Drug-induced liver injury associated with savolitinib: a novel case report and causality assessment.

BACKGROUND: Savolitinib, a small molecule inhibitor, has gained approval as the inaugural medication in China that specifically targets MET kinase. Patients with advanced non-small cell lung cancer (NSCLC) who show MET exon 14 skipping now have a new and innovative treatment option available. CASE REPORT: In this case report, we describe a patient who experienced drug-induced liver injury (DILI) due to the administration of savolitinib. After being prescribed with savolitinib (400 mg per day, oral), a 73-year-old male diagnosed with stage IV NSCLC with MET exon 14 skipping mutation experienced an increase in liver enzymes and bilirubin levels according to his laboratory tests conducted one month later. Following a 14-day course of hepatoprotective medication, the liver function reverted back to its normal state. After receiving savolitinib (200 mg per day, oral) for one week, the patient was once again diagnosed with severe liver impairment. Then savolitinib was discontinued and received treatment with hepatoprotective drugs for one week. Following the restoration of normal liver function, another attempt was made to administer a small amount of savolitinib (100 mg per day, oral). Thus far, the patient has been followed up and there has been no recurrence of liver damage. Additionally, the lung CT scan revealed ongoing tumor shrinkage with no apparent indications of spreading or metastasis. The Roussel Uclaf Causality Assessment Method (RUCAM) determined that savolitinib was "highly probable" cause of DILI. Moderate-severe was determined to be the extent of DILI severity. CONCLUSION: To the best of our understanding, this is the initial instance of DILI resulting from the use of savolitinib as a standalone treatment in a real-world setting. During the administration of savolitinib, healthcare professionals should carefully consider the potential occurrence of DILI. Administering the patient with a small amount of savolitinib resulted in a remarkable response against the tumor, leading us to speculate that the effectiveness of savolitinib might be associated with its plasma concentration. Studying the pharmacokinetics and pharmacodynamics (PK/PD) of savolitinib is beneficial for tailoring and accurately prescribing the medication to each individual.

Impact of Hypoglycemia on Hospitalized Patients With Hepatocellular Carcinoma.

Aims Hepatocellular carcinoma (HCC) is one of the common liver malignancies that presents a challenge to global healthcare. The impact and outcomes of hypoglycemia in HCC have not been studied in detail before. This study aimed to investigate the outcomes and prognosis associated with hypoglycemia in patients diagnosed with HCC, utilizing a large-scale database approach. Methods Using the Nationwide Inpatient Sample (NIS) database from 2017 to 2020, we conducted a comprehensive retrospective analysis to examine the incidence, risk factors, and clinical implications of hypoglycemia on HCC patients. The patients were divided into two groups: those with hypoglycemia and those without hypoglycemia. Univariate and multivariate logistic regression were used to conduct the analysis. STATA® version 17.0 software (StataCorp LLC, College Station, TX) was used for this purpose. Results Out of a total of 343,895 patients with HCC, the prevalence of hypoglycemia was present in 1.5% of this patient population. We found that hypoglycemia was common in the male population (68%). Compared with patients without hypoglycemia, patients who had hypoglycemia with HCC had higher mortality (42%, p-value < 0.05) and higher risks of secondary outcomes such as hepatic failure, spontaneous bacterial peritonitis (SBP), ascites, and portal vein thrombosis compared to patients who did not have hypoglycemia. The multivariate-adjusted odds ratio for hepatic failure was 2.7 (2.3-3.1), for SBP was 2.9 (1.8-3.0), for ascites was 1.6 (1.4-1.9), and for portal vein thrombosis was 1.2 (0.9-1.4). Conclusion In conclusion, hypoglycemia in HCC is associated with increased mortality and worse outcomes.

Hemophagocytic Lymphohistiocytosis (HLH) in an Elderly Male With Epstein-Barr Virus (EBV) Viremia.

This is a case of a 75-year-old male with a complicated past medical history who presented initially with weakness, fevers, exertional dyspnea, cough, and confusion. His initial workup revealed elevated aspartate transaminase (AST), alanine transaminase (ALT), bilirubin, and D-dimer. Right upper quadrant (RUQ) ultrasound revealed a partially contracted gallbladder with gallstones, so he underwent laparoscopic cholecystectomy. Due to worsening hyperbilirubinemia and anemia, he later underwent a liver biopsy which showed Epstein-Barr virus (EBV)-positive lymphoid infiltration. He developed anemia, thrombocytopenia, and low fibrinogen. He met the criteria for hemophagocytic lymphohistiocytosis (HLH) with 6/8 HLH-2004 criteria and an H score of 230 with a 96-98% probability of HLH. The patient was promptly treated with steroids, rituximab, and etoposide; however, the patient's health continued to deteriorate, and he expired. This case highlights the challenges of early diagnosis of HLH in the elderly patient population due to large differentials, confounding comorbidities, and the rarity of the diagnosis in this age range.

Association of fluoride exposure with disease burden and neurodevelopment outcomes in children in South Korea.

BACKGROUND: Community water fluoridation is an effective public health strategy for preventing dental caries, yet. Concerns exist about potential health problems. This study explores associations between tap water fluoride levels and pediatric disease burden, as well as neurodevelopmental outcomes at 6 years of age. METHODS: This nationwide population-based cohort study included children born in Korean cities with and without tap water fluoridation projects, between 2006 and 2012, aiming for a fluoride concentration of 0.8 ± 0.2 mg/L in treated tap water. Data from the National Health Insurance Service were used, spanning from birth to 2018. The relationship between exposure to fluoridated tap water and incidence of 16 childhood diseases that were previously identified as potentially linked to fluoride exposure were examined. Additionally, we evaluated the neurodevelopmental outcomes across various domains, including gross motor, fine motor, cognition, language, social skills, and self-help functions. These assessments were performed using data from a comprehensive national health screening program for children aged six years. RESULTS: A fluoride-unexposed group included 22,881 children, whereas a fluoride-exposed group comprised 29,991 children (52% males). Children in the fluoride-exposed group had a decreased risk of dental caries and bone fractures [hazard ratio (95% confidence interval, CI), 0.76 (0.63-0.93) and 0.89 (0.82-0.93), respectively] and increased risk of hepatic failures [1.85, (1.14-2.98)] compared to those in the unexposed group. Additionally, the risk ratio of abnormal neurodevelopmental screening outcomes increased by 9%, but this was statistically uncertain (95% CI, 0.95-1.26). CONCLUSIONS: Fluoridated tap water was associated with an increased risk of hepatic failure but a decreased risk of bone fractures in children. The association between fluoridated tap water and neurodevelopmental screening outcomes at 6 years remains unclear, highlighting the need for further studies to clarify this association.

Hemolytic Anemia Leading to Fulminant Hepatic Failure as the Initial Presentation of Wilson's Disease in a Young Female.

Wilson's disease (WD) is an autosomal recessive disorder that impairs copper metabolism. Copper accumulates in vital organs such as the brain, liver, and kidneys. The disease typically starts with copper accumulation in the liver and can initially present as acute hepatitis and hepatomegaly. Hemolytic anemia is a typically uncommon complication of WD. We present the case of a healthy 18-year-old female who presented with hemolytic anemia and quickly decompensated to fulminant hepatic failure requiring a liver transplant due to previously undiagnosed WD. This case recognizes the importance of early diagnosis as treatment can be lifesaving.

Application of TSPO-Specific Positron Emission Tomography Radiotracer as an Early Indicator of Acute Liver Failure Induced by Propacetamol, a Prodrug of Paracetamol.

Acetaminophen overdose is a leading cause of acute liver failure (ALF), and effective treatment depends on early prediction of disease progression. ALF diagnosis currently requires blood collection 24-72 h after APAP ingestion, necessitating repeated tests and hospitalization. Here, we assessed earlier ALF diagnosis using positron emission tomography (PET) imaging of translocator proteins (TSPOs), which are involved in molecular transport, oxidative stress, apoptosis, and energy metabolism, with the radiotracer [18F]GE180. We intraperitoneally administered propacetamol hydrochloride to male C57BL/6 mice to induce ALF. We performed in vivo PET/CT imaging 3 h later using the TSPO-specific radiotracer [18F]GE180 and quantitatively analyzed the PET images by determining the averaged standardized uptake value (SUVav) in the liver parenchyma. We assessed liver TSPO expression levels via real-time polymerase chain reaction, Western blotting, and immunohistochemistry. [18F]GE180 PET imaging 3 h after propacetamol administration (1500 mg/kg) significantly increased liver SUVav compared to controls (p = 0.001). Analyses showed a 10-fold and 4-fold increase in TSPO gene and protein expression, respectively, in the liver, 3 h after propacetamol induction compared to controls. [18F]GE180 PET visualized and quantified propacetamol-induced ALF through TSPO overexpression. These findings highlight TSPO PET's potential as a non-invasive imaging biomarker for early-stage ALF.

Thyroid storm-induced acute liver dysfunction and portal hypertension in a patient with Graves' disease: a case report.

Thyroid storm is a life-threatening condition associated with multiorgan dysfunction and decompensation. We report the case of a 41-year-old woman having Graves' disease presented with thyroid storm complicated with liver dysfunction and portal hypertension in the absence of congestive heart failure or known liver disease. After successful therapeutic management, all biological, clinical and morphological abnormalities regressed.

Graves' disease is an immune system disorder that results in the overproduction of thyroid hormones. We report the case of a 41-year-old woman with Graves' disease who presented with reversible liver dysfunction and high blood pressure in the portal vein (located in the abdomen) following the withdrawal of her treatment.

Circulating myostatin levels as a prognostic biomarker in patients with acute liver failure and late-onset hepatic failure.

AIM: Myostatin is a myokine involved in muscle mass regulation. The associations between circulating myostatin levels and clinical characteristics in patients with acute liver failure (ALF) and late-onset hepatic failure (LOHF) are unclear. METHODS: In this retrospective study, 51 patients with ALF or LOHF were included. Serum myostatin was measured using an enzyme-linked immunosorbent assay. RESULTS: Myostatin levels were significantly lower in patients with ALF and LOHF than in controls (ALF/LOHF: 2522 pg/mL, controls: 3853 pg/mL, p = 0.003). The prevalence of low myostatin in deceased patients was significantly higher than that in spontaneous survivors and patients who underwent liver transplantation. Patients with low myostatin levels had a high incidence of complications. There was a positive correlation between the psoas muscle index and serum myostatin levels. Patients with low myostatin levels had shorter 1-year transplant-free survival and shorter 1-year overall survival than patients with high myostatin levels. Low serum myostatin levels were associated with poor prognosis independent of the Japanese scoring system for ALF ≥3, King's College criteria, or model for end-stage liver disease score >30.5. The combination of serum myostatin levels and prognostic models for ALF significantly stratified patients according to 1-year prognosis. CONCLUSIONS: Low serum myostatin levels were associated with a low psoas muscle index, complication rate, and poor prognosis in patients with ALF and LOHF. Assessment of circulating myostatin levels may improve the prediction of outcomes in patients with ALF and LOHF.

Case report and literature review: A thyroid storm patient with severe acute hepatic failure treated by therapeutic plasma exchange and a double plasma molecular absorption system.

Thyroid storm (TS) leading to acute liver failure is rare but fatal in clinical practice and hepatic failure can remarkably limit medication options for TS. We successfully cured a patient with TS complicated with acute hepatic failure using therapeutic plasma exchange (TPE) and a double plasma molecular absorption system (DPMAS) and summarized the case characteristics of 10 similar critical patients reported worldwide. We recommend that patients with TS complicated with liver failure disuse propylthiouracil or methimazole. TPE should be utilized to rapidly decrease thyroid hormone levels, and DPMAS should be considered for supportive treatment in the presence of hepatic encephalopathy or dramatic bilirubin elevations.

Changing etiological spectrum of acute liver failure.

BACKGROUND AND OBJECTIVES: Acute liver failure (ALF) is an uncommon but potentially dramatic syndrome characterized by massive hepatic necrosis and has a very high mortality rate of 50% to 75% without liver transplantation. This study is aimed at analyzing the etiological spectrum of ALF patients and compare these with ALF mimics such as malaria, dengue fever and other tropical infectious diseases. METHODS: The study population included patients who presented with ALF and ALF mimics in a tertiary care center over two years. We retrospectively analyzed the patient case files and a comparison was made concerning the baseline demographic details, clinical profile, laboratory values and outcomes. RESULTS: Sixty-three patients were assessed, with 32 in ALF and 31 in ALF mimics group. The most common cause for ALF was hepatitis A virus (25%), followed by hepatitis B virus (18.7%), drug-induced liver injury (12.7%), autoimmune hepatitis (12.5%), hepatitis E virus (9.3%) and Wilson's disease (6.25%). In the ALF mimics group, malaria (58.06%) was the most common cause, followed by dengue fever (16.1%), leptospirosis (12.9%) and scrub typhus (12.9%). Patients in the ALF mimics group had significantly higher incidence of fever (p = 0.001), hepatosplenomegaly (p = 0.01), anemia (p = 0.02) and shorter jaundice to encephalopathy duration (p = 0.032) as compared to the ALF group, while higher transaminase levels (p = 0.03), bilirubin (p = 0.01), prothrombin time (p = 0.01), serum ammonia (p = 0.02) and mortality (p = 0.02) were observed in ALF patients. CONCLUSIONS: The most common cause for ALF was hepatitis A virus, followed by hepatitis B virus, while in ALF mimics it was malaria followed by dengue fever, in our study. Patients of ALF mimics can have similar presentation, but a high index of suspicion and awareness is required to identify the common infectious ALF mimics for early diagnosis.

Dengue induced acute liver failure: A meta summary of case reports.

BACKGROUND: Dengue fever is the most common cause of viral hemorrhagic fever, with more than 400 million cases being reported annually, worldwide. Even though hepatic involvement is common, acute liver failure (ALF) is a rare complication of dengue fever. AIM: To analyze the demographic profile, symptomology, hospital course and outcomes of patients presenting with ALF secondary to dengue infection by reviewing the published case reports. METHODS: A systematic search was performed from multiple databases including PubMed, Reference Citation Analysis, Science Direct, and Google Scholar. The search terms used were "dengue" OR "severe dengue" OR "dengue shock syndrome" OR "dengue haemorrhagic syndrome" OR "dengue fever" AND "acute liver failure" OR "hepatic failure" OR "liver injury". The inclusion criteria were: (1) Case reports or case series with individual patient details; (2) Reported acute liver failure secondary to dengue infection; and (3) Published in English language and on adult humans. The data were extracted for patient demographics, clinical symptomatology, clinical interventions, hospital and intensive care unit course, need for organ support and clinical outcomes. RESULTS: Data from 19 case reports fulfilling the predefined inclusion criteria were included. The median age of patients was 38 years (inter quartile range: Q3-Q1 26.5 years) with a female preponderance (52.6%). The median days from diagnosis of dengue to development of ALF was 4.5 d. The increase in aspartate aminotransferase was higher than that in alanine aminotransferase (median 4625 U/L vs 3100 U/L). All the patients had one or more organ failure, with neurological failure present in 73.7% cases. 42.1% patients required vasopressor support and hepatic encephalopathy was the most reported complication in 13 (68.4%) cases. Most of the patients were managed conservatively and 2 patients were taken up for liver transplantation. Only 1 death was reported (5.3%). CONCLUSION: Dengue infection may rarely lead to ALF. These patients may frequently require intensive care and organ support. Even though most of these patients may improve with supportive care, liver transplantation may be a therapeutic option in refractory cases.

Modulation of the crosstalk between Keap1/Nrf2/HO-1 and NF-κB signaling pathways by Tomatidine protects against inflammation/oxidative stress-driven fulminant hepatic failure in mice.

Fulminant hepatic failure (FHF) is the terminal phase of acute liver injury, which is characterized by massive hepatocyte necrosis and rapid hepatic dysfunction in patients without preexisting liver disease. There are currently no therapeutic options for such a life-threatening hepatic failure except liver transplantation; therefore, the terminal phase of the underlying acute liver injury should be avoided. Tomatidine (TOM), asteroidal alkaloid, may have different biological activities, including antioxidant and anti-inflammatory effects. Herein, the lipopolysaccharide (LPS)/D-galactosamine (D-GalN)-induced FHF mouse model was established to explore the protective potential of TOM and the underlying mechanisms of action. TOM pretreatment significantly inhibited hepatocyte necrosis and decreased serum aminotransferase activities in LPS/D-GalN-stimulated mice. TOM further increased the level of different antioxidant enzymes while reducing lipid peroxidation biomarkers in the liver. These beneficial effects of TOM were shown to be associated with targeting of NF-κB signaling pathways, where TOM repressed NF-κB activation and decreased LPS/D-GalN-induced TNF-α, IL-6, IL-1ß, and iNOS production. Moreover, TOM prevented LPS/D-GalN-induced upregulation of Keap1 expression and downregulation of Nrf2 and HO-1 expression, leading to increased Nrf2-binding activity and HO-1 levels. Besides, TOM pretreatment repressed LPS/D-GalN-induced upregulation of proliferating cell nuclear antigen (PCNA) expression, which spared the hepatocytes from damage and subsequent repair following the LPS/D-GalN challenge. Collectively, our findings revealed that TOM has a protective effect on LPS/D-GalN-induced FHF in mice, showing powerful antioxidant and anti-inflammatory effects, primarily mediated via modulating Keap1/Nrf2/HO-1 and NF-κB/TNF-α/IL-6/IL-1ß/iNOS signaling pathways.

Outcomes of liver diseases in pregnant females: A study from a tertiary care medical center in Pakistan.

Objective: To determine the etiologies and outcomes of liver disease in pregnancy in a developing country. Method: A total of 336 consecutive pregnant women with liver disease were included in this prospective cohort study conducted at the Department of Gastroenterology, Jinnah Postgraduate Medical Center, Karachi from August 2019 to August 2021. Patients' baseline demographic, clinical, and laboratory data and outcomes were collected on a pre-designed questionnaire. Results: Among all the pregnant females, the most common liver disease was acute hepatitis E virus (HEV) infection (37.2%), followed by preeclampsia (PEC)/eclampsia (EC), hemolysis, elevated liver enzymes & low platelets (HELLP) syndrome, and hyperemesis gravidarum (HG). The most common maternal complications were fulminant hepatic failure (FHF) in 14.9% and placental abruption in 11.0%. Fetal complications included intrauterine death (IUD) in 20.8% and preterm birth in 8.6%. The maternal and neonatal mortality rates were 11.6% and 39.6%, respectively. Among the predictors, low maternal weight, low body mass index (BMI), and low hemoglobin (Hb) were associated with increased maternal mortality. Low fetal weight, height, maternal systolic blood pressure (SBP), and low maternal Hb were independent predictors of fetal mortality. Conclusion: In our cohort of pregnant females in a tertiary care medical center, acute HEV was the most common liver disease, followed by PEC/EC, HELLP, and HG. Maternal and fetal deaths were alarming in this group of patients and demanded careful management.

Effects of glucagon-like peptide-1 receptor agonists on liver-related and cardiovascular mortality in patients with type 2 diabetes.

BACKGROUND: Patients with type 2 diabetes (T2D) tend to have nonalcoholic fatty liver disease (NAFLD) with poorer prognosis. We performed this research to compare the risks of cardiovascular diseases, cirrhosis, liver-related mortality, and cardiovascular mortality between glucagon-like peptide-1 receptor agonist (GLP-1 RA) use and no-use in patients with T2D without viral hepatitis. METHODS: From January 1, 2008, to December 31, 2018, we used propensity-score matching to identify 31,183 pairs of GLP-1 RA users and nonusers from Taiwan's National Health Insurance Research Database. Multivariable-adjusted Cox proportional hazards models were used to examine the outcomes between the study and control groups. RESULTS: The median (Q1, Q3) follow-up time for GLP-1 RA users and nonusers were 2.19 (1.35, 3.52) and 2.14 (1.19, 3.68) years, respectively. The all-cause mortality incidence rate was 5.67 and 13.06 per 1000 person-years for GLP-1 RA users and nonusers, respectively. Multivariable-adjusted analysis showed that GLP-1 RA use had significantly lower risks of all-cause mortality (aHR 0.48, 95%CI 0.43-0.53), cardiovascular events (aHR 0.92, 95%CI 0.86-0.99), cardiovascular death (aHR 0.57, 95%CI 0.45-0.72), and liver-related death (aHR 0.32, 95%CI 0.13-0.75). However, there was no significant difference in the risk of liver cirrhosis development, hepatic failure, and hepatocellular carcinoma compared to GLP-1 RA no-use. CONCLUSIONS: This nationwide cohort study showed that GLP-1 RA use was associated with a significantly lower risk of all-cause mortality, cardiovascular events, and cardiovascular death in patients with T2D among Taiwan population. More prospective studies are warranted to verify our results.

Causal Relationship between Angina and Hepatic Failure as Revealed by Mendelian Randomization.

BACKGROUND: Patients with angina are often suffering from comorbidities such as varying degrees of hepatic dysfunction. However, the impact of angina on the incidence of hepatic failure (HF) remains unclear. METHODS: The genetic data were retrieved from genome-wide association studies. Five Mendelian randomization methods were used to investigate the causal relationship between unstable angina (UA), stable angina (SA), and HF. The result of the Inverse variance weighted (IVW) method was deemed the principal result. In addition, we performed a comprehensive sensitivity analysis to verify the robustness of the results. RESULTS: The IVW results showed that UA (Odds ratio (OR): 2.055, 95% confidence interval (CI): 1.171-3.606, p = 0.012) was causally associated with the incidence of HF. SA (OR: 1.122, 95% CI: 0.738-1.706, p = 0.591) was not causally associated with the incidence of HF. Sensitivity analysis did not identify any bias in the results. CONCLUSIONS: UA turned out to be a risk factor for HF. SA does not have a significant causal effect on HF. Therefore, it is highly recommended that patients with chronic liver disease seek prompt medical attention and undergo regular monitoring of liver function when experiencing UA. This may help them to reduce the risk of HF.

Validation of diagnoses of liver disorders in users of systemic azole antifungal medication in Sweden.

BACKGROUND: Liver disorders are important adverse effects associated with antifungal drug treatment. However, the accuracy of Clinical International Classification of Diseases (ICD)-10 codes in identifying liver disorders for register based research is not well-established. This study aimed to determine the positive predictive value (PPV) of the ICD-10 codes for identifying patients with toxic liver disease, hepatic failure, and jaundice among patients with systemic antifungal treatment. METHODS: Data from the Swedish Prescribed Drug Register and the National Patient Register were utilized to identify adult patients who received systemic azole antifungal drugs and had a recorded diagnosis of toxic liver disease (K71.0, K71.1, K71.2, K71.6, K71.8, K71.9), hepatic failure (K72.0, K72.9), or jaundice (R17) between 2005 and 2016. The medical records of all included patients were reviewed. Prespecified criteria were used to re-evaluate and confirm each diagnosis, serving as the gold standard to calculate PPVs with 95% confidence intervals (95% CI) for each diagnostic group. RESULTS: Among the 115 included patients, 26 were diagnosed with toxic liver disease, 58 with hepatic failure, and 31 with jaundice. Toxic liver disease was confirmed in 14 out of 26 patients, yielding a PPV of 53.8% (95% CI 33.4-73.4%). Hepatic failure was confirmed in 26 out of 38 patients, resulting in a PPV of 62.1% (95% CI 48.4-74.5%). The highest PPV was found in jaundice, with 30 confirmed diagnoses out of 31, yielding a PPV of 96.8% (95% CI 83.3-99.9%). CONCLUSION: Among patients who received azole antifungal treatment and were subsequently diagnosed with a liver disorder, the PPV for the diagnosis of jaundice was high, while the PPVs for toxic liver disease and hepatic failure were lower.

A Case of Zinc Phosphide-Induced Acute Fulminant Liver Failure.

The use of rodenticides such as zinc phosphate is common in tropical countries. However, it has a toxic effect on humans when consumed or absorbed accidentally or deliberately. Although the adverse effects often only last for a short period, acute or fulminant liver failure can occur in few patients. Because the chemicals can create a wide variety of symptoms, it is essential to investigate the progression of symptoms from mild to severe so that treatment protocols can be understood and patients can receive appropriate care. In this report, we detail a case of rodenticide poisoning in a middle-aged man who, initially, had only minor symptoms but ultimately developed fulminant liver failure. In this example, we discuss the case of a 40-year-old man who intentionally consumed 10 gm of rat poison (zinc phosphide (ZnP)) and reported to our department with a complaint of nausea and three episodes of vomiting. A neurological evaluation showed that the patient had a Glasgow Coma Scale score of 9/15 (Eye(E): 2; Motor(M): 4; Verbal(V): 3). Doll's eyes were present, and the patient's pupils were semi-dilated, sluggishly reacting to light. The plantars were bilateral extensor. In the subsequent four hours, the patient developed a deep coma. The patient's lack of awareness, coagulopathy, and abnormal liver enzyme values all pointed to acute fulminant liver failure. His condition improved with supportive therapy over a period of three weeks.

Accidental iron poisoning in children - Experience from a teaching institution.

Background: Acute iron toxicity is fatal in children resulting from an accidental overdose of maternal iron tablets at home. There is scanty literature on children looking at the profile and outcome. We report a case series of five children presenting after accidental ingestion of iron tablets. Two presented with fulminant hepatic failure at 48 h, and despite supportive management and plasmapheresis in one child, both succumbed to illness. Materials and Methods: This retrospective study was conducted in the pediatric intensive care unit (PICU) of a teaching institution in South India between January 2009 and December 2019. All children with accidental iron poisoning were included in the analysis. Results: During the study period, five children presented to our PICU after accidental iron tablet ingestion. The mean age was 25.8 months [standard deviation (SD): 13.9]. All the children had consumed iron tablets from their pregnant mothers. Two children presenting with liver failure succumbed to illness. Treatment included a standard protocol of gastric lavage and desferrioxamine. Most of them (3/5) received whole bowel irrigation. We did plasmapheresis in one child who presented with fulminant hepatic failure. The majority were discharged alive (3/5). The presence of coagulopathy, acute liver failure, and delayed presentation were associated with high mortality. Conclusion: Accidental iron poisoning is prevalent in children and associated with significant mortality. Parents and caretakers must be counseled by primary care physicians and made aware of the safe storage of iron tablets.

Complex Diagnostic Dilemma of Viral Hepatitis vs. Drug-Induced Hepatitis: A Case Report.

This case report explores the intricate diagnostic challenges encountered in a 30-year-old male patient with abdominal pain, jaundice, and a history of acetaminophen use. Initially presenting as a potential case of drug-induced hepatitis due to acetaminophen overdose, the diagnosis took an unexpected turn when the patient tested positive for hepatitis B surface antigen. The case highlights the complexity of diagnosing acute hepatitis, considering multiple potential etiologies, including viral and drug-induced factors. Differential diagnoses for this case involve considering drug-induced hepatitis, autoimmune hepatitis, various viral hepatitis types, and the potential contribution of cocaine-induced hepatitis as individual possibilities or in combination. This case emphasizes the need for a comprehensive evaluation, the consideration of multiple potential causes, and the importance of ongoing monitoring and follow-up to ensure optimal patient care in cases of acute hepatitis.

A Case of Autoimmune Hepatitis Complicated by Undiagnosed Factor VII Deficiency: A Pitfall of Coagulopathy.

Prothrombin time (PT) is a key parameter for assessing the severity of liver disease. We present the case of a 37-year-old woman with severe acute liver injury due to autoimmune hepatitis. Although prednisolone drastically improved her hepatocyte function, her PT did not recover to the reference range. A review of her medical records revealed that the patient had normal transaminase levels and prolonged PT 2 years previously. Further examinations of her coagulopathy revealed that she had low factor VII activity, suggesting a diagnosis of factor VII deficiency. Our experience suggests that altered coagulopathy should be considered in cases of liver injury with an extraordinary PT.