EHEC recommended: Early neurological therapy

Hundreds of people are currently using a hemolytic-uremic syndrome in German hospitals, particularly in the north. Note the neurological disorders. The professional society recommends therefore, neurologists involved early in the therapy.
BERLIN (NES). The current wave of EHEC is special - not only because of the rare pathogen and the size of the outbreak, but also because of the neurological consequences for patients.
The German Society of Neurology (DGN) reported about half of patients with hemolytic-uremic syndrome (HUS), which may suffer from severe and sometimes irreversible neurological disorders.
As alarming call it the two Hamburg neurologist Professor Joachim Roether and Professor Christian Gerloff, that the neurological condition in spite of early plasmapheresis does not improve or even deteriorating.
Gerloff is director of neurology at the University Hospital Hamburg-Eppendorf (UKE), Roether is Chief of Neurology at the Asklepios Clinic Altona. Hamburg, Schleswig-Holstein to the trouble spot of the current wave of EHEC.
Apparently striking is the early appearance of neurological symptoms.
Gerloff, 'You can already develop simultaneously with renal and gastroenterological symptoms. " Crucial features of HUS are bloody diarrhea, hemolysis, and renal dysfunction.


On the neurological symptom complex in HUS the first professional association is one of confusion, reduced vigilance, irritability and delirium. There are also many cases in aphasia and apraxia, and disturbances of the brain stem functions. In severe cases, patients develop myoclonic seizures and sometimes that can lead to coma. The neurologists suspect the cause of these symptoms in the Shiga toxin 2, the EHEC releases. In addition to the hemolytic effect of the toxin leads to a swelling of the vascular endothelium. As a result, the toxin could also lead to a widening of the intracranial vessels and a disturbance of autoregulation in the kidneys.
Also could play the complement cascade at the neurological deficit involved. Nephrologists suggest that Shiga toxin can activate the cascade, such as by binding to the C3 convertase of the alternative activation pathway.

One therapeutic approach is the monoclonal antibody eculizumab, which inhibits the C5 convertase and therefore interrupts the terminal cascade. Initial success in the current HUS cases were hospital doctors reported already. Whether the drug is a general treatment option, however, so far the doctors can not yet be estimated.
The neurologist and Gerloff Röther argue, given the severe neurological responses for 'drastic therapeutic measures'. Also, she said eculizumab should be considered in each case. UKE on 30 patients treated so far are just that, at the Asklepios Clinic in Hamburg-Altona five. At the first neurological abnormalities to speak both in favor of early anti-shock therapy, such as anti-epileptic levetiracetam. Diagnostic method of choice is the MRI, the findings are more sensitive than CT.


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