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Mircera is a solution for injection that contains the active substance methoxy polyethylene glycolepoetin beta.
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It is available in vials and in pre-filled syringes at various strengths ranging from 50 to 1,000 micrograms per millilitre.
What is Mircera used for?
Mircera is used to treat anaemia (low red blood cell counts) that is causing symptoms in adults with chronic kidney disease (long-term, progressive decrease in the ability of the kidneys to work properly).
How is Mircera used?
Treatment with Mircera must be started under the supervision of a doctor who has experience in the management of patients with kidney disease. Mircera can be injected under the skin or into a vein. The dose and the frequency of dosing depend on whether or not Mircera is replacing another medicine used to stimulate the production of red blood cells. Doses should be adjusted according to the patient’s response, to obtain haemoglobin levels within the recommended range (between 10 and 12 grams per decilitre).
How does Mircera work?
A hormone called erythropoietin stimulates the production of red blood cells from the bone marrow.
Erythropoietin is produced by the kidneys. In patients with chronic kidney disease, the main cause of
their anaemia is a lack of natural erythropoietin. The active substance in Mircera, methoxy
polyethylene glycol-epoetin beta, works like natural erythropoietin to stimulate red blood cell
production, because it can attach itself to the same receptors as erythropoietin. However, the way it
interacts with the receptor is slightly different from natural erythropoietin, which gives it a longer
effect. It is also cleared from the body less quickly. As a result, Mircera can be given less often than
natural erythropoietin.
The active substance in Mircera is made up of epoetin beta attached to a chemical called methoxypolyethylene glycol. The epoetin beta is produced by ‘recombinant DNA technology’: it is made by a
cell that has received a gene, which makes it able to produce epoetin beta.
How has Mircera been studied?
Mircera has been studied in six main studies involving a total of 2,399 adults with anaemia associated
with chronic kidney disease. Mircera was compared with other medicines used to stimulate red blood
cell production. Two of these studies involved patients who were starting treatment for anaemia. The
first study, in 181 patients on dialysis (a blood clearance technique used in advanced kidney disease),
looked at Mircera injected into a vein every two weeks over 24 weeks and compared it with epoetin
alfa or beta. The second study, in 324 patients not on dialysis, looked at Mircera injected under the
skin every two weeks over 28 weeks, comparing it with darbepoetin alfa.
The other four studies (in 1,894 patients) were carried out in patients on dialysis who had already been
receiving medicines to stimulate red blood cell production. In these studies, patients either remained on the medicines they were already receiving, or changed to Mircera, injected into a vein or under the skin every two or four weeks. The effectiveness of the two treatment options was compared over 36
weeks. In all six studies, the main measure of effectiveness was the change in haemoglobin levels. Most
patients also received iron to prevent deficiency (low iron levels) during the studies.
What benefit has Mircera shown during the studies?
Mircera was as effective as the comparator medicines in correcting and maintaining haemoglobin
levels. In the studies of patients starting treatment for anaemia for the first time, 126 (93%) of the 135 patients on dialysis, and 158 (98%) of the 162 not on dialysis had a significant increase in haemoglobin levels with Mircera. Similar response rates were seen in the patients taking the comparator medicines. The second study showed that patients taking Mircera and those taking
darbepoetin alfa had similar increases in haemoglobin levels (around 2 g/dl).
In the studies of patients who had already been receiving medicines to stimulate red blood cell production, patients who changed to Mircera maintained their haemoglobin levels as effectively as the
patients who remained on their existing medicines. There was no overall change in haemoglobin levels
over the course of these studies with any of the treatments.
What is the risk associated with Mircera?
The most common side effect with Mircera (seen in between 1 and 10 patients in 100) is hypertension
(high blood pressure). For the full list of all side effects reported with Mircera, see the package leaflet.
Mircera must not be used in people who are hypersensitive (allergic) to methoxy polyethylene glycolepoetin beta or any of the other ingredients. It must also not be used in patients who have high blood
pressure that is not controlled Video Rating: / 5
A Division of Endocrinology, Diabetes and Bone Disease Grand Rounds presented by Paul J. Davis, MD, Professor of Medicine, Albany Medical College, and Adjunct Professor of Pharmacy at the Albany College of Pharmacy and Health Sciences
Beta-endorphin (often simply called endorphin) is a peptide neurotransmitter and hormone and one of a class of substances known as “endogenous opioids.” Its best-understood effect is natural pain inhibition, but it is also hypothesized to be involved in a number of other functions ranging from regulation of the stress response to the processing of rewarding experiences. In this video, I discuss beta-endorphin and some of its proposed functions.
TRANSCRIPT:
Beta-endorphin is a peptide neurotransmitter and hormone found in the central and peripheral nervous systems. It is one of a class of substances called endogenous opioids, which received their name because they are produced by the body and bind to the same receptors that opioid drugs like morphine bind to. The term endorphin is a blend of the words “endogenous” and “morphine.”
By binding to opioid receptors, beta-endorphin can elicit natural pain-relieving effects that have been found to be more potent than morphine. Beta-endorphin may achieve this type of analgesia by binding to opioid receptors in various regions of the nervous system. It can, for example, bind to opioid receptors in the spinal cord and inhibit the activation of neurons that transmit pain signals to the brain. And, beta-endorphin can act on opioid receptors in the brainstem that prompt the inhibition of pain signaling in the spinal cord through descending pathways.
Pain inhibition is the best-understood effect of beta-endorphin, but the peptide has also been linked to a long list of other functions. For example, beta-endorphin is released during stress and is thought to play a role in regulating the stress response as well as in the pain inhibition that can occur during acute stress. Beta-endorphin is also thought to interact with the dopamine system and be involved with rewarding experiences. Some research suggests beta-endorphin plays a role in the positive effects exercise can have on mood. And it has been associated with food intake and sexual behavior. Links between beta-endorphin and positive mood have led to a number of claims about endorphins promoting pleasure and happiness. In truth, however, much still needs to be learned about the functions of beta-endorphin in the nervous system and the role of beta-endorphin in positive mood states is still not fully understood.
References:
Corder G, Castro DC, Bruchas MR, Scherrer G. Endogenous and Exogenous Opioids in Pain. Annu Rev Neurosci. 2018 Jul 8;41:453-473. doi: 10.1146/annurev-neuro-080317-061522. Epub 2018 May 31.
Dalayeun JF, Norès JM, Bergal S. Physiology of beta-endorphins. A close-up view and a review of the literature. Biomed Pharmacother. 1993;47(8):311-20.
Dinas PC, Koutedakis Y, Flouris AD. Effects of exercise and physical activity on depression. Ir J Med Sci. 2011 Jun;180(2):319-25. doi: 10.1007/s11845-010-0633-9. Epub 2010 Nov 14.
Roth-Deri I, Green-Sadan T, Yadid G. Beta-endorphin and drug-induced reward and reinforcement. Prog Neurobiol. 2008 Sep;86(1):1-21. doi: 10.1016/j.pneurobio.2008.06.003. Epub 2008 Jun 18.
Veening JG, Barendregt HP. The effects of beta-endorphin: state change modification. Fluids Barriers CNS. 2015 Jan 29;12:3. doi: 10.1186/2045-8118-12-3. Video Rating: / 5
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A source of wise advice and rage fuelled tantrums Connie is the hormone monster we all would like guiding us. Watch some of Connie the hormone monstress’ best moments from Big Mouth.
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My precious little ravioli.
Welcome to Next of Ken and in this episode, we’re counting down 33 Times You Wished Connie Was Your Hormone Monstress. Every bit as crude, brash, and hysterical as her counterpart, Maury, Connie is also easily our favorite character on the hit Netflix show, “Big Mouth.” Played beautifully by Maya Rudolph, Connie the Hormone Monstress returns in season 2 when things with Jessi and her parents escalate to near catastrophic levels and trust us, the hilarity ensues. Clank clank!
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Substance P (SP) is an undecapeptide (a peptide composed of a chain of 11 amino acid residues) member of the tachykinin neuropeptide family. It is a neuropeptide, acting as a neurotransmitter and as a neuromodulator. The original discovery of Substance P (SP) was in 1931 by Ulf von Euler and John H. Gaddum as a tissue extract that caused an intestinal contraction in vitro. Its tissue distribution and biologic actions were further investigated over the following decades.
The endogenous receptor for substance P is neurokinin 1 receptor (NK1-receptor, NK1R) It belongs to the tachykinin receptor sub-family of GPCRs their neurokinin subtypes and neurokinin receptors that interact with SP have been reported as well. Amino acid residues that are responsible for the binding of SP and its antagonists are present in the extracellular loops and transmembrane regions of NK-1. Binding of SP to NK-1 results in internalization by the clathrin-dependent mechanism to the acidified endosomes where the complex disassociates. Subsequently, SP is degraded and NK-1 is re-expressed on the cell surface
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Women are twice as likely to suffer from anxiety as men. And while hormones can be a factor in this, cultural prejudices that persist in the education of girls cause the greatest harm. How can “normal” stress be distinguished from an anxiety disorder and which strategies are the most helpful? There’s good news: control over fear is possible, one step at a time. Listen to the talk by Psychologist Valentina Munoz, PhD, as part of Mini Psych-School 2013.
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