Volvulus is defined as the abnormal twisting of a segment of the gastrointestinal tract around its mesenteric axis, resulting in luminal obstruction with potential compromise of the mesenteric blood supply. While colonic volvulus is common in adults, small-bowel volvulus is rare and represents a surgical emergency due to the high risk of bowel ischemia, necrosis, and sepsis. Although adult primary ileal volvulus has previously been described, isolated distal ileal volvulus without identifiable secondary pathology remains uncommon. A 52-year-old female with no comorbidities presented with a three-day history of progressively worsening abdominal pain, obstipation, and abdominal distension. Clinical examination revealed right iliac fossa tenderness with a palpable cystic swelling and features suggestive of small-bowel obstruction. Radiological evaluation demonstrated dilated small-bowel loops with air-fluid levels on plain radiography, and contrast-enhanced computed tomography revealed a transition point in the distal ileum with twisted bowel loops, consistent with ileal volvulus. Emergency exploratory laparotomy revealed a 360-degree anticlockwise volvulus of approximately 20 cm of terminal ileum with irreversible ischemic changes. Resection of the gangrenous ileal segment along with limited caecal resection was performed, followed by exteriorization as a double-barrel ileocolostomy. The patient had an uneventful recovery apart from a minor surgical site infection and subsequently underwent successful stoma reversal two months later. Histopathology confirmed transmural ischemic necrosis without evidence of malignancy or tuberculosis. Preoperative diagnosis remains difficult because clinical features are nonspecific, although contrast-enhanced CT can provide important clues when ileal volvulus is suspected. Isolated distal ileal volvulus remains an uncommon entity, and maintaining a high index of suspicion together with careful interpretation of CT findings may facilitate early diagnosis and improve outcomes.

Myeloid sarcoma (MS) is an extramedullary tumor composed of immature myeloid precursor cells and represents a tissue manifestation of acute myeloid leukemia (AML). It may occur concurrently with AML, precede marrow disease, or present at relapse. Gastrointestinal (GI) involvement is uncommon and frequently poses a diagnostic challenge due to morphological overlap with lymphoid and other GI malignancies. We report the case of a 38-year-old man presenting with acute intestinal obstruction secondary to a duodenal-jejunal mass. Histopathological examination demonstrated diffuse submucosal infiltration by monomorphic abnormal cells, initially raising a differential diagnosis of lymphoma or poorly differentiated malignancy, intestinal tuberculosis, or gastrointestinal stromal tumor. Immunohistochemistry revealed strong myeloperoxidase positivity, with negativity for epithelial, lymphoid, and neuroendocrine markers, supporting myeloid lineage. Peripheral blood examination showed leukocytosis with circulating blasts and monocytic precursors. Multiparametric flow cytometry was suggestive of AML with monocytic differentiation, establishing the diagnosis of intestinal MS with concurrent AML. The present case highlights the rarity of MS presenting as an acute abdomen and surgical emergency with diagnostic challenges to the surgeon. Accurate diagnosis relies on keeping a high index of clinical suspicion, along with a multidisciplinary approach. Early identification is critical, as MS requires prompt AML-directed systemic therapy rather than localized surgical treatment.

Histoplasmosis is an endemic mycosis in certain regions of Brazil and represents a rare opportunistic infection in solid organ transplant recipients. This report describes the case of a 68-year-old female liver transplant recipient (due to Caroli disease) who presented with abdominal pain, nausea, vomiting, and a distended, tender abdomen. Abdominal computed tomography revealed parietal thickening of the bowel wall, and colonoscopy identified polymorphic ulcers and ileocecal stenosis. Given the suspicion of tuberculosis, chest computed tomography was performed, which demonstrated pulmonary opacities. Although testing for acid-fast bacilli was negative, fungal staining was positive for Histoplasma capsulatum. Antifungal therapy with amphotericin B was initiated; however, due to clinical refractoriness, surgical intervention was required, including ileocecal resection with ileo-ascending anastomosis. A reoperation was performed due to postoperative complications, resulting in the creation of a terminal ileostomy. Following this intervention, the patient showed clinical improvement and tolerated an oral diet. This case highlights an atypical presentation of disseminated histoplasmosis with pulmonary and intestinal involvement, culminating in intestinal subocclusion in a late-stage liver transplant recipient. It underscores the importance of considering histoplasmosis in the differential diagnosis of immunosuppressed patients and the need for early investigation and treatment.

Benzo[a]pyrene (BaP) is a representative environmentally persistent polycyclic aromatic hydrocarbon (PAH) that continues to enter the human diet through food-chain accumulation and food processing. The aryl hydrocarbon receptor (AHR) is a shared sensor for xenobiotic BaP and microbiota-derived tryptophan (Trp) metabolites, but how opposing ligands acting through the same receptor dictate divergent epithelial outcomes remains unclear. Here, integrating receptor engagement, AHR chromatin occupancy, and epithelial barrier function, we show that indole, a microbial Trp metabolite, counteracts BaP-induced colonic barrier injury through ligand-selective AHR regulation. AHR antagonism and knockdown attenuated BaP-induced barrier disruption and AHR signaling dysregulation, supporting AHR involvement in BaP toxicity. Indole and BaP occupied the same AHR ligand-binding pocket but displayed divergent binding modes and kinetics. Consistently, indole remodeled BaP-driven AHR chromatin occupancy and shifted enriched regulatory programs from xenobiotic metabolism toward epithelial junction, barrier maintenance, and cytoskeletal integrity. Functionally, indole restored tight-junction architecture, barrier permeability, and normalized AHR and cytochrome P450 1A1 expression under BaP challenge. In vivo, Trp and indole supplementation protected against BaP-induced colonic injury under intact microbiota. Under antibiotic-treated conditions, indole remained protective whereas Trp protection was markedly diminished, indicating that microbial conversion is required for Trp-dependent defense. These findings establish ligand-selective AHR reprogramming as a mechanism by which microbial Trp metabolites counteract BaP at the receptor interface, and identify the Trp-microbiota-indole axis as a targetable endogenous defense against health risks posed by persistent dietary pollutants.

Intestinal tuberculosis accounts for 1%-3% of all tuberculosis cases worldwide and typically arises as a secondary manifestation of hematogenous spread rather than as a primary site of infection. The condition is characterized by an insidious onset, with patients often presenting late in the disease course with non-specific gastrointestinal symptoms. At advanced stages, clinical features may include signs of bowel obstruction or perforation, closely mimicking other conditions such as colorectal malignancy, colitis, or inflammatory bowel disease, posing a significant diagnostic challenge. We report a rare case of isolated intestinal tuberculosis presenting as a partial large bowel obstruction. The patient successfully underwent a right hemicolectomy followed by anti-tuberculosis pharmacotherapy, resulting in complete restoration of normal bowel function and eradication of tuberculosis.

Amebic liver abscess (ALA), caused by Entamoeba histolytica, is the most common extraintestinal manifestation of amebiasis. However, in contemporary clinical practice, diagnosis increasingly relies on serology and polymerase chain reaction (PCR), whereas direct microscopic identification of motile trophozoites in aspirated specimens has become rarely documented. Furthermore, optimal management necessitates complete anti-amebic therapy covering both invasive tissue stages and luminal intestinal colonization to prevent relapse. Here, we report a case of a 25-year-old male with a history of splenectomy and pulmonary tuberculosis, presenting with fever, right upper quadrant pain, and cough. Imaging revealed a right hepatic lobe abscess. While abscess and blood cultures remained sterile, sputum culture grew E. coli. Fresh microscopic examination of the aspirate readily demonstrated motile, erythrophagocytic trophozoites, subsequently confirmed as E. histolytica by sequencing. Although the patient showed initial clinical improvement with metronidazole, he later developed severe bleeding and ulceration of the ascending colon, ultimately requiring partial colectomy. This case underscores the enduring diagnostic value of conventional wet-mount microscopy in the molecular era, offering a rapid and cost-effective tool. Critically, it also highlights a key therapeutic principle ALA treated with a tissue-active agent must be followed by a luminal agent to eradicate intestinal carriage. Failure to do so risks persistent colonic disease, severe complications, or treatment failure, as observed in this patient.

Methionine biosynthesis is essential for Mycobacterium tuberculosis, but the in vivo relevance of individual enzymes remains unclear. We performed transposon sequencing in Mycobacterium bovis BCG under methionine-free conditions and identified metF as a major fitness determinant. To define enzyme-specific functions, ΔmetE and ΔmetF mutants were generated in M. tuberculosis and evaluated using in vitro growth assays and a murine infection model. The ΔmetE mutant showed vitamin B12-dependent growth in minimal medium but maintained normal growth in mice, indicating that its in vitro requirement does not translate to an in vivo defect. In contrast, ΔmetF exhibited strict methionine auxotrophy in vitro and completely failed to survive or persist in murine lungs and spleens. Structural modeling showed that MetF is distinct from human homologs, supporting selective inhibition. These findings demonstrate that MetF, but not MetE, is indispensable for M. tuberculosis survival in vivo and identify MetF as a promising metabolic drug target.

Background: Active tuberculosis (TB) is increasingly recognized as a systemic thrombo-inflammatory condition capable of inducing a clinically relevant hypercoagulable state and increasing the risk of venous thromboembolism, including pulmonary embolism (PE). However, this association remains underrecognized in clinical practice, and its biological and therapeutic implications are not yet fully defined. We report two cases of active pulmonary tuberculosis complicated by PE and review the literature to highlight the temporal patterns, laboratory features, and clinical relevance of TB-associated hypercoagulability. Case Presentation: The first case involved a 65-year-old man with stage II chronic obstructive pulmonary disease in whom PE was identified concurrently with the diagnosis of active pulmonary TB. The second case concerned a 43-year-old man with severe pulmonary tuberculosis and subsequent intestinal involvement, in whom bilateral PE developed during the early intensive phase of antituberculous therapy. In both patients, laboratory evaluation demonstrated a consistent prothrombotic profile characterized by reactive thrombocytosis, elevated inflammatory markers, increased fibrinogen and D-dimer levels, and reduced protein C and protein S activity. Both patients received standard antituberculous therapy combined with therapeutic anticoagulation, with favorable clinical, laboratory, and radiological outcomes. Discussion: These cases are consistent with emerging evidence that active tuberculosis may induce a reversible infection-related hypercoagulable state through systemic inflammation, endothelial dysfunction, platelet activation, impaired fibrinolysis, and transient depletion of natural anticoagulants. They illustrate two clinically relevant temporal patterns described in the literature, namely PE detected at diagnosis and PE developing during early treatment despite appropriate therapy. The normalization of coagulation abnormalities after treatment further supports an acquired TB-related thrombo-inflammatory mechanism. Conclusions: Active tuberculosis may be complicated by pulmonary embolism both at presentation and during the early phase of treatment. Reactive thrombocytosis, elevated inflammatory markers, increased D-dimer levels, and reduced protein C and protein S activity may serve as useful indicators of TB-associated hypercoagulability. Pulmonary embolism should be considered in patients with severe tuberculosis who show unexplained deterioration or delayed recovery. Larger prospective studies are needed to clarify the role of coagulation profiling and biomarker-guided management in this setting.

Granulomatous adrenal involvement is an uncommon cause of primary adrenal dysfunction, while intestinal non-tuberculous mycobacterial (NTM) infection and Crohn's disease share substantial clinical, endoscopic, radiological, and histopathological overlap. The coexistence of these entities represents an exceptional diagnostic challenge, and epidemiological data regarding their association are currently lacking. We report the case of a 61-year-old man who presented with progressive cutaneous hyperpigmentation. Computed tomography demonstrated bilateral adrenal calcifications, calcified lymph nodes suggestive of granulomatous disease, and a calcified hepatic granuloma. Biochemical evaluation revealed markedly elevated adrenocorticotropic hormone (ACTH) levels, while morning cortisol and aldosterone.

The final part of our series of studies reports the results of a pilot study of a clinical case (patient K.), indicating that therapy enabling reconstruction of the genome of hematopoietic stem cells (HSCs) reduces the frequency of SNPs in exons of the genes associated with clonal hematopoiesis of uncertain potential in a patient with a neuroendocrine tumor of the small intestine in the terminal stage of progression. The fundamental principles of the therapy were as follows. Control samples of peripheral blood mononuclear cells (baseline) were collected from the patient. CD34+ HSCs were then mobilized and collected. The HSC genome was modified using a technology enabling ex vivo correction of the nucleotide sequences of DNA chromosomes of poorly differentiated hematopoietic progenitor cells. For this purpose, the collected leukocyte suspension enriched with CD34+ HSCs was treated with fragmented deproteinized genomic DNA obtained from approximately 100 young healthy women in labor (hDNAgr). The patient was reinfused intravenously with the treated cells. Five days before reinfusion, the patient received immunosuppressive therapy. Samples of peripheral blood mononuclear cells were also collected 4, 8, 12, and 27 months after the therapeutic intervention. Full-exome sequencing of DNA isolated from selected cell samples was performed. A group of commonly accepted clonal hematopoiesis genes was selected as a criterion demonstrating changes in the genome. The following multiplex panels were used at the initial time point as well as time points after 4, 8, and 12 months: MGIEasy Exome Capture V5 Probe set, Roche KAPA HyperExome, Nanodigmbio NEXome Plus Panel v1.0, covering the entire exome and non-coding regions of the analyzed genes adjacent to exons with ~100× coverage. A ~1000× coated panel (Nanodigmbio NanOnco Plus Panel v3.0), including the genes with mutant alleles identified at the initial time point, was used to verify the identified mutations and more accurately determine their proportions in readings at the last stage of the analysis (27 months after the therapy). Whole-exome sequencing of hDNAgr (Roche KAPA HyperExome), which is used to reconstruct the genome of HSCs whose fragments collectively constitute the complete human genome, was also performed. Although the analysis of readings of whole-exome sequencing of DNA isolated from blood samples after treatment did not reveal any currently known signs of clonal hematopoiesis with uncertain potential in the patient K., we found a significant, within the framework of the selected criterion, decrease in the frequency range of SNPs to 18 % by 27 months of follow-up in 15 % cases of the heterozygous alleles (DNMT1, SF3B1(1-2)). Subsequent analysis of the frequency of occurrence of controlled SNPs and the corresponding data on the depth of their sequencing, performed using the All-FIT algorithm, indicates that by the 27th month of follow-up, the proportion of cells carrying the basic set of SNPs significantly decreases by 12 % (confidence interval (CI) = 5-16 %). In other words, in a mixture of cells heterozygous for this SNP, a population of cells carrying a homozygote without an SNP appears. Our findings may indicate that a significant proportion of cells underwent correction of the SNP to an alternative allele, and this correction was associated with the treatment of the original HSCs with hDNAgr. The detected changes in the group of clonal hematopoiesis genes suggest the possibility of correcting other loci throughout the HSCs genome. Therefore, the clinical manifestations in the development of the disease show a pronounced positive trend, which has persisted for four years, until present. It is assumed that the positive clinical outcome after therapy with reconstructed hematopoietic stem cells is associated with an increase in the regenerative potential of HSCs, which resulted from the genetic correction of unfavorable mutations in the HSCs genome.

Lupus enteritis is a rare clinical entity with a global incidence of 0.2%-14.2%. Signs and symptoms of lupus enteritis are nonspecific, and incidence is very low; it is often misdiagnosed as tuberculosis (TB) in endemic countries like India. Also, enteritis as initial presentation is quite uncommon in systemic lupus erythematosus. We are reporting a case of a 15-year-old woman of lupus enteritis who was misdiagnosed as intestinal TB.

Gastrointestinal basidiobolomycosis (GIB) is a rare invasive fungal infection of immunocompetent hosts that is endemic to Saudi Arabia and the wider Gulf region. Its presentation overlaps with inflammatory bowel disease (IBD), intestinal tuberculosis and malignancy, and many patients reach a definitive diagnosis only after surgery. We report a 39-year-old Saudi woman who presented with a 7-day history of right lower quadrant pain and non-bloody watery diarrhea. Initial bloods showed an elevated C-reactive protein of 21.5 mg/L, an erythrocyte sedimentation rate of 44 mm/hour and an absolute eosinophil count of 0.54 × 103/µL. Contrast-enhanced computed tomography (CT) demonstrated segmental wall thickening of the terminal ileum, cecum and proximal transverse colon, with a 3×5 cm intramural cecal collection. Colonoscopy revealed ulcerated congested mucosa and an ileocecal stricture; targeted biopsies showed an eosinophil-rich granulomatous inflammation with broad, sparsely septate fungal hyphae demonstrating the Splendore-Hoeppli phenomenon, positive on Grocott methenamine silver and periodic acid-Schiff stains; and tissue culture grew Basidiobolus spp. Interventional radiology and surgical drainage were considered but were technically not feasible because of the intramural location, so the patient was managed medically with oral itraconazole at 200 mg every 8 hours for 3 days followed by 200 mg once daily, with monthly liver enzyme monitoring. Surgery was avoided. A repeat CT scan at 2 months showed near complete resolution of wall thickening, and follow-up colonoscopy at 5 months was normal. The patient self-discontinued itraconazole at 9 months because of symptom resolution and remained asymptomatic at follow-up 2 months later. Clinicians working in endemic regions should consider GIB in any patient with an ileocecal mass or abscess, eosinophilia and an IBD-like presentation, because early biopsy with fungal stains and prompt azole therapy can avert surgery.