18F-FDG PET/CT anatomic and metabolic guidance in CT-guided lung biopsies.

PURPOSE: To evaluate the role of Fluorine-18 fluorodeoxyglucose (18F-FDG) PET/CT as a metabolic guide in increasing the accuracy, diagnostic yield and safety of CT-guided percutaneous needle lung biopsy (PNB). METHODS AND MATERIALS: Retrospective analysis of 340 consecutive patients with suspicious lung nodules, masses or extensive disease that underwent lung biopsy over a 3-year period. Patients were divided into three groups; those that had PET/CT prior to the biopsy, those that had PET-CT following the biopsy and those who did not undergo PET-CT. Correlation was made with the histopathological result. RESULTS: 353 PNBs were performed (median lesion size 30 mm, 7-120 mm) with overall diagnostic rate of 83.9 % (95.8 % malignant). Biopsy success rate was 88.8 % with PET-CT pre-PNB, versus 78.9 % of 175 PNB without PET-CT upfront (p < 0.01 Fisher exact test). Correct targeting to PET-CT-maximum activity area (MAA) was present in 87.1 %. Biopsy success rate was 88.8 % for PNBs targeting the PET-CT-MAA region and only 52.8 % for PNBs not targeting the PET-CT-MAA (p < 0.0001). PET-CT pre-PNB had higher rates of PET-CT-MAA targeting compared to PET-CT post PNB (91.0 % v 80.0 %, p = 0.01). The availability of PET-CT before the PNB lead to significantly increased biopsy success rates in patients with a mass (OR:7.01p = 0.004), compared to a nodule (p = 0.498) or multiple nodules (p = 0.163). Patients with a PET-CT pre-PNB underwent fewer PNB passes (mean 2.6 v 3.1, p < 0.0001 Mann Whitney U). Serious complications were less common in PET-CT pre-PNB group (4.5 % v 10.9 %, p < 0.05). Pre-PNB PET-CT performance improvement applied to all 3 radiologists and was greatest for masses and infiltrative abnormalities. CONCLUSION: Metabolic information provided by 18F-FDG PET/CT and PNB localisation to the PET-CT maximum activity region is associated with higher diagnostic biopsy rates especially in masses and appears to account for improved performance, less needle passes and complications when available pre-biopsy.

A mini-review on Helicobacter pylori with Gastric Cancer and available treatments.

Helicobacter pylori (H. pylori) is the most thoroughly researched etiological component for stomach inflammation and malignancies. Even though there are conventional recommendations and treatment regimens for eradicating H. pylori, failure rates continue to climb. Antibiotic resistance contributes significantly to misdiagnoses, false positive results, and clinical failures, all of which raise the chance of infection recurrence. This review aims to explore the molecular mechanisms underlying drug resistance in H. pylori and discuss novel approaches for detecting genotypic resistance. Modulation of drug uptake/ efflux, biofilm, and coccoid development. Newer genome sequencing approaches capable of detecting H. pylori genotypic resistance are presented. Prolonged infection in the stomach causes major problems such as gastric cancer. The review discusses how H. pylori causes stomach cancer, recent biomarkers such as miRNAs, molecular pathways in the development of gastric cancer, and diagnostic methods and clinical trials for the disease. Efforts have been made to summarize the recent advancements made toward early diagnosis and novel therapeutic approaches for H. pylori-induced gastric cancer.

New promising routes in peptic ulcers: Toll-like receptors and semaphorins.

Peptic ulcers (PU) are one of the commonest yet problematic diseases found to be existing in the majority of the population. Today, drugs from a wide range of therapeutic classes are available for the management of the disease. Still, the complications of the condition are difficult to tackle and the side effect profile is quite a concern. The literature indicates that Toll-like receptors (TLRs) and Semaphorins (SEMAs) have been under study for their various pharmacological actions over the past few decades. Both these signalling pathways are found to regulate immunological and inflammatory responses. Moreover, receptors and signalling molecules from the family of TLRs and SEMAs are found to have bacterial recognition and antibacterial properties which are essential in eradicating Helicobacter pylori (H. pylori), one of the major causative agents of PU. Our understanding of SEMAs, a class of proteins involved in cell signalling, is relatively less developed compared to TLRs, another class of proteins involved in the immune response. SEMAs and TLRs play different roles in biological processes, with SEMAs primarily involved in guiding cell migration and axon guidance during development, while TLRs are responsible for recognizing pathogens and initiating an immune response. Here, in this review, we will discuss in detail the signalling cascade of TLRs and SEMAs and thereby understand its association with PU for future therapeutic targeting. The review also aims at providing an overview of the study that has been into exploring the role of these signalling pathways in the management of PU.

Pneumatosis coli mimicking colorectal cancer.

Pneumatosis coli (PC) is a rare condition of the gastrointestinal tract involving extraluminal gas confined within the bowel wall. We report the case of a 40-year-old gentleman presenting clinically and endoscopically with suspected colorectal cancer. In light of the patient's red flag symptoms, and carpet of polyps seen endoscopically, surgical management by an anterior resection was performed with the patient making a successful recovery. Histological analysis of the resected specimen confirmed pneumatosis coli with no evidence of colonic neoplasia. Although PC can be an incidental finding in asymptomatic patients and considered a benign condition, it can also present as a life-threatening emergency with bowel necrosis and obstruction requiring emergency surgical intervention. Also, when PC mimics malignancy, surgical management is the most appropriate step to ensure that the diagnosis of cancer is not missed.