Naunyn-Schmiedeberg's archives of pharmacology
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Naunyn Schmiedebergs Arch. Pharmacol. · Jul 2020
ReviewCOVID-19 pandemic and therapy with ibuprofen or renin-angiotensin system blockers: no need for interruptions or changes in ongoing chronic treatments.
Scientists hypothesized that drugs such as ibuprofen or renin-angiotensin system (RAS) blockers could exacerbate the novel coronavirus disease COVID-19 by upregulating the angiotensin-converting enzyme 2 (ACE2), which serves as an entry receptor for the coronavirus SARS-CoV-2. This hypothesis was taken up by the lay press and led to concerns among doctors and patients whether the use of these drugs was still safe and justified against the background of the pandemic spread of SARS-CoV-2 with an increasing number of cases and deaths. In this article, we summarize what is known about the effect of RAS blockers or non-steroidal anti-inflammatory drugs (NSAIDs) on the course of COVID-19 disease. ⋯ In view of the inconsistent and limited evidence and after weighing up the benefits and risks, we would not currently recommend discontinuing or switching an effective treatment with RAS blockers. NSAIDs should be used at the lowest effective dose for the shortest possible period. The choice of drug to treat COVID-19-associated fever or pain should be based on a benefit-risk assessment for known side effects (e.g., kidney damage, gastrointestinal ulceration).
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Naunyn Schmiedebergs Arch. Pharmacol. · Jan 2018
ReviewMigraine with prolonged aura: phenotype and treatment.
We review the published literature on migraine with prolonged aura (PA), specifically with regards to the phenotype and treatment options. PA is not uncommon. A recent study found that about 17% of migraine auras are prolonged and that 26% of patients with migraine with aura have experienced at least one PA. ⋯ The only randomised, blinded, controlled trial to date has been of nasal ketamine showing some reduction in aura severity but not duration. A small open-labelled pilot study of amiloride was also promising. Larger randomised, controlled trials are needed to establish whether any of the existing or novel compounds mentioned are significantly effective and safe.
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Tramadol is an analgesic that is used worldwide for pain, but its mechanisms of action have not been fully elucidated. The majority of studies to date have focused on activation of the μ-opioid receptor (μOR) and inhibition of monoamine reuptake as mechanisms of tramadol. Although it has been speculated that tramadol acts primarily through activation of the μOR, no evidence has revealed whether tramadol directly activates the μOR. ⋯ Several studies have shown that GPCRs and ion channels are targets for tramadol. In particular, tramadol has been shown to affect GPCRs. Here, the effects of tramadol on GPCRs, monoamine transporters, and ion channels are presented with a discussion of recent research on the mechanisms of tramadol.
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Naunyn Schmiedebergs Arch. Pharmacol. · Sep 2011
ReviewThe role of morphine in regulation of cancer cell growth.
Morphine is considered the "gold standard" for relieving pain and is currently one of the most effective drugs available clinically for the management of severe pain associated with cancer. In addition to its use in the treatment of pain, morphine appears to be important in the regulation of neoplastic tissue. Although morphine acts directly on the central nervous system to relieve pain, its activities on peripheral tissues are responsible for many of the secondary complications. ⋯ Various signaling pathways have been suggested to be involved in these extra-analgesic effects of morphine. Suppression of immune system by morphine is an additional complication. This review provides an update on the influence of morphine on the growth and migration potential of tumor cells.
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Naunyn Schmiedebergs Arch. Pharmacol. · Mar 2011
ReviewTherapeutic effects of Clostridium botulinum C3 exoenzyme.
C3 exoenzyme from Clostridium botulinum, specifically ADP-ribosylates small GTP-binding proteins RhoA, B, and C. ADP-ribosylation causes functional inactivation of Rho proteins resulting in cessation of the complete downstream signaling. Rho proteins are general regulators of a lot of essential cellular functions, among others, the neuronal growth cone. ⋯ Whereas full-length C3 also acts on astrocytes and microglia to induce-at least in an in vitro model-inflammation and glial scar formation, C3(154-182) peptide is inert and seems only to act on neurons. In addition to its axono- and dendritotrophic effects on cultured primary hippocampal neurons, C3(154-182) peptide enhanced functional recovery and regeneration in a mouse model of spinal cord injury. Thus, in a proof-of-principle experiment, C3 peptide was shown to be efficacious in post-traumatic neuro-regeneration.