Intestinal Ca2+ absorption revisited: A molecular and clinical approach

Ca2+has an important role in the maintenance of the skeleton and is involved in the main physiological processes.Its homeostasis is controlled by the intestine,kidney,bone and parathyroid glands.The intestinal Ca2+absorption occurs mainly via the paracellular and the transcellular pathways.The proteins involved in both ways are regulated by calcitriol and other hormones as well as dietary factors.Fibroblast growth factor 23(FGF-23)is a strong antagonist of vitamin D action.Part of the intestinal Ca2+movement seems to be vitamin D independent.Intestinal Ca2+absorption changes according to different physiological conditions.It is promoted under high Ca2+demands such as growth,pregnancy,lactation,dietary Ca2+deficiency and high physical activity.In contrast,the intestinal Ca2+transport decreases with aging.Oxidative stress inhibits the intestinal Ca2+absorption whereas the antioxidants counteract the effects of prooxidants leading to the normalization of this physiological process.Several pathologies such as celiac disease,inflammatory bowel diseases,Turner syndrome and others occur with inhibition of intestinal Ca2+absorption,some hypercalciurias show Ca2+hyperabsorption,most of these alterations are related to the vitamin D endocrine system.Further research work should be accomplished in order not only to know more molecular details but also to detect possible therapeutic targets to ameliorate or avoid the consequences of altered intestinal Ca2+absorption.

Pathological Observation of Blood Stasis Syndrome in Non-diabetic Peripheral Neuropathies:A Retrospective Analysis Based on Nerve Biopsy

Objective To investigate the pathological features of blood stasis syndrome(BSS)in non-diabetic peripheral neuropathy.Methods Clinical data of 31 patients with non-diabetic peripheral neuropathy who had undergone nerve biopsy during December 2004 and December 2010 in Xuanwu Hospital Capital Medical University were retrospectively analyzed.According to Chinese medicine(CM)syndrome differentiation and signs,26 patients were blood stasis type and 5 patients were non-blood stasis type.Clinical and pathological data were compared in detail.Results Clinically,although both groups shared similar symptoms of limb numbness,weakness and sensory disturbances,the prevalence of neuralgia was much grievous in BSS group(73.1%,26/31)compared with the non-BSS group(0%,0/5).As for signs,dermal nutrients disturbance(84.6%,22/26),dark or purple tongue(100.0%,26/26),and sublingual varices(80.7%,21/26)were more common in the BSS group than the non-BSS group(0%,60%,20%,respectively).The prevalence of qi deficiency cases(19/26)in the BSS group was significantly higher compared with the non-BSS group(1/5).The unique histological manifestations of BSS were axonal degeneration(16/26 vs 2/5 in non-BSS group),which was the hallmark of ischemia.Cases with BSS had prominent microangiopathy(61.5%,16/26),manifested as epineurium vasculitis(inflammatory cell infiltrated to the vessel wall,obliteration and recanalization,vascular proliferation,extravascular hemosiderin deposition),angiotelectasis,proliferation and hyaline degeneration of endoneurium capillary.In the BSS group,impaired blood-nerve barrier was indicated by sub-perineurial edema(46.2%,11/26)and endoneurial edema(15.4%,4/26).The Renaut body(15.4%,4/26)and amyloid deposition(3.8%,1/26)found in the BSS group were absent in the non-BSS group.Conclusions BBS was common in non-diabetic peripheral neuropathies.The nerves exhibited ischemic alteration of primary axon degeneration and secondary demyelination.The interstitial tissue revealed microcirculation impairment,blood-nerve barrier disturbance,amyloid deposition and proliferation changes.The high prevalence of qi deficiency also highlights the therapy of promotion of blood circulation and removal of blood stasis.