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- Hypoparathyroidism after Roux-en-Y gastric bypass - a challenge for clinical management: a case report. [JOURNAL ARTICLE]
- J Med Case Rep 2014 Oct 28; 8(1):357.
In this report, we describe challenges we encountered in the clinical management of a patient with hypoparathyroidism who had previously undergone a bariatric procedure.We report the case of a 38-year-old Caucasian woman who had undergone a Roux-en-Y gastric bypass procedure for treatment of obesity. She also had a past history of right lobectomy to treat a benign thyroid nodule. Another thyroid nodule was diagnosed after her bariatric surgery, so a new thyroid surgery was performed. Permanent hypoparathyroidism occurred after the second thyroid surgery. A Roux-en-Y gastric bypass resulted in important weight loss, but the preferential site of calcium absorption was bypassed. The lack of endogenous parathyroid hormone secretion due to post-surgical hypoparathyroidism abolished the physiological mechanism that compensates the reduced calcium absorption, which was a challenge for us to overcome. In this report, we describe our clinical therapeutic choices to maintain normocalcemia and normophosphatemia in this patient. Higher doses of exogenous calcium citrate, calcitriol and cholecalciferol were used, but hypocalcemia was still present. To improve vitamin D absorption with resultant improvement of calcium homeostasis, we speculated that adding pancrelipase to meals would increase lipid absorption and possibly fat-soluble vitamins, including vitamin D. Only after the addition of pancrelipase did the patient improve without weight regain according to clinical and laboratory assessments.The use of exogenous pancreatic enzymes improved calcium homeostasis in this bariatric patient. The role of these enzymes on vitamin D absorption and subsequent rise in calcium levels in hypoparathyroid patients who undergo bariatric procedures need further investigation.
- Vitamin d prevents endothelial damage induced by increased neutrophil extracellular traps formation in patients with systemic lupus erythematosus. [Journal Article]
- Acta Med Indones 2014 Jul; 46(3):189-98.
to investigate the effects of Vitamin D calcitriol/1,25(OH)2D3 on NETosis in systemic lupus erythematosus (SLE) patients with hypovitamin D.neutrophlis of five SLE patients with hypovitamin D were divided into 4 groups, P0 (0 nM/control), P1 (1 nM), P2 (10 nM), and P3 (100 nM) as cultured samples. Phorbol Myristate Acetate (PMA) was used to stimulate NETs formation. The supernatant was separated and cocultured with HUVECs. Externalization of Neutrophil Elastase (NE) and Myeloperoxidase (MPO) during NETosis was measured by immunofluorescence and ELISA respectively. Early and late apoptosis of endothelial cell was measured by flowcytometry using cell death kit (Annexin V and PI antibody).this study showed significant decrease in early apoptosis with 10 nM of 1,25(OH)2D3 compared to control group. Significance of NE externalization found in all treatment groups (p<0.05), while MPO absorbance in the same tendency but not statistically significant. Further analysis also found a moderate positive correlation between NE externalizations with early apoptosis.vitamin D 1,25(OH)2D3 could reduce endothelial damage by decreasing NETosis activity. This result may reveal the possibility of Vitamin D as supplementary therapy for SLE patients with hypovitamin D to prevent endothelial damage.
- THE ACTIVE FORM OF VITAMIN D, CALCITRIOL, INDUCES A COMPLEX DUAL UP-REGULATION OF ENDOTHELIN AND NITRIC OXIDE IN CULTURED ENDOTHELIAL CELLS. [JOURNAL ARTICLE]
- Am J Physiol Endocrinol Metab 2014 Oct 21.:ajpendo.00156.2014.
Despite the presence of vitamin D receptor (VDR) in endothelial cells, the effect of vitamin D on endothelial function is unknown. An unbalanced production of vasoactive endothelial factors, such as nitric oxide (NO) or endothelin-1 (ET-1), results in endothelial dysfunction, which can alter the normal cardiovascular function. Present experiments were devoted to assess the effect of active vitamin D (calcitriol) on the synthesis of endothelial vasoactive factors. Results: In cells, calcitriol increased ET-1 and NO productions, measured by ELISA and fluorimetric assay, respectively. Calcitriol also increased endothelin-converting enzyme-1 (ECE-1) and endothelial-nitric oxide synthase (eNOS) activities, their mRNA (qPCR), protein expressions (Western-blot) and promoter activities (transfection assays). Calcitriol did not change prepro-ET-1 mRNA. The effect was specific of VDR activation because when VDR was silenced by siRNA, the observed effects disappeared. Mechanisms involved in each up-regulation differed. ECE-1 up-regulation depended on AP-1 activation, whereas, eNOS up-regulation depended directly on VDR activation. To evaluate the in vivo consequences of acute calcitriol treatment, normal Wistar rats were treated with a single i.p injection of 400 ng/kg of calcitriol and sacrificed 24h later. Results confirmed those observed in cells: production and expression of both factors were increased by calcitriol. Besides, calcitriol-treated rats showed a slight rise in mean blood pressure, which decreased when pretreated with FR-901533, an ECE-1 antagonist. Conclusions: Calcitriol increases the synthesis of both ET-1 and NO in endothelial cells. However, the ET-1 up-regulation seems to be biologically more relevant, as animals acutely treated with calcitriol show slight increases of blood pressure.
- Impact of Vitamin D on Infectious Disease: A Systematic Review of Controlled Trials. [JOURNAL ARTICLE]
- Am J Med Sci 2014 Oct 20.
Observational studies have linked vitamin D status and infectious disease. This association is supported by the presence of the vitamin D receptor and CYP27B1 in immune cells. This review aims to consolidate data from clinical trials that used vitamin D for the treatment or prevention of infectious disease.The authors searched the term "(vitamin D OR ergocalciferol OR cholecalciferol OR vitamin D2 OR vitamin D3 OR calcitriol) AND (infection OR tuberculosis OR sepsis OR pneumonia)" with limits preset to manuscripts published in English and with human subjects. They identified controlled trials that measured infectious outcomes (eg, incidence and severity of disease, time to disease resolution or recurrence, measures of clinical improvement, mortality). Studies that used analog, topical or micronutrient formulations of vitamin D, assessed only vitamin D status or lacked a comparison group were excluded. The references from eligible manuscripts and from 2 recent reviews were scanned for additional manuscripts.One thousand two hundred eighty-four manuscripts were identified with our search terms, with 60 papers still eligible after review of the title and abstract. Full review of these papers, their references and 2 related reviews yielded 38 manuscripts.Although some prospective studies show positive results regarding vitamin D on infectious disease, several robust studies are negative. Factors such as high variability between studies, the difference in individual responsiveness to vitamin D and study designs that do not primarily investigate infectious outcomes may mask the effects of vitamin D on infections.
- Checkpoint kinase Chk2 controls renal Cyp27b1 expression, calcitriol formation, and calcium-phosphate metabolism. [JOURNAL ARTICLE]
- Pflugers Arch 2014 Oct 17.
Checkpoint kinase 2 (Chk2) is the main effector kinase of ataxia telangiectasia mutated (ATM) and responsible for cell cycle regulation. ATM signaling has been shown to upregulate interferon-regulating factor-1 (IRF-1), a transcription factor also expressed in the kidney. Calcitriol (1,25 (OH)2D3), a major regulator of mineral metabolism, is generated by 25-hydroxyvitamin D 1α-hydroxylase in the kidney. Since 25-hydroxyvitamin D 1α-hydroxylase expression is enhanced by IRF-1, the present study explored the role of Chk2 for calcitriol formation and mineral metabolism. Chk2-deficient mice (chk2 (-/-)) were compared to wild-type mice (chk2 (+/+)). Transcript levels of renal 25-hydroxyvitamin D 1α-hydroxylase, Chk2, and IRF-1 were determined by RT-PCR; Klotho expression by Western blotting; bone density by μCT analysis; serum or plasma 1,25 (OH)2D3, PTH, and C-terminal FGF23 concentrations by immunoassays; and serum, fecal, and urinary calcium and phosphate concentrations by photometry. The renal expression of IRF-1 and 25-hydroxyvitamin D 1α-hydroxylase as well as serum 1,25 (OH)2D3 and FGF23 levels were significantly lower in chk2 (-/-) mice compared to chk2 (+/+) mice. Plasma PTH was not different between the genotypes. Renal calcium and phosphate excretion were significantly higher in chk2 (-/-) mice than in chk2 (+/+) mice despite hypophosphatemia and normocalcemia. Bone density was not different between the genotypes. We conclude that Chk2 regulates renal 25-hydroxyvitamin D 1α-hydroxylase expression thereby impacting on calcium and phosphate metabolism.
- Epicardial adipose tissue inflammation is related to vitamin D deficiency in patients affected by coronary artery disease. [JOURNAL ARTICLE]
- Nutr Metab Cardiovasc Dis 2014 Sep 19.
Alterations in epicardial adipose tissue (EAT) biology (i.e. increased fat thickness and inflammation) have been described in coronary artery disease (CAD) patients. In addition to its classic role in the regulation of calcium-phosphate homeostasis, vitamin D may exert immune-regulatory and anti-inflammatory effects. Whether EAT inflammation may be linked to vitamin D deficiency is still unknown. In the present study we evaluated plasma 25-hydroxycholecalciferol (25OHD) level in CAD patients and its relationship with EAT ability to locally metabolize vitamin D, EAT expression of inflammation-related molecules and EAT thickness.Plasma 25OHD level was quantified by an immunoluminometric assay. EAT expression of inflammation-related molecules (MCP-1, PTX3, TNFα, IL-6, adiponectin), vitamin D receptor (VDR), CYP27B1 (25OHD-activating enzyme) and CYP24A1 (1,25-dihydroxycholecalciferol-metabolizing enzyme) was performed by microarray. EAT thickness was quantified by echocardiography. Median plasma 25OHD level was 10.85 ng/mL and 83% of CAD patients displayed 25OHD level below 20 ng/mL. At decreasing plasma 25OHD concentration, we observed a down-regulation in CYP27B1 and CYP24A1 level and an increased expression of VDR and pro-inflammatory cytokines (MCP-1, PTX3, TNFα, IL-6) at EAT level. No correlation was observed between plasma 25OHD level and EAT thickness.Our data suggest an increased activation of inflammatory pathways at EAT level possibly related to systemic and local vitamin D deficiency in CAD patients. Whether maintaining an optimal vitamin D status may be helpful to reduce EAT inflammation and to prevent CAD and its progression needs further investigation.
- Increased oxygen consumption observed in phorbol 12-myristate 13-acetate stimulated human cultured promonocytic U937 cell lines treated with calcitriol and retinoic acid. [Journal Article]
- Asian Pac J Trop Med 2014 Sep.:S272-7.
To investigate the effect of phorbol 12-myristate 13-acetate (PMA) and formyl-methionyl-leucyl-phenylalanine (FMLP) on oxygen consumption of differentiated and non-differentiated immune cell lines by retinoic acid and calcitriol treatment which might be useful in subsequent elicitation of immunological action during immunosuppressive states.PMA and FMLP were used to artificially stimulate reactive oxygen production in cultured promonocytic U937 cell line. Paralleled samples of the cultured cells were separately prepared with calcitriol (1, 25- dihydroxyvitamin D3) and retinoic acid followed by a 72-hour incubation period. The rate of respiratory burst was measured using the Clark oxygen electrode.The average increase in cell concentrations per mL observed was significantly higher in retinoic acid-treated cells (9×10(6) cells/mL) when compared with calcitriol-treated samples (4×10(6) cells/mL). There was a marked increase in oxygen consumption of the calcitriol-treated cell lines against the retinoic acid-treated ones. Exposure of differentiated U937 cells to PMA and FMLP increased significantly (P<0.05) in their oxygen consumption when compared with the control. PMA calcitriol-treated cells resulted in 55% oxygen consumption more than the control while FMLP oxygen consumption increased 78% by comparison with the control.The result demonstrated that calcitriol may serve as a physiological promoter of normal differentiation of precursor cells which may exert an immunological action. This effect could elicit a marker potential and increase immune cell activity of the host especially in immunosuppressed diseased states.
- Cinacalcet administration by gastrostomy tube in a child receiving peritoneal dialysis. [Journal Article]
- J Pediatr Pharmacol Ther 2014 Jul; 19(3):202-5.
A 2-year-old male with chronic kidney disease with secondary hyperparathyroidism developed hypercalcemia while receiving calcitriol, without achieving a serum parathyroid hormone concentration within the goal range. Cinacalcet 15 mg (1.2 mg/kg), crushed and administered via gastrostomy tube, was added to the patient's therapy. This therapy was effective in achieving targeted laboratory parameters in our patient despite instructions in the prescribing information that cinacalcet should always be taken whole.
- The origin and metabolism of vitamin D in rainbow trout. [JOURNAL ARTICLE]
- J Steroid Biochem Mol Biol 2014 Oct 9.
An explanation for the origin and the high concentration of vitamin D (cholecalciferol) in some species of fish is still not apparent. Because fish may live in deep water and may, thus, not be exposed to solar ultraviolet (UV) light, it is commonly assumed that vitamin D found in their livers and adipose tissue has been derived from a food chain, originating in zooplankton exposed to UV light at the water surface. To investigate the metabolism and possible origin of vitamin D in fish, rainbow trout were reared from eggs, in the absence of light, and were fed a vitamin D-free diet. When small quantities of radioactively-labelled vitamin D were injected or fed to these trout, much of the radioactivity was found as excreted metabolites in bile. Hence, even when they are vitamin D deficient, trout vigorously catabolise and excrete exogenous vitamin D. The main vitamin D metabolite found in plasma of non-deficient trout was 1,25-dihydroxycholecalciferol [1,25(OH)2D3]. This was produced in the liver by an enzyme process that was strongly stimulated in vitamin D deficiency. When vitamin D was fed for several weeks to vitamin D-deficient trout, plasma 1,25(OH)2D3 levels rose to 180pg/ml and the fish became hypercacemic. When vitamin D-deficient fish were inadvertently exposed to 60W incandescent light for 24h, they became moribund and died. It was subsequently found that vitamin D-deficient trout can produce vitamin D in skin when exposed to blue light at wavelengths between 380 and 480nm. It is concluded that trout, like terrestrial vertebrates, produce 1,25(OH)2D3 as the functional form of vitamin D and that this has an effect on calcium homeostasis. Furthermore, vitamin D is formed in the skin of these fish by the photochemical action of visible light on 7-dehydrocholesterol. Elucidation of the physicochemical mechanism of this process requires further research.
- Oral manifestations of hyperparathyroidism secondary to familial hypophosphatemic rickets. [Journal Article]
- Pediatr Dent 2014; 36(5):422-4.
A 14-year-old male with familial hypophosphatemic rickets, being treated with oral phosphate and calcitriol therapy, presented to the Division of Pediatric Dentistry, Children's Hospital of Pittsburgh of the University of Pittsburgh Medical Center, Pittsburgh, Pa. A panoramic radiograph showed multifocal, multilocular lesions in the mandible leading to surgical exploration and biopsy. Histopathological evaluation of the largest lesion showed features consistent with central giant cell granuloma. Given the patient's history, hyperparathyroidism was suspected. Laboratory data showed an elevated parathyroid hormone of 152 pg/ml (normal range equals nine to 69). This confirmed the diagnosis of multiple brown tumors in the mandible associated with secondary hyperparathyroidism, which was attributed to high-dose phosphate treatment. After endocrinology consultation, calcitriol therapy was increased. Improvement of the patient's brown tumors is expected with medical therapy. The purpose of this case report was to raise awareness among pediatric dentists about the maxillofacial ramifications of secondary hyperparathyroidism.