BACKGROUND Chronic hepatitis B (CHB) is a significant public health problem. Most of the global burden of CHB is due to mother-to-child transmission, since perinatal infections lead to a high rate of chronicity. Spontaneous seroclearance of hepatitis B surface antigen (HBsAg) in CHB happens at a rate of 1% per year. Treatment options for CHB in children are available starting at 1 year of age. Current paediatric guidelines recommend treating children with hepatitis B envelope antigen (HBeAg) positive hepatitis with elevated serum transaminases levels for at least 6 months. Treatment is not indicated for children with HBeAg positive infection and normal transaminases. In 2024, the World Health Organization unified criteria for initiating antiviral treatment in children older than 12 years and in adults. Recent, preliminary evidence showed that antiviral therapy in infants and children younger than 2 years to 3 years of age with CHB infection led to higher rates of HBsAg loss than in adults and older children. AIM To evaluate the available evidence about treatment of CHB in young children and discuss the potential impact of early treatment. METHODS We searched the literature to identify studies reporting cases of HBsAg loss in children treated with antiviral drugs. We included only studies in which treatment-naïve patients started treatment before 2 years of age. RESULTS We identified 6 studies reporting results of CHB treatment, particularly HBsAg loss rates, hepatitis B virus DNA undetectability, and HBeAg loss. CONCLUSION Studies conducted on young children showed a higher HBsAg loss rate compared to those reached in older children and adults, offering new perspectives on the treatment of CHB. Further studies are needed to assess the effect of early treatment in larger populations and over a longer follow-up period.

Background and Aims: Tuberculosis remains a major public health problem, and the emergence of drug-resistant forms significantly complicates its management, particularly in resource-limited countries such as the Republic of Guinea. Thus, this study is to assess the management of patients with drug-resistant pulmonary tuberculosis at the Matam Tuberculosis Center (CAT), in order to identify shortcomings and propose areas for improvement. Methodology: During 12 months, a descriptive and analytical cross-sectional study was conducted at the Matam Tuberculosis Center (CAT). Sociodemographic, clinical, bacteriological, and treatment-related data were collected. A total of 152 sputum samples were analyzed using the GeneXpert MTB/RIF assay and fluorescence microscopy. Results: Among the152 pulmonary tuberculosis patients, GeneXpert MTB/RIF detected 32% of cases compared to 22% by fluorescence microscopy, confirming its superior diagnostic performance. Hematological findings revealed a high prevalence of anemia (98%), mainly microcytic along with leukocytosis and lymphopenia, reflecting chronic inflammation and immune alterations. Biochemical abnormalities, including elevated transaminases and creatinine (31%), suggest treatment-related hepatic and renal effects. The treatment success rate reached 94%, exceeding WHO targets, indicating effective patient management despite persistent challenges related to drug resistance and adherence. Conclusion: Drug-resistant tuberculosis remains a major challenge in Conakry. Strengthening early detection, improving treatment monitoring, and ensuring strict adherence to treatment protocols are essential to improving patient care.

Objective: To summarize the characteristics and prognosis of infantile cholestasis caused by McCune-Albright syndrome (MAS). Methods: A retrospective case series study was conducted. Clinical data was collected and analyzed from four infantile cholestasis cases caused by MAS at Pediatric Liver Center, Children's Hospital of Fudan University from February 2016 to October 2025. Descriptive analysis was performed on their clinical characteristics, biochemical examinations, liver ultrasound, liver histopathology, genetic testing, treatment, and prognosis. Results: Among the 4 children (2 males and 2 females), the age of onset was the neonatal period, and presented with jaundice as the initial symptom. Three cases (case 1-3) had pale stools. Mild hepatomegaly was present in all patients. Biochemical examinations revealed elevated gamma-glutamyl transferase (GGT) levels, which were 124, 128, 78, and 258 U/L, accompanied by severely elevated alanine aminotransferase and aspartate aminotransferase levels, with peak values of 2 312 and 1 742 U/L. Liver histology in case 1 and case 3 at 2 months of age showed cholestasis, fibrous tissue hyperplasia, separation of lobules of liver, mild bile ducts hyperplasiamild. Follow-up liver histopathology in case 1 at 1.3 years of age revealed significant improvement in inflammation and fibrosis. Liver histopathology in case 4 at 3.2 years of age showed mild cholestasis, mild inflammation in the portal areas and reduced number of intrahepatic bile ducts. While the cholestasis subsided spontaneously by approximately 8 months of age, liver transaminase abnormalities could last for several years, and only 1 case (case 3) returned to normal after 1.9 years. Café-au-lait spots were present at birth in 3 cases (case 1, 3, 4) and appeared at 2 months of age in 1 case (case 2). Precocious puberty and bony abnormality occurred later than the onset of cholestasis. The results of whole exon sequencing of blood samples from all the four cases were negative, whereas GNAS variant was identified in the liver tissue of case 4. Conclusions: MAS can involve the liver. In infancy, it can present as high-GGT cholestasis accompanied by severely elevated transaminases. Although jaundice may resolve spontaneously in infants, abnormal transaminase levels can persist. Detection of GNAS variants in liver tissue may facilitate early diagnosis.

The management of acne patients treated with isotretinoin has evolved quite markedly over the last years: from simply reporting elevated transaminase levels and lipids to a deeper insight into the mechanisms of these changes, development of effective correction methods, and to more clarity on patient selection criteria. Comorbid conditions that can affect safety and tolerability of systemic retinoids require special consideration. This article presents a clinical case of a 15-year-old female patient with severe, extensive, and treatment-resistant acne (IGA 4). The patient had been suffering from rashes over her face, chest, and back for three years. Her comorbidities included class I obesity (BMI 31.2), insulin resistance, hyperprolactinemia, and functional menstrual cycle disorders. The patient had a history of apathy and depressive episodes (she was emotionally stable at the time of therapy). The previous therapy with antiseptics and topical antibiotics has proved to be ineffective. Given the resistance and severity of the disease, isotretinoin was prescribed at a starting dose of 30 mg/day (0.36 mg/kg/day). After one month, improvements were noted: a decrease in sebum secretion and the number of inflammatory lesions. At 2.5 month of therapy, acute abdominal pain syndrome developed due to dietary inconsistency. Laboratory tests showed elevated transaminase levels (ALT, AST), and the abdominal ultrasound examination revealed signs of cholelithiasis. The acute condition was resolved. The isotretinoin dosage was temporally tapered to 10 mg/day, and a diet was recommended. After laboratory parameters and clinical status returned to normal, the dosage was gradually increased to 20 mg/day, and then to the initial therapeutic dose (30 mg/day). At the time of this writing, the patient was completing a course of isotretinoin therapy; the skin process regressed with development of stable clinical remission. The presented case demonstrates the potential to safely continue isotretinoin therapy with transient transaminase elevations, including in patients with comorbidities. Isotretinoin tapering, dietary therapy, and follow-up laboratory monitoring allow to maintain commitment to the treatment and achieve the target cumulative dose without discontinuation of the drug therapy.

Background & Objective: To compare the efficacy and safety of two human epidermal growth factor receptor 2 (HER2)-targeting antibody-drug conjugates (ADCs), disitamab vedotin (RC48) and trastuzumab deruxtecan (DS-8201), in patients with the HER2 altered solid tumors. Methodology: We conducted a preliminary real-world comparative study, which included a case of a patient with HER2 exon 20 insertion mutated lung adenocarcinoma and a retrospective analysis of 18 patients treated at Air Force Medical Hospital, PLA, Beijing between 2021 and 2025. Patients received either RC48 (n=12) or DS-8201 (n=6). The primary endpoints were objective response and adverse events, evaluated using RECIST 1.1 criteria and standard toxicity assessments. Results: The case patient exhibited primary resistance and severe gastrointestinal toxicity to RC48 but achieved partial remission (PR) with DS-8201. In the cohort analysis, DS-8201 demonstrated a significantly superior PR of 66.67% compared to 8.33% for RC48 (P = 0.022). The adverse event profiles differed notably: DS-8201 was primarily associated with elevated transaminases and fatigue, while RC48 more frequently caused myelosuppression and hyperbilirubinemia. Conclusion: DS-8201 demonstrates potential as one of the effective salvage therapies following RC48 failure in HER2 altered solid tumors, showing significantly better disease control and a distinct, manageable toxicity profile. These findings highlight the importance of selecting personalized ADCs based on molecular subtypes and toxicity factors and provide a basis for future, larger-scale prospective studies.

Abnormal liver enzyme elevations with positive antinuclear antibodies (ANA) frequently prompt investigation for autoimmune hepatitis after common causes such as viral hepatitis or drug-induced liver injury have been excluded. Current guidelines recommend liver biopsy for suspected autoimmune hepatitis, but its utility in patients with only mild transaminase elevation remains uncertain. This study evaluated the diagnostic yield of liver biopsy in such patients, particularly when alanine aminotransferase is below 101 U/L. We retrospectively analysed 313 adults who underwent percutaneous liver biopsy at the University Hospital Heidelberg between 2019 and 2024 for unexplained liver enzyme elevation including suspected autoimmune hepatitis. Clinical data were extracted, and histology was classified according to the 2022 International Autoimmune Hepatitis Pathology Group consensus recommendations. Patients with malignancy, post-transplant biopsy, or incomplete data were excluded. The median age was 49 years; 55.3% were female. Median alanine aminotransferase and aspartate aminotransferase were 161 U/L and 106 U/L, respectively. Antinuclear antibodies were positive in 61.3% of cases. 22.4% of antinuclear antibody positive and 15.7% of antinuclear antibody negative patients had autoimmune hepatitis compatible histology. Among patients with positive antinuclear antibodies and alanine aminotransferase < 101 U/L, only 9% showed autoimmune hepatitis compatible histology and 3.8% (three patients) required long-term immunosuppression. Two of these three patients had compensated liver cirrhosis. Liver biopsy provides limited additional diagnostic value in ANA-positive, non-cirrhotic patients with alanine aminotransferase < 101 U/L and no alternative suspected aetiology. In such cases, the procedure can be safely deferred, reserving biopsy for higher enzyme elevations or unclear differential diagnoses.

This study aimed to assess the efficacy and safety of intensity-modulated radiotherapy (IMRT) combined with regorafenib with or without immune checkpoint inhibitors (ICIs) as a second- or later-line treatment for advanced hepatocellular carcinoma (HCC). Patients diagnosed with advanced HCC who had received RT combined with concurrent or sequential regorafenib treatment or regorafenib plus ICIs after failures of at least one line of systemic treatment in a single center from April 2018 to August 2022 were retrospectively reviewed. Progression-free survival (PFS) was the primary endpoint, while overall survival (OS), objective response rate (ORR), disease control rate (DCR), and toxicity were the secondary endpoints. Fifty patients were included, with 44 (88.0%) in BCLC stage C, 37 (74.0%) having portal vein tumor thrombosis (PVTT), and 12 (24.0%) with extrahepatic metastasis. Thirty-eight patients received conventional fractionated RT (56.4Gy/22-28f), while 12 received hyperfractionated RT (50Gy/5-10f). Twenty-six were treated concurrently with regorafenib and 24 sequentially. ICIs were applied in 34 patients. For the entire cohort, when measured from the start of RT initiation, the median PFS and OS were 10.9 months and not reached. The corresponding 2-year PFS and OS rates were 25.3% and 53.5%, respectively. When assessed from regorafenib initiation, the median PFS and OS were 5.9 months and not reached, with 2-year PFS and OS rates of 22.8% and 54.9%, respectively. For tumors in the RT field, the ORR was 74.0% (RECIST) and 92.0% (mRECIST). The most common grade 3 toxicities were hand-foot syndrome (16.0%), thrombocytopenia (8.0%), dermatitis (8.0%), and transaminase elevation (6.0%). IMRT concurrently or sequentially combined with regorafenib with or without ICIs is an effective, well-tolerated, and promising regimen as second-line or further-line treatment in patients with advanced HCC.

High-normal and abnormal alanine transaminase levels linked to increased risk of hepatoma following treatment for chronic hepatitis C.

The antimetabolite methotrexate (MTX) was originally used in chemotherapeutic treatment for cancer. Since the early 1980s, MTX has become indispensable in the treatment of rheumatoid arthritis and is established worldwide as the standard of care for the treatment of many inflammatory rheumatic diseases. The mechanism of action of MTX is not completely understood; the adenosine signaling pathway likely plays arole. There are several undesired side-effects associated with MTX (e.g., nausea, elevated transaminase levels, and cytopenia). Based on numerous case reports, it is also postulated that there is MTX-induced osteopathy, which manifests as bone pain and insufficiency fractures. The present article presents the current data and evaluates it critically.

Clinical study of recombinant human thrombopoietin in platelet engraftment following autologous hematopoietic stem cell transplantation.

CD19 CAR-T therapy induces remission in refractory autoimmune hemolytic anemia with ITP and antiphospholipid syndrome.

Statin is often under-prescribed in patients with metabolic dysfunction-associated steatotic liver disease (MASLD) due to fear of hepatotoxicity. Limited studies examine the safety of statin in MASLD prospectively. We evaluated the safety of statins in a cohort with biopsy proven MASLD. The study cohort comprised patients with biopsy proven MASLD between 2009 and 2022, with clinical data prospectively collected. We compared the liver profiles of patients with or without statins, at baseline and follow-up. We evaluated risk of statin-related hepatotoxicity in a subgroup of patients with advanced fibrosis or higher baseline transaminase elevation. There were 215 patients with biopsy proven MASLD, 115(53.5%) were female. The median age of all patients was 59.9years. A total of 115(53.5%) patients received statins. Simvastatin and atorvastatin were most used (89.5%). NAFLD activity scores and fibrosis stage were similar between the two cohorts. Baseline ALT was higher in the non-statins' cohort (73 U/L vs 57.5 U/L, p < 0.01). The median duration of statins use was 63months. At follow-up in comparison to baseline, ALT was significantly lower in both statins (57.5 U/L vs 45 U/L, p < 0.01), and non-statins cohort (73 U/L vs 43 U/L, p < 0.01). There was no significant difference in liver enzyme between the cohorts at follow-up. In subgroup of patients with advanced fibrosis, statins use was not associated with worsening of liver enzymes or liver stiffness. In this cohort with biopsy proven MASLD, the use of statins was well tolerated and not associated with worsening liver enzymes or fibrosis.

Shwachman-Diamond syndrome (SDS) is an inherited bone marrow failure disorder, and its hepatic phenotype is poorly defined. Our objective was to systematically characterize the prevalence, features, and outcomes of liver injury in a multicenter SDS cohort. Retrospective registry study of 171 patients with biallelic Shwachman-Bodian-Diamond syndrome (SBDS) mutations and evaluable hepatic data. Clinical, laboratory, imaging, elastography, and biopsy findings were extracted from medical records. Chronic hepatitis (CH) was observed in 94 of 171 patients (55%), with a median age at onset of 1.0 year (range 0.04-37.9). At presentation, 71% had alanine aminotransferase (ALT) ≥ 2× upper limit of normal (ULN) (interquartile range [IQR] 81-228.5 U/mL). In contrast, adult-onset CH (n = 5) was characterized by only mild (1-2× ULN) transaminase elevations. CH persisted for a median of 6 years, with resolution in 36% of cases. Hematopoietic stem cell transplantation (HSCT) exposure and liver-related mortality did not differ between patients with and without CH. Ultrasound (226 studies) was the principal imaging modality; 55% of scans in the CH cohort displayed increased echogenicity with preserved size, mirroring no-CH findings. Elastography (n = 41) showed comparable liver stiffness, though controlled attenuation parameter (CAP)-defined steatosis was more common without CH (40% vs. 18%). Biopsies (n = 30) revealed hepatitis (69%) and fibrosis (65%) in pediatric CH, whereas adults showed universal steatosis, often with fibrosis or cirrhosis. Liver disease is common in individuals with SDS. Longitudinal prospective surveillance and mechanistic studies are needed to inform targeted prevention and therapy.

Aim: This the study aimed to describe the etiologic distribution, clinical characteristics, and outcomes of hypertransaminasemia in children.Material and Methods: This retrospective cohort study was conducted using electronic medical records of children aged 1 month–18 years who presented with persistent transaminase elevation between January 2023 and July 2024. Hypertransaminasemia was defined as alanine aminotransferase (ALT) &amp;gt;45 IU/L and/or aspartate aminotransferase (AST) &amp;gt;50 IU/L on at least two measurements with elevation persisting for at least 3 months. Patients with extrahepatic cholestasis or insufficient data were excluded. Demographic, clinical, laboratory, and imaging findings were collected, and etiologies were categorized. Subgroup analyses were performed based on cholestasis and ALT &amp;gt;10× the upper limit of normal (ULN).Results: Among 6886 first-time clinic visits, 214 children (3.1%) met the inclusion criteria. The cohort was predominantly male (55.6%) with a median age of 2.3 years, and parental consanguinity was notably high (79.9%). Infectious causes accounted for the majority of cases (65%), while metabolic/genetic disorders (9.3%), drug-induced liver injury (7%), metabolic dysfunction–associated steatotic liver disease (MASLD) (3.3%), and autoimmune disease (1.4%) were less frequent; 14% remained idiopathic. ALT &amp;gt;10×ULN was observed in 20.6% of patients, and cholestasis in 25.7%. Although these subgroups showed higher biochemical abnormalities, their etiologic patterns and normalization times were similar to the overall cohort. Follow-up data were available for 172 patients (80.4%); among them, transaminase levels normalized in 128 (74.4%), with a median time to normalization of 37.5 days (IQR 26.6–70).Conclusion: Hypertransaminasemia appears to be strongly influenced by regional factors, and establishing standardized pediatric reference ranges in Türkiye would substantially improve diagnostic accuracy.

Classical congenital galactosaemia continues to be associated with high mortality and long-term disability in affected infants, even with expanded neonatal screening in Ukraine. The purpose of the work is to highlight the diagnostic and management challenges associated with this rare inborn error of metabolism in neonates, particularly in settings with limited clinical experience among neonatologists, based on a single-centre observation. Material and methods of the study. The report describes the clinical course, diagnostic evaluation, and management of a newborn diagnosed with classical (type I) congenital galactosaemia. Diagnostic investigations comprised clinical examination, serial biochemical analyses (including serum bilirubin fractions and liver enzymes), chest radiography, abdominal ultrasonography with Doppler assessment, ophthalmoscopic fundus examination, and postmortem histopathological analysis. Results of the study. A full-term male infant with classical congenital galactosaemia presented with a severe clinical course culminating in death. The infant was delivered by caesarean section to a 38-year-old mother with a significant somatic and obstetric history. At birth, the newborn was in satisfactory condition and remained with the mother for the first 6 days of life while receiving exclusive breastfeeding. Jaundice developed on day 4 of life as the sole initial clinical manifestation. Expanded neonatal screening for 21 inherited metabolic disorders was performed on day 3. Progressive indirect hyperbilirubinaemia ensued despite intensive phototherapy. From day 7, clinical deterioration became evident, characterised by systemic intoxication, persistent hyperbilirubinaemia, hepatomegaly, and neurological abnormalities (hypotonia and hyporeflexia). The infant was transferred to a second-level neonatal care unit. On day 9, haemorrhagic syndrome developed in association with worsening biochemical parameters (rising conjugated bilirubin and hepatic transaminases), necessitating transfer to the neonatal intensive care unit with a provisional diagnosis of early-onset haemorrhagic disease, perinatal infection, and haemolytic jaundice. Ophthalmoscopic examination on day 13 revealed vitreous haemorrhages in the left eye. On day 14, the initial neonatal screening result was reported as positive for galactosaemia type I and was confirmed by repeat testing. Despite maximal supportive care, progressive multiorgan failure ensued, including severe intoxication, respiratory insufficiency, worsening neurological status, and disseminated intravascular coagulation, leading to death on day 14 of life. The diagnosis was confirmed postmortem by histopathological examination and the repeated positive screening result. Conclusions. Classical congenital galactosaemia typically presents with nonspecific early symptoms, and the current turnaround time for expanded neonatal screening results in Ukraine is approximately 10 days. Neonatologists should maintain a high index of suspicion in the presence of progressive jaundice with significant hyperbilirubinaemia, hepatomegaly with elevated transaminases, coagulopathy, and vitreous haemorrhages. Immediate initiation of a galactose-free and lactose-free formula is warranted pending confirmatory screening results.

Background/Objectives: Hepatitis E virus (HEV) infection is an increasingly recognized cause of acute hepatitis in Europe, but short-term in-hospital laboratory dynamics remain insufficiently described in hospitalized cohorts. We aimed to characterize admission biochemical abnormalities and paired admission-to-discharge laboratory changes in hospitalized patients with acute hepatitis E from Craiova, Romania, with exploratory sex- and age-stratified analyses. Methods: We conducted a single-center retrospective observational study including 40 consecutive hospitalized patients with acute hepatitis E during 2024-2025. Admission and discharge laboratory values were compared at the within-patient level, and exploratory subgroup analyses by sex and age class were performed. Given the limited sample size, multivariable analyses were restricted to parsimonious age-adjusted models for selected endpoints. Results: The cohort comprised 22 females (55%) and 18 males (45%), with a mean age of 53.05 ± 21.44 years; two in-hospital deaths occurred. At admission, marked transaminase elevation and frequent hyperbilirubinemia were observed, with 70% of patients having total bilirubin ≥ 2 mg/dL and 40% ≥ 10 mg/dL. During hospitalization, ALT and AST declined markedly, whereas total and direct bilirubin improved more modestly, indicating slower resolution of jaundice/cholestatic abnormalities. Platelets increased, while prothrombin index changes were heterogeneous. Male patients had higher bilirubin values at admission and discharge and more frequent clinically relevant hyperbilirubinemia thresholds; however, these findings should be interpreted cautiously given the small sample size, the retrospective design, and the absence of standardized clinical confounders and mechanistic data. Exploratory age-stratified analyses did not identify robust differences after multiplicity control. Conclusions: In hospitalized hepatitis E, hepatocellular injury markers improved rapidly during hospitalization, whereas cholestatic abnormalities resolved more slowly and often remained clinically relevant at discharge. The observed sex-related cholestatic pattern should be considered exploratory and requires confirmation in larger studies with standardized clinical covariates and longer follow-up. These findings support closer monitoring of bilirubin trajectories at discharge, particularly in male patients, and highlight the need for integrating laboratory dynamics into short-term clinical assessment of hospitalized HEV cases.

Systematic toxicokinetic analysis and early hepatic effects evaluation of BbF following acute oral exposure in mice.

Transient abnormal myelopoiesis (TAM) in Down syndrome (DS) typically causes acute neonatal liver failure; however, late-onset chronic sequelae remain undercharacterized. We report two patients who, despite achieving hematologic remission, developed a persistent non-fatal inflammatory liver phenotype. Unlike the catastrophic neonatal hemochromatosis-like pathway, these cases exhibited sustained transaminase elevations and fibrotic markers triggered by immune bias rather than blast burden. We propose a two-track model of DS-TAM hepatic sequelae: (i) an acute fatal pathway, and (ii) a chronic residual inflammatory phenotype. These findings expand the clinical spectrum of TAM-associated liver disease, necessitating long-term hepatic surveillance beyond hematologic remission.

The ductus venosus plays a critical role in fetal circulation. Postnatal persistence of the ductus venosus (PDV) is associated with secondary portal vein hypoplasia and results in a porto-systemic shunt. In this extremely rare case, we present a 6-year-old male diagnosed with PDV, who had a history of elevated liver enzymes and mild hepatic dysfunction first detected at 11 months of age. Due to the presence of PDV, endovascular closure was planned. Portal venous pressure was measured as 10 mmHg both before and after balloon occlusion. Percutaneous occlusion was successfully performed using a vascular plug. Post-intervention ultrasonography confirmed complete occlusion of the ductus venosus and increased portal vein flow. During follow-up, liver function tests returned to normal; a slight elevation in transaminases persists. PDV is a rare congenital vascular anomaly that may present with a wide spectrum of clinical symptoms. While some patients may be diagnosed during early infancy due to cholestatic jaundice, hepatic dysfunction, or hyperammonaemia, others may remain asymptomatic and undiagnosed for years. Endovascular closure represents a minimally invasive treatment option. A balloon occlusion test to measure portal venous pressure is recommended before and after the procedure to evaluate the safety of shunt closure.

Pulmonary tuberculosis remains a major cause of morbidity and mortality, particularly in high-endemic countries. The aim of our study was to analyze the clinical and paraclinical differences between tuberculosis patients presenting electrolyte disorders and those without such abnormalities. Identifying profiles of tuberculosis patients at risk of hydroelectrolytic disorders therefore represents an important clinical challenge. We conducted a retrospective descriptive and analytical study over three years, from June 1, 2021 to June 1, 2024, including 40 patients with pulmonary tuberculosis hospitalized in the pulmonology department of the 20 August Hospital in Casablanca. Patients were divided into two groups: Group A (with electrolyte disorders, n=20) and Group B (without disorders, n=20). Hyponatremia was the most frequent hydroelectrolytic disorder (42.5%). Hypocalcemia, hypokalemia, and hyperkalemia were each observed in 5% of cases. These abnormalities were significantly associated with low BMI, tachycardia, anemia, neutrophilia, lymphopenia, hypoproteinemia, and hypoalbuminemia (p&lt;0.01, Fisher test). Moderate associations were observed for rhonchi and elevated transaminases (p&lt;0.05). Other elements such as bronchial syndrome, vomiting, fever, lower limb edema, and the presence of miliary tuberculosis showed significance with the Chi-square test (p&lt;0.05), but not with Fisher’s test. Mean CRP, urea, GOT, and GPT levels were significantly higher in Group A according to Student’s t-test. These results highlight the central role of systemic inflammation and the syndrome of inappropriate antidiuretic hormone secretion (SIADH) in the development of electrolyte imbalances, particularly hyponatremia. Adverse effects of anti-tuberculosis drugs (nephrotoxicity, hepatotoxicity, digestive disorders, and disturbances of vitamin D metabolism) may also contribute to their occurrence.