Since we are at MD Anderson this week. Reposting this report.
MD Anderson Masto Researcher. Takes only confirmed diagnosis.
https://tmsforacure.org/physician-database/database/srdan-verstovsek/
Systemic Mastocytosis, Version 2.2019, NCCN Clinical Practice Guidelines in Oncology
47.2 Year olds reportedly most miserable.
Gastrointestinal Exaggeration of Mast Cells in Pediatric Patients: A
Localized Process without a Worrisome Concern? A Report of 3 cases and a Review of the Literature
"Allergic diseases with mast cell exaggeration
Mast cells, of a non-pathological variety, are modestly elevated and likely genetically constitutive, in all allergic disease, including: allergic rhinitis, asthma, atopic dermatitis and eosinophilic esophagitis. The clinical presentation and the continued demonstration of the allergic disease process are intimately tied to tissue based mast
cell activation. In some situations, the over-production of mast cell mediators results in anaphylaxis or a constellation of anaphylaxis-associated symptoms (secondary mast cell activation syndrome) [13].
The literature supports increased mast cells in the allergic diseases, and a published report in adults
suggested a cut-off of <20 mast cells/HPF (as measured in GI tissue) as within normal limits; and if examined the specific markers of CD25 and CD2+ are negative [11,14]."
Next-generation sequencing in systemic mastocytosis: Derivation of a mutation-augmented clinical prognostic model for survival
Animesh Pardanani,* Terra Lasho, Yoseph Elala, Emnet Wassie, Christy Finke, Kaaren K. Reichard, Dong Chen, Curtis A. Hanson, Rhett P. Ketterling, and Ayalew Tefferi
"In routine practice, the World Health Organization classification of systemic mastocytosis (SM) is also the de facto prognostic system; a core value is distinguishing indolent (ISM) from advanced SM (includes aggressive SM [ASM], SM with associated hematological neoplasm [SM-AHN] and mast cell leukemia [MCL]).
We sequenced 27 genes in 150 SM patients to identify mutations that could be integrated into a clinical-molecular prognostic model for survival.
Forty four patients (29%) had ISM, 25 (17%) ASM, 80 (53%) SM-AHN and 1 (0.7%) MCL; overall KITD816V prevalence was 75%.
In 87 patients, 148 non-KIT mutations were detected; the most frequently mutated genes were TET2 (29%), ASXL1 (17%), and CBL (11%), with significantly higher mutation frequency in SM-AHN>ASM>ISM (P<0.0001).
In advanced SM, ASXL1 and RUNX1 mutations were associated with inferior survival. In multivariate analysis, age>60 years (HR52.4), hemoglobin<10 g/dL or transfusion dependence (HR51.7), platelet count<150 3 109/L (HR53.2), serum albumin<3.5 g/dL (HR52.6), and ASXL1 mutation (HR52.3) were associated with inferior survival.
A mutation-augmented prognostic scoring system (MAPSS) based on these parameters stratified advanced SM patients into high-, intermediate-, and low-risk groups with median survival of 5, 21 and 86 months, respectively (P<0.0001). These data should optimize riskstratification and treatment selection for advanced SM patients."
American Journal of Hematology, Vol. 91, No. 9, September 2016
If you have MCAS generated IBS officer, you could understand…
Maybe he is, I wasn’t aware we didnt treat Shirefolk >:p next on pharmacy stories from Mordor
NOTE: RX warning can cause long toes and excessively hairy feet.
Hi all, a member wants to know, if you have a hot tub, what sanitizing and maintaining chemicals can you tolerate??
A not so subtle reminder!
More MD Anderson contributors.
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