TY - JOUR A1 - Bohnert, S. A1 - Monoranu, C. - M. A1 - Siauw, C. A1 - Al-Tinawi, F. A1 - Bohnert, M. T1 - Tödliche Hirnmassenblutung infolge Vitamin-K-Mangels bei einem 9 Wochen alten Säugling JF - Rechtsmedizin N2 - Intrakranielle Blutungen sind im Säuglingsalter seltene, aber lebensbedrohende Ereignisse. Neben Gefäßmissbildungen, Stoffwechseldefekten sowie Störungen der Blutgerinnung kommen v. a. nichtakzidentielle Traumata, Schütteltrauma in Betracht. Die klinische Diagnostik umfasst hinsichtlich der Blutungsgenese neben Sonographie und MRT als apparatives Verfahren auch eine Fundoskopie sowie laborchemische Analysen, insbesondere der Gerinnungsparameter. Für die Blutgerinnung ist das fettlösliche Vitamin K essenziell: Frühe, klassische und späte Vitamin-K-Mangel-Blutungen werden dabei unterschieden. Um ein gehäuftes Wiederauftreten von Vitamin-K-Mangel-Blutungen bei Neugeborenen und jungen Säuglingen zu verhindern, bedarf es einer hinreichenden Aufklärung der Eltern. Eine Verweigerung der Prophylaxe scheint Folge einer weltanschaulich begründeten Ablehnung der Schulmedizin und ein zunehmendes Phänomen in wohlhabenden Industrieländern zu sein. N2 - Intracranial hemorrhages in infants are rare but life-threatening events. Apart from vascular malformations, metabolic disorders and coagulopathies, nonaccidental trauma, in particular shaken baby syndrome must be taken into consideration. Clinical diagnostic tests and procedures to further evaluate the etiology of the hemorrhage include sonography and magnetic resonance imaging (MRI) as imaging procedures as well as fundoscopy and laboratory tests, especially with respect to coagulation parameters. Fat-soluble vitamin K is essential for blood coagulation. A differentiation is made between classical and delayed hemorrhages due to vitamin K deficiency. In order to avoid an increased recurrence of bleeding due to vitamin K deficiency in neonates and young infants, an adequate clarification for the parents is necessary. A refusal of prophylaxis seems to be the result of an ideologically founded rejection of classical medicine and an increasing phenomenon in affluent industrial countries. KW - Intrakranielle Blutung KW - Schütteltrauma KW - Vitamin-K-Mangel-Blutung KW - Prophylaxe KW - intracranial bleeding KW - shaken baby syndrome KW - vitamin k deficiency bleeding KW - prophylaxis Y1 - 2020 U6 - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-232475 SN - 0937-9819 VL - 30 ER - TY - JOUR A1 - Riederer, P. A1 - Monoranu, C. A1 - Strobel, S. A1 - Iordache, T. A1 - Sian-Hülsmann, J. T1 - Iron as the concert master in the pathogenic orchestra playing in sporadic Parkinson's disease JF - Journal of Neural Transmission N2 - About 60 years ago, the discovery of a deficiency of dopamine in the nigro-striatal system led to a variety of symptomatic therapeutic strategies to supplement dopamine and to substantially improve the quality of life of patients with Parkinson's disease (PD). Since these seminal developments, neuropathological, neurochemical, molecular biological and genetic discoveries contributed to elucidate the pathology of PD. Oxidative stress, the consequences of reactive oxidative species, reduced antioxidative capacity including loss of glutathione, excitotoxicity, mitochondrial dysfunction, proteasomal dysfunction, apoptosis, lysosomal dysfunction, autophagy, suggested to be causal for ɑ-synuclein fibril formation and aggregation and contributing to neuroinflammation and neural cell death underlying this devastating disorder. However, there are no final conclusions about the triggered pathological mechanism(s) and the follow-up of pathological dysfunctions. Nevertheless, it is a fact, that iron, a major component of oxidative reactions, as well as neuromelanin, the major intraneuronal chelator of iron, undergo an age-dependent increase. And ageing is a major risk factor for PD. Iron is significantly increased in the substantia nigra pars compacta (SNpc) of PD. Reasons for this finding include disturbances in iron-related import and export mechanisms across the blood-brain barrier (BBB), localized opening of the BBB at the nigro-striatal tract including brain vessel pathology. Whether this pathology is of primary or secondary importance is not known. We assume that there is a better fit to the top-down hypotheses and pathogens entering the brain via the olfactory system, then to the bottom-up (gut-brain) hypothesis of PD pathology. Triggers for the bottom-up, the dual-hit and the top-down pathologies include chemicals, viruses and bacteria. If so, hepcidin, a regulator of iron absorption and its distribution into tissues, is suggested to play a major role in the pathogenesis of iron dyshomeostasis and risk for initiating and progressing ɑ-synuclein pathology. The role of glial components to the pathology of PD is still unknown. However, the dramatic loss of glutathione (GSH), which is mainly synthesized in glia, suggests dysfunction of this process, or GSH uptake into neurons. Loss of GSH and increase in SNpc iron concentration have been suggested to be early, may be even pre-symptomatic processes in the pathology of PD, despite the fact that they are progression factors. The role of glial ferritin isoforms has not been studied so far in detail in human post-mortem brain tissue and a close insight into their role in PD is called upon. In conclusion, "iron" is a major player in the pathology of PD. Selective chelation of excess iron at the site of the substantia nigra, where a dysfunction of the BBB is suggested, with peripherally acting iron chelators is suggested to contribute to the portfolio and therapeutic armamentarium of anti-Parkinson medications. KW - SARS-CoV-2 KW - iron in parkinsonism KW - parkinson’s disease KW - iiron transporter KW - neuromelanin KW - iron pathology KW - neuroinflammation KW - iron model KW - ferroptosis KW - ɑ-Synuclein and iron KW - virus–iron interaction KW - COVID-19 KW - hepcidin Y1 - 2021 U6 - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-268539 SN - 1435-1463 VL - 128 IS - 10 ER -