The operative mortality for biliary tract obstruction due to malignancy is high. In 1981 a controlled clinical trial of pre-operative percutaneous drainage was started at the Royal Postgraduate Medical School. At the time of percutaneous transhepatic cholangiography patients were randomized either to laparotomy or to pre-operative percutaneous transhepatic biliary drainage ( PTBD ) followed by laparotomy. Only patients with malignant biliary tract obstruction and serum bilirubin greater than 100 mumol/l were included. Seventy patients entered the trial, and five were withdrawn. Of the 65 remaining, 31 underwent laparotomy and 34 had pre-operative PTBD followed by laparotomy. The median duration of drainage was 18 days and during this time the median bilirubin fell from 305 to 115 mumol/l. Five patients required early surgery for complications of PTBD and two died within 30 days of surgery. The mortality for laparotomy was 19 per cent (6/31) compared with 32 per cent (11/34) for drainage plus laparotomy. This trial highlights the hazards of PTBD in high risk patients and has failed to demonstrate a reduction in mortality with the use of pre-operative PTBD .

OBJECTIVE.The purpose of this study was to determine the effects of percutaneous transcatheter coil embolization of pulmonary arteriovenous malformations on arterial oxygen saturation, pulmonary gas exchange, anatomic right-to-left shunt, and lung function and to assess the complications of the procedure.

Chronic inflammation has been shown to contribute to the development of a wide variety of disorders by means of a number of proposed mechanisms. Depression and cognitive impairment are two such disorders which may share a closely linked inflammatory etiology. The ability of inflammatory mediators to alter the activity of enzymes, from key metabolic pathways, may help explain the connection between these disorders. The chronic up-regulation of the kynurenine pathway results in an imbalance in critical neuroactive compounds involving the reduction of tryptophan and elevation of tryptophan metabolites. Such imbalances have established implications in both depression and cognitive impairment. This may implicate the immune system as a potential therapeutic target in the treatment of these disorders. The most common treatment modalities currently utilized, involve drug interventions which act on downstream targets. Such treatments help to reestablish protein balances, but fail to treat the inflammatory basis of the disorder. The use of anti-inflammatory interventions, such as regular exercise, may therefore, contribute to the effectiveness of current drug interventions in the treatment of both depression and cognitive impairment.

Study design: Review article. Objectives: The objective of this study is to provide an overview of the many factors that contribute to the chronic inflammatory state typically observed following spinal cord injury (SCI). Methods: Literature review. Results: Not applicable. Conclusion: SCI is typically characterized by a low-grade inflammatory state due to a number of factors. As bidirectional communication exists between the nervous, endocrine and immune systems, damage to the spinal cord may translate into both endocrinal and immune impairment. Damage to the autonomic nervous system may induce immune dysfunction directly, through the loss of neural innervation of lymphoid organs, or indirectly by inducing endocrinal impairment. In addition, damage to the somatic nervous system and the corresponding loss of motor and sensory function increases the likelihood of developing a number of secondary health complications and metabolic disorders associated with a state of inflammation. Lastly, numerous related disorders associated with a state of chronic inflammation have been found to be at a substantially higher prevalence following SCI. Together, such factors help explain the chronic inflammatory state and immune impairment typically observed following SCI. An understanding of the interactions between systems, both in health and disease, and the many causes of chronic inflammation may aid in the effective future treatment of immune dysfunction and related disorders following SCI.

BackgroundThe purpose of the present study was to examine the efficacy of targeting inflammation as a means of improving mood following spinal cord injury (SCI) and explore the potential mechanisms of action.MethodsThe study was a randomized, parallel-group, controlled, clinical trial (NCT02099890) whereby 20 participants with varying levels and severities of SCI were randomized (3:2) to either the treatment group, consisting of a 12-week anti-inflammatory diet, or control group. Outcome measures were assessed at baseline, 1 and 3 months, and consisted of CES-D scores of depression, markers of inflammation as assessed by various pro- and anti-inflammatory cytokines and several amino acids related to depression.ResultsA significant group × time interaction was found for CES-D (Center for Epidemiologic studies Depression Scale) score (p = 0.01), the TRP/LNAA (tryptophan/large neutral amino acid) ratio (p = 0.04), the composite score of pro-inflammatory cytokines (p = 0.04), IL-1β (interleukin-1 beta) (p = 0.04), and IFN-γ (interferon gamma) (p = 0.03). Pearson’s r correlation showed significance between the ∆IL-1β and both the ∆CES-D score (r = 0.740, p < 0.01) and the ∆KYN/TRP (kynurenine/tryptophan) ratio (r = 0.536, p = 0.02). The ∆KYN/TRP ratio was also significantly correlated with the ∆CES-D score (r = 0.586, p = 0.01). Mediation analysis showed that the relationship between the ∆KYN/TRP ratio and the ∆CES-D score was mediated by the ∆IL-1β. Subgroup analysis showed that participants with high CES-D scores had significantly higher concentrations of IL-1β, and all correlations were maintained or strengthened within this subgroup.ConclusionsOverall, the results demonstrated the effectiveness of targeting inflammation as a means of improving mood in SCI, with potential mechanisms relating to the reduction in IL-1β and improvements in levels of neuroactive compounds related to the kynurenine pathway. Due to the limited sample size, results should be interpreted with caution; however, they are worthy of further examination due to the potential impact of inflammation on depression.Trial registrationClinicalTrials.gov ID: NCT02099890.

In a prospective study of 65 patients with bile duct obstruction, various radiologic modalities were compared for their capability to demonstrate the level and cause of obstruction and to indicate accurately tumor resectability. Ultrasound (US) was performed in 65 patients, computed tomography (CT) in 51, direct cholangiography (DC) in 57, and angiography in 35. The level of obstruction was correctly indicated by US in 95% of patients and by CT in 90%, and the cause was correctly indicated by US in 88%, by CT in 63%, and by DC in 89%. In predicting tumor resectability, US was correct in 71% of patients, compared with 42% for CT, 58% for DC, and 25% for angiography. US therefore appears to be the single most useful modality in the evaluation bile duct obstruction.

BackgroundThe purpose of the present study was to examine the effectiveness of an anti-inflammatory intervention as a treatment for neuropathic pain following spinal cord injury (SCI).MethodsThis randomized, parallel-group, controlled clinical trial (NCT02099890) examined 20 participants with varying levels and severities of SCI, randomized (3:2) to either a 12-week anti-inflammatory diet, or control group. Outcome measures consisted of self-determined indices of pain as assessed using the neuropathic pain questionnaire (NPQ) and markers of inflammation as assessed by various pro- and anti-inflammatory cytokines, as well as the eicosanoids PGE2 and LTB4.ResultsA significant group × time interaction was found for sensory pain scores (p < 0.01). A Mann-Whitney test revealed that the change scores (3-month baseline) were significantly different between groups for IFN-y (U = 13.0, p = 0.01), IL-1β (U = 14.0, p = 0.01), and IL-2 (U = 12.0, p = 0.01). A Friedman test revealed the treatment group had a significant reduction in IFN-y (x2 = 8.67, p = 0.01), IL-1β (x2 = 17.78, p < 0.01), IL-6 (x2 = 6.17, p < 0.05), while the control group showed no significant change in any inflammatory mediator. A stepwise backward elimination multiple regression analysis showed that the change in sensory neuropathic pain was a function of the change in the proinflammatory cytokines IL-2 and IFN-y, as well as the eicosanoid PGE2 (R = 0.689, R2 = 0.474).ConclusionsOverall, the results of the study demonstrate the efficacy of targeting inflammation as a means of treating neuropathic pain in SCI, with a potential mechanism relating to the reduction in proinflammatory cytokines and PGE2.Trial registrationClinicalTrials.gov, NCT02099890Electronic supplementary materialThe online version of this article (doi:10.1186/s12974-016-0625-4) contains supplementary material, which is available to authorized users.

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