Association between small‐intestinal bacterial overgrowth and deep vein thrombosis in patients with spinal cord injuries

Chen, Xuan; Zhang, Lu; Xie, Ning; Xu, Hong‐Liang; Lian, Yajun

doi:10.1111/jth.13583

Cited by 16 publications

(10 citation statements)

References 35 publications

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“…Further, the reported incidence rate of DVT varied, ranged from 10% to 30% [23]. A previous study in Chinese patients with DVT found that 20.2% patients experienced DVT in the following 3-month after SCI [24]. Consistent with those results, our study showed that 18.8% of the SCI patients were determined as DVT in the follow-up of 1-month.…”

Section: Discussionsupporting

confidence: 87%

Association between plasma macrophage migration inhibitor factor and deep vein thrombosis in patients with spinal cord injuries

Zheng

Wang

et al. 2019

Aging

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The patients with spinal cord injury (SCI) suffered significantly higher risk of deep vein thrombosis (DVT) than normal population. The aim was to assess the clinical significance of macrophage migration inhibitory factor (MIF) as the risk factor for DVT in acute SCI patients. 207 Chinese patients were enrolled in this study, including thirty-nine (39) patients (18.8 %; 95 %CI: 13.5 %–24.2 %) diagnosed as DVT at the follow-up of 1 month. Nine (9) of the 39 patients (23.1%) were suspected of thrombosis before the screening. The MIF levels in plasma of DVT patients were significantly higher than DVT-free patients. The risks of DVT would be increased by 11 % (OR unadjusted : 1.11; 95% CI, 1.06–1.17, P<0.001) and 8 % (OR adjusted : 1.08; 1.03–1.14, P=0.001), for each additional 1 ng/ml of MIF level. Furthermore, after MIF was combined with established risk factors, area under the receiver operating characteristic curve (standard error) was increased from 0.82(0.035) to 0.85(0.030). The results showed the potential association between the high MIF levels in plasma and elevated DVT risk in SCI patients, which may assist on early intervention.

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Section: Discussionsupporting

confidence: 87%

Association between plasma macrophage migration inhibitor factor and deep vein thrombosis in patients with spinal cord injuries

Zheng

Wang

et al. 2019

Aging

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“…Although gastrointestinal symptoms are frequently observed in patients with SCI, there are few reports of SIBO in SCI patients. Cheng et al report that 39% (145 of 377) of SCI patients were diagnosed with SIBO based on the glucose hydrogen/methane breath test [ 22 ]. However, the prevalence of SIBO among SCI patients as confirmed by the consensus diagnostic criteria of the presence of more than 10 5 CFU/mL bacteria or any amount of E. coli in upper digestive tract content is unknown.…”

Section: Discussionmentioning

confidence: 99%

“…A certain proportion of the patients with SCI show constipation in spite of the coexisting SIBO. Cheng et al reported that in patients with both SCI and SIBO, 22% showed constipation [ 22 ]. We believe that the, factors leading to constipation in our patient were stronger than those leading to diarrhea.…”

Section: Discussionmentioning

confidence: 99%

Small intestinal bacterial overgrowth as a cause of protracted wound healing and vitamin D deficiency in a spinal cord injured patient with a sacral pressure sore: a case report

et al. 2020

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Background Pressure sores are sometimes refractory to treatment, often due to malnutrition. Small intestinal bacterial overgrowth (SIBO) obstructs absorption in the digestive tract and causes malnutrition. However, little is known about the association between pressure sore wound healing and SIBO. Here, we report a case of a patient with a refractory sacral pressure sore and SIBO. Case presentation A 66-year-old woman who was spinal cord injured 14 years before visiting our hospital presented with the chief complaint of a sacral pressure sore, 10.0 × 6.5 cm in size, which was refractory to treatment. Physical examination showed abdominal distension and emaciation, with a body mass index of 15. Further examination revealed elevated serum alkaline phosphatase (1260 U/L), bilateral tibial fracture, multiple rib fracture, and osteoporosis. We diagnosed the patient with osteomalacia with vitamin D deficiency. Despite oral supplementation, serum levels of calcium, phosphorous, and vitamin D remained low. Also, despite concentrative wound therapy for the sacral pressure sore by plastic surgeons, no wound healing was achieved. Due to a suspicion of disturbances in nutrient absorption, we performed bacterial examination of collected gastric and duodenal fluid, which showed high numbers of bacteria in gastric content (10 4 E. coli , 10 5 Streptococcus species, and 10 5 Neisseria species) and duodenal content (10 6 E. coli , 10 4 Candida glabrata ). Therefore, we diagnosed the patient with SIBO and started selective decontamination of the digestive tract using polymyxin B sulfate and amphotericin B. After starting treatment for SIBO, the sacral pressure sore began to heal and was nearly healed after 285 days. The patient’s serum levels of calcium, phosphorous, vitamin D, and other fat-soluble vitamins also gradually increased after starting treatment for SIBO. Conclusion We report a case of a patient with a refractory sacral pressure sore that healed after starting treatment for SIBO. We conclude that SIBO may be an overlooked cause of malnutrition and poor wound healing in patients with chronic pressure sores.

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“…A known example is small intestinal bacterial overgrowth (SIBO), a malabsorption syndrome, which is referred to as an increase in the number of bacteria in the proximal part of small bowel or dysbiosis manifested as the presence of bacteria characteristic for colon. Cheng et al 85 showed the DVT as a dangerous complication associated with SIBO during posttraumatic hospitalization in patients after spinal cord injury. SIBO syndrome leads to increased bowel permeability with enhanced adsorption of LPS and other bacterial products.…”

Section: Gut Microbiome and Cardiovascular Diseasesmentioning

confidence: 99%

<p>Microbial Modulation of Coagulation Disorders in Venous Thromboembolism</p>

Lichota

Gwoździński

Szewczyk

2020

JIR

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Venous thromboembolism (VTE), including deep vein thrombosis (DVT) and pulmonary embolism (PE), is the third leading cause of cardiovascular death in the world. Important risk factors of thrombosis include bed restraint, surgery, major trauma, long journeys, inflammation, pregnancy, and oral contraceptives, previous venous thromboembolism, cancer, and bacterial infections. Sepsis increases the risk of blood clot formation 2-20 times. In this review, we discussed various mechanisms related to the role of bacteria in venous thrombosis also taking into consideration the role of the human microbiome. Many known bacteria, such as Helicobacter pylori, Chlamydia pneumoniae, Mycoplasma pneumoniae, Haemophilus influenzae, Streptococcus pneumoniae, Staphylococcus aureus, and Escherichia coli, causing infections may increase the risk of thrombotic complications through platelet activation or may lead to an inflammatory reaction involving the fibrinolytic system. Additionally, the bacteria participate in the production of factors causing or increasing the risk of cardiovascular diseases. An example can be trimethylamine N-oxide (TMAO) but also uremic toxins (indoxyl sulfate), short-chain fatty acids (SCFA) phytoestrogens, and bile acids. Finally, we presented the involvement of many bacteria in the development of venous thromboembolism and other cardiovascular diseases.

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Association between small‐intestinal bacterial overgrowth and deep vein thrombosis in patients with spinal cord injuries

Cited by 16 publications

References 35 publications

Association between plasma macrophage migration inhibitor factor and deep vein thrombosis in patients with spinal cord injuries

Association between plasma macrophage migration inhibitor factor and deep vein thrombosis in patients with spinal cord injuries

Small intestinal bacterial overgrowth as a cause of protracted wound healing and vitamin D deficiency in a spinal cord injured patient with a sacral pressure sore: a case report

<p>Microbial Modulation of Coagulation Disorders in Venous Thromboembolism</p>

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