Re: j epstein
thnks for the time jay, current issue is parasteis on walking , severe spinal stenosis. L4 L5 foraminal and central. 8 mm. however I have ZERO!! pain. , can bike swim sit sleep . zero pain , its only the parastesia. . 1 it is elimanted by medrol pack. I can jog if need be, cortizone shots didnt give relief at all. ?
blood history, with some outliers. blood has not changed much in 10 years. tryglyerides. ( double recessive gene) beteween 400-600. Idl 200. hdl 24-27... parathryoid high 108. calcium 9.7. low testostereone 150. some constipation. take magnesium.. some ED. weight is up 10 pounds to 194. . 65 years old statins difficult muscle cramps and little goofy.. did allergy test, trees?. ,
5 episodes of angio edema . lip . medrol . thought low level chronic inflamation.
hi Jeff,
Better for us to speak today or tomorrow? I have a another call today which I can move back to later or if you prefer tomorrow morning also works.My skype is Drjaylombard770 Reviewing your MRI now
Now is fine if good for you my Skype is jeevacation. The name you sent does not show or 561 6555 7626
845 596 7989
Nice speaking. Will connect dots:
Calcif Tissue Int. 2015 May;96(5):410-6. doi: 10.1007/s00223-015-9969-5. Epub 2015 Feb 20.
Dickkopf-1 and sclerostin serum levels in patients with systemic mastocytosis.
Rossini M1, Viapiana O, Zanotti R, Tripi G, Perbellini O, Idolazzi L, Bonifacio M, Adami S, Gatti D.
Author information
Abstract
Bone involvement, mainly osteoporosis but also osteosclerosis, is frequent in patients with indolent systemic mastocytosis (ISM). The recent characterization of the canonical Wnt/p-catenin pathway in the regulation of bone remodeling provided important insights for our understanding of the pathophysiology of a number of conditions. The regulation of Wnt pathway in bone is predominantly driven by the production of receptor inhibitors such as Dickkopf-1 (DKK1) and sclerostin (SOST). This study aimed to explore if the various bone involvements in patients with ISM might be explained by variations in serum levels of DKK1 and SOST. This is a cross-sectional study in an adult ISM cohort (13 men and 13 women with diagnosed ISM) and fifty-two healthy sex and age-matched controls. Early morning, fasting and venous sampling was obtained in all subjects. The main outcome measures were serum bone-specific alkaline phosphatase (bALP), C-terminal telopeptides of type I collagene (CTX), DKK1, SOST, parathyroid hormone (PTH), bone mineral density, and prevalent vertebral fractures. Mean DKK1 serum levels were about two-folds higher in patients, than in controls (65,0 ± 43.3 vs. 33.1 ± 19.4 pmol/L, respectively; p < 0.001), irrespective of the presence of osteoporotic or diffuse osteosclerotic bone involvement. DKK1 serum levels were positively correlated with PTH and both CTX and bALP. Mean SOST serum levels were not significantly different in patients versus controls, and we did not observe any significant correlation between SOST and any available clinical or laboratory parameters, with the only exception of a positive correlation with age. In conclusion, in our study, we observed that DKK1, but not SOST, serum levels significantly increased in ISM patients with various bone involvements, and correlated with PTH and bone turnover markers. Our results suggest that the Wnt/p-catenin pathway is not primarily involved in the pathophysiology of the array of bone involvement in ISM.
J Nippon Med Sch. 2002 Aug;69(4):347-54.
Morphological and histochemical characteristics of mast cells and the content of in-tissue histamine in various pathological parathyroids: do mast cells participate in hormone secretion in human parathyroids?
Iwamura T1, Shimizu K, Tanaka S.
Author information
Abstract
The possibility of the participation of mast cells in human parathyroid hormone secretion was studied with regard to the frequency, distribution, and sub-types of mast cells and the content of in-tissue histamine, a chemical mediator in mast-cell granules, in human parathyroids with various pathological conditions. The above factors were compared between those of a 'normal' parathyroid group and those of 'pathological' parathyroids associated with adenoma and hyperplasia. Specimens were scanned for the mean value of the mast cellnumber per field of microscopic view and for the ratio of the mast cell number in glandular parenchymal tissue to that in interstitial tissue. The activated state of the mast cells was examined through classifying the mast cells into two sub-types, mucosal mast cells and connective-tissue mast cells. The high-performance liquid chromatography (HPLC) method was used for assay of in-tissue histamine. The frequency of mast cells showed no difference between the groups, whereas the distribution of mast cells, showed a distinct difference. The occurrence rate of mast cells in glandular parenchymal tissue in the 'pathological' group presented an increase as compared with that in the 'normal' group. Furthermore, the occurrence rate of mucosal mast cells in an activated state also showed an increase. This suggests that mast cellsare likely to participate in parathyroid hormone secretion. The histamine-content in the 'normal' group was significantly larger than that in the 'pathological' group, which was a different outcome from that observed in mast cells from the results of light microscopy. This may require taking into consideration the difference in the histamine content of the mast cells themselves between that of mucosal mast cells and connective-tissue mast cells.
Not to overwhelm you, so last article...
J Investig Allergol Clin Immunol. 2013;23(3):212.
Nonhistaminergic idiopathic angioedema may be a presentation of mast cell activation syndrome.
Afrin LB.
Comment on
Nonhistaminergic idiopathic angioedema: clinical response to icatibant. [J Investig Allergol Clin Immunol. 2012]