When looking at test results with your doctor, read the data sheet online from ARUP, Quest, or Mayo.
In measurement of a set, accuracy is closeness of the measurements to a specific value, while precision is the closeness of the measurements to each other.
Specificity and sensitivity
Specificity and sensitivity reveal the likelihood of false negatives and false positives. To be effective a pathology test is expected to detect abnormalities with certainty.
How likely is it that an individual has the disease that the test suggests?
What are the chances that an individual has a certain disorder even though a test for it was negative?
Specificity is the ability of a test to correctly exclude individuals who do not have a given disease or disorder.
For example, a certain test may have proven to be 90% specific.
If 100 healthy individuals are tested with that method, only 90 of those 100 healthy people will be found to be “normal” (disease-free). The other 10 people also do not have the disease, but their test results seem to indicate they do. For that 10% their “abnormal” findings are a misleading false-positive result.
The more specific a test is, the fewer “false-positive” results it produces. A false-positive result can lead to misdiagnosis and unnecessary, possibly challenging or life-altering, diagnostic procedures and therapies.
It is important to confirm a diagnosis that requires dangerous therapy and a test’s specificity is one of the crucial indicators.
Although few if any tests succeed in diagnosing disease correctly 100% of the time, most tests produce only a small proportion of false-positive or false-negative results.
Laboratories are required through laboratory accreditation to use the most sensitive and specific tests available.
Sensitivity is the ability of a test to correctly identify people who have a given disease or disorder. For example, a certain test may have proven to be 90% sensitive.
That is, if 100 people known to have a certain disease are tested with that method, the test will correctly identify 90 of those 100 cases of disease.
The other 10 people who were tested also have the disease but the test will fail to detect it. For that 10%, the finding of a “normal” result is a misleading false-negative result.
A test’s sensitivity becomes particularly important when you are seeking to exclude a dangerous disease.
The more sensitive a test, the fewer “false-negative” results it produces. A false-negative result fails to identify disease states even though they are present.
Impressive new system. Real time status feedback in the ER for each patient. Time from arrival 5 minutes.
Mast Cell Activation Disease and Microbiotic Interactions
Lawrence B. Afrin, MD and Alexander Khoruts
Conveying a new understanding that all MC disease features inappropriate MC activation, the new toplevel designation MCAD encompasses various types of rare mastocytosis and likely prevalent MCAS.
The apparent uniqueness in each patient with MCAD of constitutively activating mutational patterns in KIT and other MC regulatory elements likely is the principal driver of not only the specific clinical presentation, and therapeutic response profile, in each patient but also the great heterogeneity across this population.
The complex systems biology of microbiota are just beginning to be elucidated, but it is clear that there are innumerable interactions with normal MCs, creating the potential for exponentially more complex interactions with the abnormal MCs of MCAD. Much more research lies ahead.
And Dexamethasone and Aristocort and Solmedrol
My friend Cathy found this paper.
Restless Legs Syndrome Is Associated With Mast Cell Activation Syndrome
Leonard B Weinstock et al. J Clin Sleep Med. 2020.
RLS appears to be associated with MCAS. Effects of mast cell mediators, inflammation, immune mechanisms, dysautonomia, or hypoxia may theoretically activate RLS in MCAS.
Great paper. Other papers detail the neuropsychiatric impacts of mast cell mediators on modulating the blood brain barrier this would only make sense.
After 25 years of progressive suffering and all the inxreasing dosage rotation of “seizure/Parkinson’s” meds, periodic infusions of ferritin sulfate at Mayo to keep serum ferritin levels over 100 ng/ml has almost eliminated her symptoms. Takes about 4 to 6 weeks after infusion to get enough across BBB. After initial series, one a year for maintenance to keep brain ferritin levels sufficient for production of GABA/glutamate and dopamine. Good series about it on video at John’s Hopkins neurology website.
Heads up for those with SM
YOUR HELP IS NEEDED!
Blueprint Medicines, together with The Mastocytosis Society, Inc. (TMS) and a working group of physicians and patient advocates, has launched a new survey aimed at better defining the daily experience of patients living with systemic mastocytosis through the Mast Cell Connect (MCC) registry.
This survey asks about patient symptoms as well as details about how these symptoms impact your daily life. We plan to use the information to educate a broader community of Health Care Professionals and bring the patient experience to the forefront of SM education.
If you are a patient living with SM and a member of the MCC registry, please log-in to complete the important survey.
If you’re interested in registering for Mast Cell Connect, visit https://www.mastcellconnect.org/
Thank you so much!
Recall on certain Impax-Amneal generic Adrenaclik injectors
Impax Laboratories, LLC, a wholly owned subsidiary of Amneal Pharmaceuticals LLC, is providing important safety information concerning its Epinephrine Injection, USP Auto-Injector 0.3 mg. Impax is writing to inform you that some Epinephrine Injection, USP Auto-Injector 0.3 mg devices may not contain the yellow “stop collar” component (see pictures below). The yellow “stop collar” is one of several components that work together to assure proper dosing of the auto-injector. If the auto-injector is missing a yellow “stop collar” component, it has the potential safety risk of delivering a double dose of the product to a consumer. An overdose of epinephrine has the potential to cause severe patient harm or death.
If you have received Amneal or Impax’s Epinephrine Injection, USP Auto-Injector 0.3 mg after December 20, 2018, Impax is requesting that you immediately perform a visual inspection (Steps 1-5) as described below to confirm the presence of the yellow “stop collar”:
Carefully inspect for the presence of the yellow “stop collar.”
If yellow “stop collar” is present, then the product is safe to use. No further action is necessary.
If the yellow “stop collar” is missing, call or e-mail Amneal Drug Safety Department using the contact information below, for instructions for the return and replacement of the auto-injector:
AMNEAL PHARMACEUTICALS DRUG SAFETY DEPARTMENT
Phone: 1(877) 835-5472
Mail: Amneal Pharmaceuticals, 50 Horseblock Road, Brookhaven, New York 11719
After weeks of high dose steroids…It’s clobbering time
Y’all know I prefer to see the lighter side of everything…now THIS is good!!!
COVID-19’s deadliness for men is revealing why researchers should have been studying immune system sex differences years ago
Expensive, but if you are extremely sensitive, here is a starting point. Remember though everyone is different. What triggers you, may not trigger me.
The role of mast cells in allergic inflammation
Respiratory Medicine (2012)106, 9-14
The histochemical characteristics of human basophils and tissue mast cells were described over a century ago by Paul Ehrlich. When mast cells are activated by an allergen that binds to serum IgE attached to their FcɛRI receptors, they release cytokines, eicosanoids and their secretory granules. Mast cells are now thought to exert critical proinflammatory functions, as well as potential immunoregulatory roles, in various immune disorders through the release of mediators such as histamine, leukotrienes, cytokines chemokines, and neutral proteases (chymase and tryptase). The aim of this review is to describe the role of mast cells in allergic inflammation.
Mast cells interact directly with bacteria and appear to play a vital role in host defense against pathogens. Drugs, such as glucocorticoids, cyclosporine and cromolyn have been shown to have inhibitory effects on mast cell degranulation and mediator release. This review shows that mast cells play an active role in such diverse diseases as asthma, rhinitis, middle ear infection, and pulmonary fibrosis.
In conclusion, mast cells may not only contribute to the chronic airway inflammatory response, remodeling and symptomatology, but they may also have a central role in the initiation of the allergic immune response, that is providing signals inducing IgE synthesis by B-lymphocytes and inducing Th2 lymphocyte differentiation.
Physiological Roles of Mast Cells: Collegium Internationale Allergologicum Update 2019
Varricchi G., et.al.
Mast cells are immune cells which have a widespread distribution in nearly all tissues. These cells and their mediators are canonically viewed as primary effector cells in allergic disorders.
However, in the last years, mast cells have gained recognition for their involvement in several physiological and pathological conditions. They are highly heterogeneous immune cells displaying a constellation of surface receptors and producing a wide spectrum of inflammatory and immunomodulatory mediators.
These features enable the cells to act as sentinels in harmful situations as well as respond to metabolic and immune changes in their microenvironment.
Moreover, they communicate with many immune and nonimmune cells implicated in several immunological responses. Although mast cells contribute to host responses in experimental infections, there is no satisfactory model to study how they contribute to infection outcome in humans.
Mast cells modulate physiological and pathological angiogenesis and lymphangiogenesis, but their role in tumor initiation and development is still controversial. Cardiac mast cells store and release several mediators that can exert multiple effects in the homeostatic control of different cardiometabolic functions.
Although mast cells and their mediators have been simplistically associated with detrimental roles in allergic disorders, there is increasing evidence that they can also have homeostatic or protective roles in several pathophysiological processes. These findings may reflect the functional heterogeneity of different subsets of mast cells.
Emerging Roles of Mast Cells in the Regulation of Lymphatic Immuno-Physiology
Sarit Pal, Shubhankar Nath, ￼Cynthia J. Meininger, and Anatoliy A. Gashev
"Mast cells (MCs) are abundant in almost all vascularized tissues. Furthermore, their anatomical proximity to lymphatic vessels and their ability to synthesize, store and release a large array of inflammatory and vasoactive mediators emphasize their significance in the regulation of the lymphatic vascular functions.
As a major secretory cell of the innate immune system, MCs maintain their steady-state granule release under normal physiological conditions; however, the inflammatory response potentiates their ability to synthesize and secrete these mediators.
Activation of MCs in response to inflammatory signals can trigger adaptive immune responses by dendritic cell-directed T cell activation. In addition, through the secretion of various mediators, cytokines and growth factors, MCs not only facilitate interaction and migration of immune cells, but also influence lymphatic permeability, contractility, and vascular remodeling as well as immune cell trafficking through the lymphatic vessels.
In summary, the consequences of these events directly affect the lymphatic niche, influencing inflammation at multiple levels.
In this review, we have summarized the recent advancements in our understanding of the MC biology in the context of the lymphatic vascular system. We have further highlighted the MC-lymphatic interaction axis from the standpoint of the tumor microenvironment."
Neutrophils, basophils, eosinophils, and mast cells. Their granules contain enzymes that damage or digest pathogens and release inflammatory mediators into the bloodstream.