scholarly journals Diversity of Gut Microbiota Affecting Serum Level of Undercarboxylated Osteocalcin in Patients with Crohn’s Disease

Nutrients ◽  
2019 ◽  
Vol 11 (7) ◽  
pp. 1541 ◽  
Author(s):  
Kohei Wagatsuma ◽  
Satoshi Yamada ◽  
Misora Ao ◽  
Minoru Matsuura ◽  
Hidemi Tsuji ◽  
...  
Keyword(s):  
Polymerase Chain Reaction ◽  
Crohn’S Disease ◽  
Gut Microbiota ◽  
Vitamin K ◽  
Intestinal Bacteria ◽  
Undercarboxylated Osteocalcin ◽  
Vitamin K Deficiency ◽  
Chain Reaction ◽  
K Deficiency ◽  
Polymerase Chain

Several reports have indicated a possible link between decreasing plasma levels of vitamin K and bone mineral density. It has been suggested that intestinal bacteria contribute to maintenance of vitamin K. Several factors are involved in the reduction of vitamin K in patients with Crohn’s disease (CD). We aimed to assess the relationship between gut microbiota and alternative indicators of vitamin K deficiency in patients with CD. We collected the feces of 26 patients with clinically inactive CD. We extracted 16S rRNA from the intestinal bacteria in the feces and amplified it by polymerase chain reaction. The generated polymerase chain reaction product was analyzed using a 16S metagenomic approach by Illumina Miseq platform. Serum undercarboxylated osteocalcin concentration was used as an alternative indicator of vitamin K deficiency. There was a significant negative correlation between serum undercarboxylated osteocalcin and mean Chao1 index in cases of low activity. The diversity of the gut microbiota was significantly lower, and Ruminococcaceae and Lachnospiraceae were significantly decreased in the vitamin K-deficient group in comparison to the vitamin K-normal group. Taken together, these data suggested the significance of investigating the gut microbiota even in patients with clinically inactive CD for improving patients’ vitamin K status.

Is vitamin K deficiency a risk factor for osteoporosis in Crohn's disease?

The Lancet ◽  
2001 ◽  
Vol 357 (9273) ◽  
pp. 1995-1996 ◽  
Author(s):  
Pawel Szulc ◽  
Pierre Jean Meunier
Keyword(s):  
Risk Factor ◽  
Crohn’S Disease ◽  
Crohn's Disease ◽  
Vitamin K ◽  
Vitamin K Deficiency ◽  
K Deficiency

scholarly journals Search for Mycobacterium paratuberculosis DNA in orofacial granulomatosis and oral Crohn’s disease tissue by polymerase chain reaction

Gut ◽  
1997 ◽  
Vol 41 (5) ◽  
pp. 646-650 ◽  
Author(s):  
M P Riggio ◽  
J Gibson ◽  
A Lennon ◽  
D Wray ◽  
D G MacDonald
Keyword(s):  
Polymerase Chain Reaction ◽  
Crohn’S Disease ◽  
Crohn's Disease ◽  
Oral Lesions ◽  
Mycobacterium Paratuberculosis ◽  
Chain Reaction ◽  
Pcr Assay ◽  
Orofacial Granulomatosis ◽  
Polymerase Chain ◽  
Normal Controls

Background—Although intestinal Crohn’s disease has long been suspected to have a mycobacterial cause, possible mycobacterial involvement in orofacial granulomatosis (OFG) and oral lesions of Crohn’s disease has not yet been investigated.Aims—As the slow growingMycobacterium paratuberculosis has been implicated in the aetiology of intestinal Crohn’s disease, the potential involvement of this mycobacterial species in OFG and oral lesions of Crohn’s disease was investigated.Patients—To attempt detection of the organism in OFG and oral Crohn’s disease tissue samples, a polymerase chain reaction (PCR) assay was used on archival formalin fixed, paraffin wax embedded oral tissue sections from 30 patients with OFG, seven with Crohn’s disease, and 12 normal controls.Methods—The PCR assay used was based on primers targeting the 5′ region of the multicopy IS900 DNA insertion element of the M paratuberculosis genome. In order to achieve maximum sensitivity, two rounds of PCR were carried out and amplicons confirmed by Southern blot hybridisation to a digoxigenin labelled IS900 DNA probe.Results—None of the OFG and oral lesions of Crohn’s disease samples were positive forMparatuberculosis and all normal controls were also negative.Conclusions—These results suggest that M paratuberculosis may not be a major aetiological agent in OFG or oral Crohn’s disease lesions, although the use of paraffin wax embedded tissue as opposed to fresh tissue as a sample source could underestimate the true prevalence of the organism.

scholarly journals Difference in the metabolism of vitamin K between liver and bone in vitamin K-deficient rats

2002 ◽  
Vol 87 (4) ◽  
pp. 307-314 ◽  
Author(s):  
Toshiro Sato ◽  
Yutaka Ohtani ◽  
Yoko Yamada ◽  
Sanshiroh Saitoh ◽  
Hiroshi Harada
Keyword(s):  
Body Weight ◽  
Vitamin K ◽  
Initial Level ◽  
Undercarboxylated Osteocalcin ◽  
Vitamin K Deficiency ◽  
Dose Administration ◽  
Osteocalcin Level ◽  
Short Period ◽  
K Deficiency ◽  
The Difference

The difference between vitamin K metabolism in the liver and that in the bone of vitamin K-deficient rats was examined. After 17 d administration of vitamin K-deficient food, vitamin K in the liver was almost depleted, and prothrombin time (PT) was prolonged. Serum total osteocalcin level was slightly decreased by vitamin K deficiency, whereas serum undercarboxylated osteocalcin level did not change. The level of menaquinone (MK)-4 as well as that of phylloquinone was decreased, but approximately 40 % of the initial level still existed in the femur after the 17 d period. A single-dose administration of vitamin K (250 nmol/kg body weight) markedly increased vitamin K level in the liver but not in the femur. These results suggest that the turnover of vitamin K in the bone is slower than that in the liver, and bone metabolism may be little affected by the short period of intake of vitamin K-deficient food. However, intake of a larger amount of vitamin K is required for its accumulation in the bone than in the liver. Furthermore, the counteracting effect of MK-7 on prolonged PT in vitamin K-deficient rats was found to be higher than phylloquinone or MK-4.

Mo1291 The Role of Tissue Tuberculosis Polymerase Chain Reaction for Diagnosis of Crohn's Disease in Taiwan

2016 ◽  
Vol 150 (4) ◽  
pp. S689
Author(s):  
Chia-Jung Kuo ◽  
Cheng-Yu Lin ◽  
Cheng-Tang Chiu ◽  
Ming-Yao Su ◽  
Wey-Ran Lin
Keyword(s):  
Polymerase Chain Reaction ◽  
Crohn’S Disease ◽  
Crohn's Disease ◽  
Chain Reaction ◽  
Polymerase Chain
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