Gabriel Samasca

The segmental colitis associated with diverticulosis (SCAD) is a particular presentation of the diverticular disease. Its effective management hinges on accurate diagnosis, prognosis, and ongoing therapeutic monitoring. Although SCAD generally follows a benign clinical trajectory, it remains the subject of intensive investigation. Recent advances in the field have yielded new opportunities to improve clinical outcomes for individuals with SCAD by informing diagnostic precision, risk stratification, and personalized treatment strategies.

Adverse effects of chemotherapeutic agents remain a significant clinical challenge in the management of gastric cancer. Across the literature, discussions of chemotherapy consistently document a range of toxicities, underscoring that even when treatment halts disease progression, it can leave substantial clinical sequelae. Chemotherapy can impact virtually every organ system, producing multiorgan toxicity with meaningful implications for patient quality of life and treatment feasibility. When initiating a new chemotherapy regimen, prior lack of therapeutic benefit is often associated with difficult recovery or inability to tolerate subsequent chemotherapy, thereby constraining future therapeutic options. Given these considerations and the current absence of universally personalized treatment, a multidisciplinary team—comprising a medical oncologist, gastroenterologist, and internist—is essential to the planning and execution of chemotherapy regimens. We recommend that these chemotherapy regimens be administered within internal medicine departments, in collaboration with the medical oncologist and gastroenterologist, because in many cases the adverse effects outweigh the potential benefits of chemotherapy.

Background and Objectives: The technique of complete mesocolic excision (CME) for colonic cancer is being advocated to improve the local control of the disease and increase the long-term survival. However, even with an open approach, CME is a complex technique and has not yet been adopted as standard care. Laparoscopy has been proven to bring significant advantages to colorectal surgery but performing a laparoscopic CME (Lap-CME) for colonic cancer is even more technically demanding than CME in open surgery. The purpose of this study is to evaluate whether Lap-CME can be offered as a standard procedure for patients with colonic cancer and to compare the results with those obtained after a conventional, open technique. Materials and methods: This study included 100 consecutive patients with colonic cancer, who were operated on by the same surgical team using a standardized medial-to-lateral open or laparoscopic complete mesocolic excision technique. The perioperative data was prospectively recorded in a database and retrospectively analyzed with the aim of identifying the proportion of patients that received Lap-CME, to evaluate the success rate of the procedure and to identify whether there are differences in the oncological quality of CME between the laparoscopic and open surgery groups. Results: Most of the patients enrolled in this study were in the advanced stages of the disease, with the incidence of pT3 tumors being 67% and the mean tumor size averaging 4.5 cm. Laparoscopic CME was performed in 39% of cases overall, with 41.4% being right colectomies, 42.5% being left colectomies and 16.1% being transverse colectomies. All of the parameters relevant to the oncological quality of resection, namely total lymph node count, resection margins, or the completeness of resection, were similar between the open and laparoscopic groups both when analyzed for the entire cohort or when analyzed for specific subgroups according to the tumor location (right, transverse, or left colon) or stage of the disease (pT3 or stage III). Conclusions: Laparoscopic complete mesocolic excision for colonic cancer can be offered as a standard procedure by experienced surgical teams in carefully selected patients and provides oncological results similar to those obtained with open surgery.

Spondyloarthropathies (SpAs) represent a diverse group of seronegative immune-mediated inflammatory diseases characterized by a genetic predisposition and an association with human leukocyte antigen-B27. This narrative review aims to explore juvenile spondyloarthropathies (JSpAs), their classification, clinical manifestations, diagnostic challenges, and contemporary treatment strategies. According to the International League of Associations for Rheumatology criteria, JSpAs include several specific forms: enthesitis-related arthritis, psoriatic arthritis, and undifferentiated arthritis. Despite established classifications, the terms and definitions surrounding these conditions can often lead to confusion among healthcare professionals. This ambiguity underscores the need for a standardized approach to nosological classification. The clinical presentation of JSpAs can be multifaceted, encompassing both articular and extra-articular manifestations. Articular symptoms may include enthesitis and varying forms of arthritis, while extra-articular involvement can range from uveitis to gastrointestinal, cardiovascular, pulmonary, neurological, and renal complications. These diverse manifestations highlight the systemic nature of the disease and the importance of a holistic approach to diagnosis and treatment. While laboratory tests for SpAs are often non-specific, imaging modalities such as musculoskeletal ultrasound and magnetic resonance imaging play a crucial role in the early detection of inflammatory lesions. These imaging techniques can provide valuable insights into disease progression and aid in the formulation of appropriate treatment plans. Current treatment guidelines advocate for a “stepwise” approach to therapy, beginning with nonsteroidal anti-inflammatory drugs and progressing to glucocorticoids, disease-modifying antirheumatic drugs, and biological agents, particularly anti-tumor necrosis factor alpha agents. The primary objective of treatment is to achieve clinical remission or, at a minimum, to attain low disease activity. Regular monitoring of disease activity is imperative; however, the lack of validated assessment tools for the pediatric population remains a significant challenge. JSpAs pose unique challenges in terms of diagnosis and management due to their diverse manifestations and the complexities of their classification. Ongoing research and clinical efforts are essential to refine our understanding of these conditions, improve treatment outcomes, and enhance quality of life for affected children and their families. Effective management hinges on early detection, individualized treatment plans, and continuous monitoring, ensuring that patients receive the most appropriate care tailored to their specific needs.

Introduction: Anastomotic fistula is the most feared complication in colorectal surgery. It requires early diagnosis followed by urgent treatment. In this study, we analyzed the dynamics of C-reactive protein (CRP) as a marker for early detection of anastomotic fistula. Methods: A prospective study was conducted among 83 patients who underwent colorectal resection with anastomosis at the First Surgical Department, County Emergency University Clinical Hospital, Cluj Napoca, Romania. The CRP and leukocyte values were recorded at admission and on postoperative days 3, 5, 7, and 9. Total serum protein values were measured on postoperative days 3, 5, and 7, and albumin values were measured on postoperative day 3. Results: Only CRP values showed substantial postoperative variations. At postoperative days 3, 5, and 7, serum CRP levels in patients with anastomotic fistula were higher than those in patients without anastomotic fistula, with differences at postoperative days 5 (P <.001) and 7 (P <.001) being statistically significant. Discussion: A steady decrease in CRP values after postoperative day 3 is a strong sign that the development of anastomotic fistula is unlikely. An increase or a flat decrease in CRP value at postoperative days 5 and 7 with a serum value at or close to 100 mg/L suggests an increased probability for development of anastomotic fistula.

Background/Objectives: Indocyanine green (ICG)-guided near-infrared (NIR) fluorescence imaging represents a potentially advantageous approach for the identification of lymphatic drainage pathways. This study was undertaken to evaluate the efficacy of ICG-guided NIR fluorescence in mapping lymphatic drainage and facilitating sentinel lymph node biopsy (SLNB) in patients diagnosed with colon cancer. Methods: A prospective cohort of 30 consecutive patients with colon cancer undergoing surgical resection at our institution was enrolled in this study. Peritumoral injection of ICG was performed to facilitate intraoperative identification of sentinel lymph nodes (SLNs). Identified SLNs were marked and excised ex vivo following specimen retrieval. All the retrieved specimens were submitted for histopathological analysis using hematoxylin and eosin (H&E) staining. SLNs that were negative for metastatic disease upon H&E staining underwent further examination via immunohistochemistry (IHC). Results: Successful identification of SLNs was achieved in 83.33% of cases. The false positive rate was 6.6%, and the false negative rate was 8%, respectively. Atypical lymphatic drainage patterns were observed in 6.6% of the patients. Notably, the patients exhibiting atypical lymphatic drainage subsequently developed metastases during the follow-up period. Immunohistochemical analysis failed to detect micrometastases in SLNs that were initially deemed negative based on H&E staining. Conclusions: NIR–ICG fluorescence is a safe, reliable, and technically feasible method for performing SLNB in patients with colon cancer. Furthermore, this technique offers the potential for intraoperative identification of atypical lymphatic drainage pathways, which may have significant implications for determining the optimal extent of standard lymphadenectomy.

The escalating global prevalence of fungal and bacterial co-infections underscores the significant and multifaceted impact of ubiquitous microorganisms on both environmental equilibria and human well-being. The human microbiome, a complex ecosystem of bacterial communities, harbors opportunistic pathogens capable of inducing superinfections or concurrent infections with Candida spp. The intricate interplay, exemplified by the interaction between Candida albicans and diverse bacteria, necessitates rigorous investigation to elucidate mechanisms by which this polymicrobial behavior potentiates fungal virulence, particularly in immunocompromised individuals. Our study aims to comprehensively examine the ramifications of these interactions, with a specific focus on their influence on fungal virulence and the consequent exacerbation of disease severity. Achieving a comprehensive understanding of these complex relationships is paramount for informing effective clinical management strategies for infectious diseases, and the accurate identification of fungal–bacterial co-infections holds substantial implications for optimizing clinical treatment paradigms, especially in vulnerable immunocompromised hosts.

Gastrointestinal cancers (GIC), encompassing colonic, rectal, and gastric malignancies, rank among the most prevalent cancer types globally, contributing significantly to cancer-related mortality. In the scientific literature, various syndromes associated with colorectal and gastric cancers have been elucidated, highlighting the intricate interplay between genetic factors and disease manifestation. The primary objective of this study was to conduct a genetic exploration aimed at elucidating these associations and identifying shared genetic determinants across these cancer types. Notably, considerable research has focused on the KRAS gene mutations, polymorphisms in nucleic acids, the Wnt signaling pathway, and the role of chemokine ligands in tumorigenesis. While investigations into natural plant extracts as potential therapeutic agents are still in their nascent stages, they represent a promising avenue for future research. Ongoing studies are essential to uncover suitable biomarkers that could facilitate the identification and understanding of the genetic links between these GIC. This exploration not only seeks to enhance our comprehension of the underlying genetic architecture but also aims to inform the development of targeted therapies and preventive strategies.

Gastric cancer (GC) remains a significant public health concern because of its lethality, underscoring the need for deeper insights into its molecular mechanisms. Recent studies have increasingly highlighted the role of epigenetic modifications as critical players in cancer progression. Despite their importance, research specifically addressing epigenetic factors in GC is relatively scarce. This paper seeks to bridge that gap by examining recent literature that elucidates the epigenetic landscape associated with GC. The investigation of long noncoding RNAs (lncRNAs) has revealed their substantial involvement in gene dysregulation and epigenetic alterations within GC tumors. Notably, lncRNAs such as LINC00853 and LINC01266 have been identified as significant contributors to the epigenetic modulation of gene expression. Furthermore, the overexpression of KAT5 and GPX4 has been shown to mitigate the antiproliferative effects resulting from the depletion of circRHOT1, suggesting a complex interplay between these molecules in GC pathophysiology. Another pivotal aspect of epigenetic regulation in GC involves modifications in N6-methyladenosine (m6A), which play crucial roles in mRNA maturation processes such as splicing, export, degradation, and translation. m6A modifications are known for their influence on various cancer-related pathways, thus presenting a potential avenue for targeted interventions. Our findings indicate that the most pronounced instances of epigenetic dysregulation in GC can be traced back to the effects of long lncRNAs and alterations in m6A modification patterns. This underscores the urgent need for comprehensive investigations into these epigenetic factors, as a deeper understanding could lead to enhanced diagnostic markers and innovative therapeutic strategies. The integration of genetic and epigenetic considerations is essential for advancing the field of GC research. This synthesis of recent findings concerning epigenetic regulation offers valuable insights that could inform future studies and therapeutic developments. There is a critical need for ongoing research to elucidate the complexities of epigenetic modifications in GC, ultimately improving patient outcomes through tailored interventions.

Researchers have performed numerous studies on immunotherapy because of the high death rate associated with gastric cancer (GC). GC immunotherapy research has made tremendous progress, and we wanted to provide an update on this topic. On the basis of this update, we suggest performing a new medical evaluation before initiating immunotherapy in patients with GC to increase the success rate of immunotherapies. We propose that before patients start GC immunotherapy, they should be evaluated and given a score of one to two points for the following factors: immunopathological features, molecular and genomic features, potential consequences for bacterial pathogens, potential immunotherapeutic resistance and hyperprogressive illness, and the potential to use biomarkers to gauge their prognosis and immunotherapy responses to optimize immunotherapy following surgery. The proposed scoring system could also help in the diagnosis of GC. With all the advances in genetics, immunology, and microbiology, the diagnosis of GC could be improved, not changed. Currently, patients diagnosed with GC undergo surgical resection as the only permanent solution. Patients who meet the maximum score from the presented proposal could be eligible immediately after diagnosis for immunotherapy. Therefore, immunotherapy could be a first-line option for clinicians.