Skin Lesions with Loss of Tissue and Cutaneous-Onset Sepsis: The Skin Infection-Sepsis Relationship.

Infectious and inflammatory dermatoses featuring skin lesions with loss of tissue expose skin layers to microbial invasions, disrupt the normal skin microbiome, and potentially lead to sepsis. However, literature data on the incidence of cutaneous-onset sepsis are scarce. This retrospective observational study assessed hospital admissions for primary skin lesions without bacterial infections and sepsis during 2020-2022 in the largest emergency hospital in NE Romania. Of 509 patients, 441 had infected lesions, 78 had sepsis caused by venous ulcers from microbial eczema cellulitis, superinfected bullous dermatoses, erysipelas, and erythroderma. Cultured samples revealed S. aureus, P. aeruginosa, and E. coli; and K. pneumoniae and S. ß-hemolytic associated with sepsis, even if this was rarer. Clinical manifestations included ulcerations, erosions, fissures, excoriations, bullae, vesicles, pruritus, tumefaction, edema, fever, chills, pain, adenopathy, and mildly altered mental status. Underlying chronic heart failure, atrial fibrillation, anemia, and type-1 diabetes mellitus were comorbidities associated with infection and sepsis. Significant associations and risk factors, including their combined effects, are discussed to draw attention to the need for further research and adequate management to prevent sepsis in adult patients of any age presenting with infected skin lesions (especially cellulitis) and comorbidities (especially type 1 diabetes mellitus and anemia).

Vascular endothelial growth factor - key mediator of angiogenesis and promising therapeutical target in ulcerative colitis.

Ulcerative colitis (UC) is an inflammatory bowel disease, triggered by an inappropriate immune response of colonic mucosa. Angiogenesis is an important part of inflammatory process, enhancing inflammation in a vicious circle that aggravates mucosal damage and remodeling. The most important pathway for angiogenesis in ulcerative colitis involves vascular endothelial growth factor (VEGF) and endoglin (CD105) and can be used as target for adjuvant therapy in order to improve patients' outcome. We present a retrospective cohort study evaluating mucosal expression of VEGF and CD105 and their correlation with patients' evolution and risk of relapse. In our study, patients with UC have correlated increases of VEGF expression and microvessel density (evaluated with CD105 staining), sustaining the hypothesis that angiogenesis is not just a passive process driven by inflammation, but an active player of mucosal lesions in ulcerative colitis.

Different effects of anti-TNF-alpha biologic drugs on the small bowel macroscopic inflammation in patients with ankylosing spondylitis.

BACKGROUND & AIMS: Considering the ability of anti-TNF alpha drugs to lower the burden intestinal inflammation in patients with inflammatory bowel disease (IBD), and the similarity between IBD and ankylosing spondylitis (AS) regarding inflammatory intestinal involvement, we aimed to investigate the impact of anti-TNF alpha biologic therapy on subclinical intestinal inflammation in AS patients. METHODS: Between January 2008 and December 2013, 38 AS patients and 23 controls were enrolled in the study and investigated with small bowel videocapsule endoscopy examination and ileocolonoscopy. Each tertile of the small bowel (proximal, mid and distal) was assessed by calculating the Lewis score based on the image stream. RESULTS: The Lewis scores were significantly higher in the AS group compared to controls (580.9 ± 818 vs. 81 ± 121, p<0.001). 16 patients (42.1%) were on anti-TNF alpha therapy (Adalimumab (n = 5), Infliximab (n = 5) or Etanercept (n = 6)).31.3% of them used NSAIDs simultaneously, compared with 77.3% of the other patients (p<0.01). Their Lewis scores were lower compared to the other patients for the entire small bowel (306 ± 164 vs. 790 ± 1038, p = 0.015), its proximal and distal tertiles (238 ± 154 vs. 560 ± 543, p = 0.021, and 140 ± 189 vs. 300 ± 220, p = 0.027, respectively). The Lewis score was also lower in patients receiving Adalimumab/Infliximab compared to those on Etanercept for the entire bowel and its distal tertile (262 ± 165 vs. 380 ± 148, p = 0.069 and 62 ± 101 vs. 273 ± 236, p = 0.060, respectively). CONCLUSION: Anti-TNF alpha therapy in patients with AS reduces the subclinical intestinal inflammation, but the magnitude seems to depend upon the class anti-TNF alpha agent used (Clinical Trials. gov NCT00768950).

First Pillcam Colon 2 capsule images of Whipple's disease: Case report and review of the literature.

Whipple's disease is a rare chronic systemic infection determined by the Gram-positive bacillus Tropheryma whipplei. The infection usually mainly involves the small bowel, but sometimes other organs are affected as well. Since the current standard clinical and biological tests are nonspecific, diagnosis is very difficult and relies on histopathology. Here we present the case of a 52-year-old man with chronic diarrhea and weight loss whose symptoms had been evolving for 2 years and whose diagnosis came unexpectedly after capsule examination. Diagnosis was confirmed by the histopathologic examination of endoscopic biopsy samples, and treatment with co-trimoxazole resulted in remission of symptoms. We present the first images of Whipple's disease obtained with the Pillcam Colon 2 video capsule system.

NSAID-induced deleterious effects on the proximal and mid small bowel in seronegative spondyloarthropathy patients.

AIM: To investigate the small bowel of seronegative spondyloarthropathy (SpA) patients in order to ascertain the presence of mucosal lesions. METHODS: Between January 2008 and June 2010, 54 consecutive patients were enrolled and submitted to a video capsule endoscopy (VCE) examination. History and demographic data were taken, as well as the history of non-steroidal anti-inflammatory drug (NSAID) consumption. After reading each VCE recording, a capsule endoscopy scoring index for small bowel mucosal inflammatory change (Lewis score) was calculated. Statistical analysis of the data was performed. RESULTS: The Lewis score for the whole cohort was 397.73. It was higher in the NSAID consumption subgroup (P = 0.036). The difference in Lewis score between NSAID users and non-users was reproduced for the first and second proximal tertiles of the small bowel, but not for its distal third (P values of 0.036, 0.001 and 0.18, respectively). There was no statistical significant difference between the groups with regard to age or sex of the patients. CONCLUSION: The intestinal inflammatory involvement of SpA patients is more prominent in NSAID users for the proximal/mid small bowel, but not for its distal part.

The influence of Helicobacter pylori presence on the immunophenotype of inflammatory infiltrate in gastric diseases.

The first medical hypothesis about the possible relationship between chronic inflammatory response and carcinogenesis belongs to Virchow and it was published in 1893. In these days, multiple studies demonstrate the certain involvement of chronic inflammation as trigger of progression towards malignancy. The fact that in 1994, the International Agency for Research on Cancer considered Helicobacter pylori as first class carcinogenic agent, is postulating the existence of the pathogenical chain carcinogenesis, of chronic inflammatory lesions as it was described by Correa, as a first step. Our study including 75 patients who underwent surgical procedures for gastric lesions uses immunohistochemical studies for lymphocytes phenotyping, to identify the nature of inflammatory cells involved, correlating the results with the presence of Helicobacter pylori. We tried to bring new information needed for establish to what extent the chronic inflammation of gastric mucosa is a response to the presence of bacteria and is implicated in tumorigenesis. We used T cells antibodies: CD3, CD4, CD5, CD8, CD57, GranzymeB and B cells antibodies: Cd20 and CD23. Our results revealed the presence of immune cellular response to Helicobacter pylori in gastric mucosa, based on T helper, cytotoxic and NK cells. B cells have a minor role in this response. CD4+ cells seem to be involved in local protection response as well as in carcinogenesis, while CD8+ have a minor or no role in carcinogenesis.

Bowel lesions in spondyloarthritides.

The gut can play an important role in the pathogenesis of many rheumatic conditions; this is also true for spondyloarthropathies, ileocolonoscopic studies revealing the prevalence of histological gut inflammation in more than half of these patients. Furthermore, in patients with spondyloarthritis, an evolution to clinical inflammatory bowel disease has been observed in 20% of patients with an initial subclinical chronic gut inflammation, indicating that joint and bowel inflammation are somehow connected. The presence of chronic gut inflammation can be the first sign of Crohn's disease, and it is being speculated that early treatment of the gut inflammation could prevent this evolution when the appropriate drugs become available. Moreover, the medication employed in treating these patients has the potential of influencing the inflammatory bowel lesions, in a negative (NSAIDs) or positive way (DMARDs, corticosteroids, biologic agents), and there are reports trying to prove that the spondylarthropathic ileo-colonic inflammation represents, at least in part, iatrogenic COX-2 driven damage. Therefore, there are "obscure" fields regarding the issue of gut inflammation in spondyloarthropathies, which need focused research, but taking into consideration the complex treatment strategies applied in patients with these kinds of diseases, this is not an easy task to perform.