamivir: Case series and overview of causal relationships
Rokuro Hama
Following restrictions on the use of NSAIDs as antipyretics for children in Japan in 2000 [37], the proportion of NSAIDs users among cases of Reye?s syndrome and/or influenza-associated encephalopathy decreased from about 30% to below 10% and the proportion of case fatalities resulting from
influenza associated encephalopathy decreased from about 30% to about 10%. Two years (i.e. two winter seasons) elapsed during which the
proportion of case fatality of influenza-associated encephalopathy decreased, before the marketing of Tamiflu dry syrup for children in Japan commenced in September 2002.
This new type of encephalopathy among infants was first found in the winter of 2002/2003 just after the marketing of Tamiflu dry syrup for children had started. However a similar adult case of sudden death had been already reported in March 2001 [MHLWB01-529], just after the Tamiflu capsule was marketed in February 2nd 2001 in Japan.
Times of onset of most sudden deaths and of neuropsychiatric symptoms are very similar. These facts also suggest that the majority of sudden deaths and
neuropsychiatric symptoms after taking Tamiflu are different from the pattern observed with infection-associated encephalopathy including Reye?s syndrome and/or influenza-associated encephalopathy.
Epithelial Na+ channel (ENaC), Na+/K+-ATPase pumps, and several aquaporin water channels are the best described molecular transporters in the lung when pathological conditions lead to the development of pulmonary oedema. Lung oedema results from the impairment of alveolar cells and/or capillary endothelial cells, both of which actively transport fluids from the alveolar space to the blood vessels. In acute lung injury (ALI), especially in severe sepsis (systemic inflammatory response by infection), an inflammatory process damages the capillary endothelium rather than the alveolar epithelium, resulting in high permeability of the lung capillaries to fluid, which leads to clinical pulmonary oedema. In contrast to the endothelium, the alveolar epithelium is often spared in ALI, and the rate of alveolar fluid clearance (AFC) in ALI can therefore be maintained and perhaps even increased.
Although the role of Tamiflu in the development of lung oedema in two of the autopsied cases is not completely clarified, it is at least
possible that severe hypoxia induced by the respiratory suppressive action of oseltamivir might have contributed to the induction of lung oedema just prior to respiratory arrest in both cases.
There is only one reported case of acute hemorrhagic colitis induced by Tamiflu but in that instance an allergic mechanism was involved. However, among the
80 fatal cases now known, bleeding episodes were described in eight, including one case without severe infection, sepsis or multiorgan failure.
One certainly cannot exclude the possibility that activation of normal human plasminogen by human neulaminidase (sialidase) might be inhibited by OCB, in which case normal fibrinolysis might be affected,
resulting in abnormal coagulopathy including DIC.
After the submission of this paper, three investigators found equivocally that P-glycoprotein is the efflux transporter of oseltamivir at the BBB."
http://www.npojip.org/english/published-paperJRS431.pdf
"Disseminated intravascular coagulation (
DIC): leads to the
formation of small blood clots inside the blood vessels throughout the body. As the small clots consume all the available coagulation proteins and platelets, normal coagulation is disrupted and
abnormal bleeding occurs from the skin, the digestive tract, the
respiratory tract and surgical wounds." http://en.wikipedia.org
/wiki/Disseminated_intravascular_coagulation
