Vol 54, No 1 (2026)

Background: The incidence of cancer in acromegaly varies substantially, ranging from 6.8% to 21.3%. Population-based studies have revealed differences both in the tumor types and in the risk factors for cancer development in acromegaly.

Aim: To assess the frequency and structure of malignancies in patients with acromegaly from a single region of the Russian Federation and to identify possible clinical and biochemical predictors of cancer risk in these patients.

Methods: A retrospective observational single-cohort study was performed. Data from the acromegaly registry of the Moscow Region as of December 1, 2025, were analyzed. The frequency and structure of malignancies were studied in the cohort of acromegaly patients. Clinical and biochemical characteristics, features of acromegaly course, prevalence of comorbidities, and treatment modalities were compared between acromegaly patients with and without cancer.

Results: Among 423 patients with acromegaly included in the Moscow Region registry, 75 (17.7%) had malignancies, and 7 of them had multiple primary cancers. A total of 82 malignant tumors were recorded, 4 of which were diagnosed before the onset of acromegaly symptoms. The most commonly affected sites were the thyroid (18/82, 22.0%), colon (16/82, 19.5%), breast (13/82, 15.9%), and uterus (11/82, 13.4%). Patients with cancer were older at the time of acromegaly diagnosis (mean ± SD, median [LQ; UQ]: 51.5 ± 13.9, 54 [41; 62] vs 48.0 ± 13.5, 49 [38; 58] years, p = 0.036) and at the last visit (66.7 ± 12.5, 69 [61; 75] vs 60.1 ± 13.5, 61.5 [50; 70] years, p = 0.004), and had a significantly longer time to remission of acromegaly (8.9 ± 9.2, 5 [3; 12] vs 5.6 ± 5.6, 4 [2; 7] years, p = 0.021). Growth hormone (GH) and insulin-like growth factor-1 (IGF-1) levels at both acromegaly diagnosis and the last visit did not differ between groups. In the cancer group, the frequency of primary hyperparathyroidism (10.7% vs 3.9%, p = 0.009; odds ratio (OR) 3.303, 95% confidence interval (CI) 1.300–8.392) and glucose metabolism disorders (68.9% vs 54.1%, p = 0.021; OR 1.879, 95% CI 1.097–3.219) was significantly higher. Moreover, patients with cancer had significantly higher prolactin levels at acromegaly diagnosis (6080 ± 13045, 1767 [1060; 2500] vs 2098 ± 4183, 1138 [724; 1939] mIU/L, p = 0.022), although the frequency of hyperprolactinemia did not differ (24.2% vs 22.1%, p = 0.700).

Conclusion: In the Moscow Region, the most frequent cancers in acromegaly patients were those of the thyroid, colon, breast, and uterus. Risk factors for cancer in acromegaly included longer duration of active acromegaly (but not the degree of GH or IGF-1 elevation), as well as the presence of glucose metabolism disorders and primary hyperparathyroidism.

Background: Liver fibrosis is a manifestation of chronic liver diseases (CLD) and a key prognostic factor for their progression. The development of non-invasive quantitative magnetic resonance imaging (MRI) techniques that are robust to the influence of liver tissue composition is important for fibrosis stage stratification. The extracellular volume fraction (ECV) reflects the volume of the extracellular matrix and can be considered a specific quantitative marker of fibrotic changes.

Aim: To evaluate the diagnostic performance of liver and spleen ECV for stratifying liver fibrosis stages and to analyze the effect of steatosis on the robustness of the diagnostic characteristics of the technique.

Methods: This single-center, observational, retrospective, two-sample, comparative study included 427 patients with CLD and 111 patients without CLD examined in inpatient and outpatient settings between November 2024 and July 2025. Fibrosis staging was performed using the Metavir scale (F0–F4). Liver and spleen ECV were calculated based on T1 mapping using the MOLLI 5(3)3 protocol before and 10 minutes after intravenous contrast injection according to the formula: ECV = (1 - Hct) × (ΔR1_organ / ΔR1_aorta). Steatosis stratification was performed based on the proton density fat fraction, forming subgroups of patients without steatosis and with steatosis. ROC analysis was performed to assess diagnostic performance when discriminating ≥ F2, ≥ F3, and F4.

Results: The study cohort comprised 538 patients (276 women and 262 men, mean age 47.2 ± 14.2 years). Distribution by fibrosis stage: F0 – 228 (of which 111 had no CLD), F1 – 126, F2 – 79, F3 – 40, F4 – 65. No steatosis was found in 287 patients, while 251 had steatosis. Liver and spleen ECV values progressively increased with advancing fibrosis from F0 to F4. Pairwise differences between adjacent stages remained statistically significant (FDR < 0.05). For detecting clinically significant fibrosis (≥ F2), the AUC for liver ECV was 0.865 in patients without steatosis and 0.872 in those with steatosis; for ≥ F3, 0.939 and 0.977; and for F4, 0.976 and 1.000, respectively. For spleen ECV, when detecting stage ≥ F2, the AUC was 0.779 and 0.866; for ≥ F3, 0.882 and 0.911; and for F4, 0.940 and 1.000, without and with steatosis, respectively.

Conclusion: Liver ECV is a highly informative quantitative biomarker of liver fibrotic changes in CLD. The diagnostic performance of the technique increases at later fibrosis stages and remains robust in the presence of steatosis. Spleen ECV provides additional diagnostic value, mainly for assessing severe fibrosis and liver cirrhosis.

Helicobacter pylori infection remains a key risk factor for chronic gastritis, peptic ulcer disease, and gastric adenocarcinoma. However, the efficacy of standard eradication regimens is substantially declining due to rising antibiotic resistance and frequent therapy-related adverse effects. In this context, interest in adjuvant strategies is growing, including the use of probiotics and postbiotics / metabiotics capable of increasing eradication rates and improving treatment tolerability through strain-specific mechanisms of action and modulation of the gastrointestinal microbiota.

This review focuses on the postbiotic / metabiotic Limosilactobacillus reuteri DSM 17648, which has demonstrated anti-H. pylori activity that persists after inactivation and is independent of H. pylori antibiotic resistance. The article discusses the main mechanisms of action of L. reuteri DSM 17648, including strain-specific coaggregation with H. pylori, competitive blocking of pathogen adhesion to gastric epithelium, inhibition of H. pylori virulence factors, masking of its adhesins, as well as the production of antimicrobial and anti-inflammatory metabolites (organic acids, reuterin, exopolysaccharides, etc.) that contribute to reduced expression of urease, vacA, and cagA genes and attenuation of the inflammatory response in the gastric mucosa.

A review of major clinical studies in adults and children is provided, including randomized placebo-controlled trials in Europe and Asia, which have shown that adding L. reuteri DSM 17648 to standard triple therapy increases H. pylori eradication rates by an average of 10–20%, reduces bacterial load (as assessed by urea breath test), alleviates dyspeptic symptoms, and decreases the frequency of gastrointestinal adverse effects by 20–40% compared to eradication therapy alone. Data from pediatric studies are separately examined, confirming the efficacy and favorable safety profile of the metabiotic during courses of up to 56 days, as well as the absence of serious adverse events in patients across different age groups.

Based on cumulative experimental and clinical evidence, practical aspects of L. reuteri DSM 17648 use are discussed, including its incorporation into standard H. pylori eradication regimens and as monotherapy (in infected individuals without immediate eradication indications, between antibiotic courses, and in special patient populations), its place in current guidelines (Maastricht VI, Russian clinical guidelines), and future perspectives for use in combined and alternative therapeutic regimens, including the potential to reduce gastric cancer risk in infected individuals through its multifaceted impact on bacterial load, H. pylori virulence factors, inflammation, and gastric mucosal barrier function.

Niemann-Pick disease type C (NP-C) is a rare, progressive, autosomal recessive neurodegenerative disorder with onset at various ages, caused by pathogenic variants in the NPC1 or NPC2 genes. In the late-infantile form of NP-C, the development of psychotic symptoms at onset or during the course of the disease in preschool children has not been described in the literature. We report a clinical case of a 6-year-old female patient who, from the first days of life, had prolonged jaundice, hepatosplenomegaly and haemorrhagic episodes. Early development was age-appropriate, but from the age of 4 years speech regression began, and from the age of 5 years progressive behavioral disturbances appeared. The key feature was the development of rare and severe psychotic symptoms at preschool age in the late-infantile form of NP-C: inappropriate laughing without reason, talking to a mirror, night wandering around the house, aggressive jealousy of a younger brother, grabbing a kitchen knife, self-aggression (scratching until bleeding), insomnia and withdrawal. Simultaneously, daytime enuresis, ataxia and upward gaze palsy – a pathognomonic sign of NP-C – appeared. Video-electroencephalography monitoring revealed epileptic encephalopathy with continuous spike-and-wave activity during sleep with a pharmacoresistant course. Whole-exome sequencing identified compound heterozygous mutations c.3019C>G + c.3742_3745delCTCA in NPC1, and blood oxysterol levels were markedly elevated. Subsequently, pathogenetic therapy with miglustat was initiated.

Psychotic manifestations in NP-C can mimic childhood schizophrenia or psychotic disorder, but their combination with hepatosplenomegaly, ataxia and supranuclear gaze palsy should immediately direct the physician towards biochemical and genetic testing for NP-C.