Andreea Clim

Background and Objectives: Ménétrier’s disease (MD) is an exceptionally rare hypertrophic gastropathy characterized by foveolar hyperplasia, gastric acid suppression, and protein-losing enteropathy. Congenital gallbladder duplication is a rare biliary anomaly associated with independent pathological risks and surgical complications. Case Presentation: We report the case of a 34-year-old male presenting with chronic epigastric and right hypochondriac pain, alongside persistent, uninvestigated polycythemia. Upper endoscopy and histopathology revealed diffuse foveolar hyperplasia with cystic oxyntic gland dilatation and active Helicobacter pylori infection, confirming MD. Magnetic resonance cholangiopancreatography demonstrated a double gallbladder with independent cystic ducts. Successful H. pylori eradication was achieved, and hematological workup ruled out primary myeloproliferative neoplasm. Conclusions: To our knowledge, this is the first reported case of concurrent MD, and double gallbladder. This report underscores the necessity of a systematic diagnostic approach combining advanced imaging and histopathology to manage complex, overlapping abdominal pathologies.

Introduction: Celiac disease (CD) is a prevalent autoimmune enteropathy that remains significantly underdiagnosed due to its multifaceted diagnostic pathway and diverse clinical presentations. While duodenal biopsy has historically served as the diagnostic gold standard, its clinical primacy has been challenged by the burden of invasive endoscopy and potential histological misinterpretation. Material and Methods: We conducted a prospective diagnostic accuracy study involving consecutive adult patients with suspected CD to evaluate the performance of serological markers against histological findings. Results: The study included 139 patients, with a female predominance of 105 (75.5%). Histological evaluation revealed Marsh 3a–c in 100 patients (71.9%), whereas Marsh 1–2 was observed in 39 patients (28.1%). Sixty-one patients (43.9%) presented with high-titer ≥10×ULN tTG-IgA levels, while 78 patients (56.1%) fell below this threshold. To determine the independent predictors of Marsh 3a–c, we performed a logistic regression analysis. In the univariate analysis, both tTG-IgA (OR: 1.880; 95% CI: 1.458–2.426; p < 0.001) and non-smoker status (OR: 1.865; 95% CI: 1.283–2.709; p = 0.002) were significantly associated with VA. After adjusting for confounding variables in the multivariate model, both factors remained highly significant (p < 0.001 and p = 0.014, respectively). The diagnostic performance of the ≥10×ULN tTG-IgA threshold for detecting VA was confirmed by AUROC of 0.737, CI 0.646–0.827, p < 0.001, with a sensitivity of 55.0% and a specificity of 84.6%, a PPV of 90.2% and a NPVof 42.3% (33/78), underscoring that while the ≥10×ULN tTG-IgA threshold is highly specific for atrophy, lower titers do not reliably exclude it in adults. Conclusions: In conclusion, our study demonstrates that the ≥10×ULN tTG-IgA threshold provides a reliable diagnostic surrogate for VA in adult CD. While high cut-off values minimize false positives, a diagnostic gap remains for patients with lower antibody levels or those influenced by modifiers such as smoking. The low sensitivity of the high threshold reinforces the continued necessity of duodenal biopsy for symptomatic patients with lower-range antibody elevations to avoid a significant diagnostic gap.

Chronic delta hepatitis is a global health problem. Although a smaller percentage of chronic HBV-infected patients are coinfected with the hepatitis delta virus, these patients have a higher risk of an accelerated progression to fulminant “delta hepatitis”, cirrhosis, hepatic decompensation, and hepatocellular carcinoma, putting a financial strain on the healthcare system and increasing the need for a liver transplant. Since its discovery, tremendous efforts have been directed toward understanding the intricate pathogenic mechanisms, discovering the complex viral replication process, the essential replicative intermediates, and cell division-mediated viral spread, which enables virion viability. The consideration of the interaction between HBV and HDV is crucial in the process of developing novel pharmaceuticals. Until just recently, interferon-based therapy was the only treatment available worldwide. This review aims to present the recent advancements in understanding the life cycle of HDV, which have consequently facilitated the development of innovative drug classes. Additionally, we will examine the antiviral strategies currently in phases II and III of development, including bulevirtide (an entry inhibitor), lonafarnib (a prenylation inhibitor), and REP 2139 (an HBsAg release inhibitor).

Potential celiac disease (PCD) is characterized by the absence of villous atrophy on duodenal biopsies (Marsh 0 or 1) despite positive celiac serology and HLA DQ2 or DQ8 heterodimers. Recent epidemiological studies report that PCD represents one fifth of the total CD diagnoses. Compared to patients with CD, the majority of adult patients with PCD show lower rates of nutrient deficiencies and extraintestinal symptoms at diagnosis. Recommending a gluten-free diet (GFD) to PCD patients depends on whether they have symptoms or not. A significant clinical improvement is reported by symptomatic patients, but for asymptomatic PCD, diet implementation is still a matter of debate. Some questions remain to be answered: does PCD serve as an intermediary phase leading to the progression of true CD? Is it reasonable to hypothesize that PCD and active CD represent different manifestations of the same condition? Is there a potential for both underdiagnosis and overdiagnosis of CD in those who may have the condition? Additional research is required to address these inquiries and ascertain the specific subset of people with potential progression to overt CD, as well as to determine the potential advantages of early implementation of a GFD for these individuals. The investigation of risk factors in CD warrants examination of variables such as the timing of diagnosis, the genetic profile, the extent of gluten exposure, and the composition of the microbiome.

Over the past 100 years, cardiovascular disease (CVD) has become a leading cause of mortality and morbidity in developed countries, and similar trends have occurred for chronic liver disease. Subsequent research also indicated that people with non-alcoholic fatty liver disease (NAFLD) had a twofold increased risk of CV events and that this risk was doubled in those with liver fibrosis. However, no validated CVD risk score specific for NAFLD patients has yet been validated, as traditional risk scores tend to underestimate the CV risk in NAFLD patients. From a practical perspective, identifying NAFLD patients and assessing severity of liver fibrosis when concurrent atherosclerotic risk factors are already established may serve as an important criterion in new CV risk scores. The current review aims to assess current risk scores and their utility for the prediction of CV events among patients with NAFLD.

Without a doubt, a majority of diseases are food-pattern-related. However, one disease stands out as an increasingly more common autoimmune-mediated enteropathy triggered by the ingestion of gluten. Celiac disease (CD) is an old disease, with changing clinical patterns, affecting any age, including infancy and adolescence, and becoming more frequent among the elderly. The gluten-free diet (GFD) has been the sole provider of clinical, serological, and histological improvement for patients with CD for more than seven decades. Nowadays, complete avoidance of dietary gluten is rarely possible because of the wide availability of wheat and other processed foods that contain even more gluten, to the detriment of gluten-free products. Undeniably, there is a definite need for replacing the burdensome GFD. An add-on therapy that could control the dietary transgressions and inadvertent gluten consumption that can possibly lead to overt CD should be considered while on GFD. Nevertheless, future drugs should be able to provide patients some freedom to self-manage CD and increase food independence, while actively reducing exposure and mucosal damage and alleviating GI symptoms. Numerous clinical trials assessing different molecules have already been performed with favorable outcomes, and hopefully they will soon be available for patient use.

Treponema pallidum infection has emerged in recent years as an important community threat and burden to the health care system. Here, we report the case of a patient with cholestatic liver disease secondary to late latent syphilis. A 41 year-old male patient was referred to the clinic for assessment of an abnormal liver function panel. Ultrasound of the abdomen demonstrated an intense liver echogenicity, normal bile ducts, and no ascites. Virologic study revealed negative results for antibodies against common viral hepatitis and metabolic and autoimmune disease. The patient was tested for syphilis and a positive result was reported. The patient was diagnosed with late latent syphilis and syphilitic hepatitis and initiated benzathine penicillin at G 7.2 million units total, delivered as three doses of 2.4 million units intramuscular each at one-week intervals. He was assessed monthly and by the end of the sixth month, he had nonreactive VDRL (seroconversion), which confirmed recovery. Syphilitic hepatitis is an overlooked type of hepatitis and should be kept in mind as a differential diagnosis in an abnormal liver panel of uncertain etiology. Health care providers should be advised that higher levels of ALP may be the single landmark in cases of syphilitic hepatitis.