Liver Function Tests Research Articles

Liver damage in patients hospitalized with acute decompensated heart failure, depending on the degree of glucose metabolism disorder

Aim. To study the frequency of cardiohepatic syndrome and steatosis by the value of controlled attenuation parameter (CAP), fibrosis, and their combination, depending on the degree of glucose metabolism disorder in patients with acute decompensated heart failure (ADHF).Materials and methods. The study included 280 patients (53% men, average age 70.1 ± 10.8 years) with ADHF: 72.5% of patients had a history of arterial hypertension, 60% of patients had coronary heart disease. The HbA1c test was performed in all patients to assess the status of glucose metabolism. The patients were divided into groups depending on the results obtained: at HbA1c values < 5.7%, patients were included in the group without glucose metabolism disorders, at HbA1c 5.7–6.4% – in the prediabetes group, at HbA1c ≥ 6.5% – in the type 2 diabetes group. All patients underwent a standard physical examination at admission and at discharge. Clinical and comprehensive assessments of congestion were performed – NT-proBNP, lung ultrasound, liver fibroscan with CAP, and bioelectrical impedance analysis of body composition.Results. The frequency of glucose metabolism disorders in patients hospitalized with ADHF was 57.5% (n = 161), while prediabetes was detected in 17.1% (n = 48) and type 2 diabetes – in 40.4% (n = 113) of patients. We revealed significantly higher incidence of steatosis by CAP value (69 vs. 42%, p < 0.001), fibrosis (80 vs. 64%, p < 0.001), and their combination (59 vs. 30%, p < 0.001), as well as cardiohepatic syndrome (87 vs. 61%, p < 0.001) in patients with ADHF and glucose metabolism disorders compared to individuals with ADHF without glucose metabolism disorders, respectively. The group of ADHF patients with glucose metabolism disorders and a combination of steatosis / fibrosis was characterized by more pronounced manifestations of metabolic syndrome, impaired kidney and liver function, and more pronounced manifestations (both clinical and laboratory) of congestion.Conclusion. In patients with ADHF with glucose metabolism disorders, liver function test and liver fibroscan with CAP allow for identifying the most severe group of patients with a combination of steatosis/fibrosis and pronounced congestion.

Utility of Quantitative Assessment of Tc-99m-diethylenetriamine-penta-acetic acid-galactosyl Human Serum Albumin SPECT/CT in the Identification of Severe Liver Fibrosis: Its Complementary Diagnostic Value with Other Liver Function Indices.

To evaluate the value of Tc-99m-diethylenetriamine-penta-acetic acid-galactosyl human serum albumin (99mTc-GSA) single photon emission computed tomography (SPECT) for assessing liver fibrosis, and to assess its complementary value to other liver function indices such as fibrosis-4 (FIB-4) index and indocyanine green (ICG) clearance test parameters (ICG-R15 and ICG-K). Seventy-eight patients with chronic liver disease and hepatocellular carcinoma who underwent 99mTc-GSA scintigraphy and other liver function tests including ICG test and FIB-4 index prior to hepatectomy were studied. 99mTc-GSA imaging was performed with SPECT/CT scanner (Discovery NM/CT 670). Immediately after injection of 99mTc-GSA, dynamic imaging was performed for 20min, followed by SPECT data acquisition for 6min. LHL15 which is a conventional index by 99mTc-GSA planar images, and liver uptake ration (LUR) was measured from 99mTc-GSA SPECT images. From the liver resection specimens, the degree of liver fibrosis was graded according to the Ludwig scale (F0-4). Significant differences in LUR, LHL15, ICG-R15, ICG-K, platelet count and FIB-4 index were found between the F0-3 and F4 liver fibrosis patient groups (P < 0.05). Multivariate logistic regression analysis revealed that LUR and ICG-K were independent factors for identifying severe liver fibrosis (F4). Area under the curve of receiver operating curve analysis for the logistic regression model using LUR and ICG-K was 0.83. In the patient group with higher FIB-4 (≥ 3.16), the diagnostic performance of LUR for detecting severe liver fibrosis was significantly better than LHL15 (AUC: 0.83 vs. 0.75, P = 0.048). In the high FIB-4 index group, the sensitivity and specificity for identifying F4 was 88% and 85%, respectively, with LUR cutoff value of 41.2%. LUR, measured by 99mTc-GSA SPECT, is a useful indicator for identifying sever liver fibrosis. Particularly in patients with high FIB-4 index (≥ 3.16), LUR can be a valuable indicator to identify severe liver fibrosis with high diagnostic accuracy.

Turmeric supplement-associated hepatitis: a clinicopathological series of 11 cases highlighting pan-lobular and zone 3 injury.

Although turmeric is commonly ingested and well tolerated, there is increasing evidence that over-the-counter turmeric supplements can cause drug-induced liver injury. We sought to thoroughly characterise clinicopathological features of patients for whom liver injury was attributed clinically to turmeric supplements. We identified 11 patients via retrospective pathology archive review: 10 females (91%) and one male, with a median age of 58 years (range = 37-66 years). Six patients (55%) were asymptomatic with abnormal liver function tests, while five patients (45%) presented with malaise and/or jaundice. Ten patients (91%) showed predominant transaminase abnormalities, while one exhibited predominant alkaline phosphatase elevation. Histologically, biopsies showed acute hepatitis (eight cases, 73%, including five pan-lobular and three zone 3-predominant inflammation), scattered lobular aggregates of histiocytes (two; 18%) and a chronic hepatitis pattern of injury (one; 9%). Mild bile duct injury was present in five biopsies (45%). All patients stopped ingesting turmeric supplements after presenting with liver injury, and four patients additionally received steroid therapy; liver function tests normalised in all patients. Roussel Uclaf causality assessment method (RUCAM) analysis estimated the likelihood of turmeric supplement-associated liver injury to be probable (eight cases) and possible (three). Histological features in the 'possible' cases were consistent with drug-induced injury, highlighting the added benefit of histological analysis relative to RUCAM analysis isolation. This study underscores the need to obtain a full history of over-the-counter medications and supplements when investigating aetiologies for liver injury, including supplements purportedly containing innocuous compounds such as turmeric.

Proximity predicament: a rare case of hydatid cyst in the porta hepatis region

Hydatid cysts near the porta hepatis present notable medical challenges due to their intricate positioning and potential influence on crucial structures within the liver and its vicinity. While relatively rare, their presence can lead to intricate medical scenarios because of their proximity to vital liver and bile duct structures, but their occurrence can present complex medical situations due to their proximity to critical structures in the liver and bile ducts. We present an unusual case of a 33-year-old male with no known comorbidities presented to the outpatient department of general surgery with pain, insidious in onset and gradually progressive, in the right hypochondrial region for the past 3 months, along with mild fever, reduced appetite, and weight loss of 3 kg. Managing hepatic cysts, especially when near the porta hepatis, poses significant diagnostic challenges. Imaging scans revealed multiple hypodense lesions suggestive of hepatic cysts, with the largest one measuring 5 cm × 8 cm in segment VI. Native post-contrast lesions were also observed in the right lower lobe. Although hepatic duct dilation was not observed, the presence of a cyst near the porta hepatis an atypical site for hydatid cyst, complicated potential PAIR procedures (puncture, aspirate, injection, re-aspirate), raising concerns about the risk of damaging vital structures like the hepatic artery or major bile duct. A multidisciplinary approach engaged interventional radiology to evaluate PAIRS feasibility. PAIRS was performed successfully, except for the cyst near the porta hepatis to avoid complications. Despite this, the patient continued to experience abdominal discomfort post-operation, although liver function tests improved in the postop period. This case underscores the uncommon occurrence of hydatid cysts near the porta hepatis and highlights the need for additional research to comprehend its prevalence and causes. Further investigation is crucial to enhance our understanding of the epidemiology and optimal management strategies involving PAIRS in such challenging cases.

Efficacy and safety of Dapagliflozin and Glimepiride in combination with Metformin: Randomized clinical trial

Objective: To identify the effective treatment option between dapagliflozin-metformin and glimepiride-metformin combination in patients with type 2 diabetes who were inadequately controlled with metformin monotherapy. Study design and setting: The present study is randomized, conducted for 12 weeks at the National Medical center, Karachi, Pakistan. Methodology: The patients were divided into 2 treatment groups; group A was given dapagliflozin-metformin combination, while group B was given glimepiride-metformin combination. The efficacy endpoint of groups was estimated by hemoglobin A1c and fasting blood glucose levels at 0-, 6- and 12-week. While, safety endpoints were identified by analyzing liver function tests, lipid profile tests, renal function test, and urine analysis. The significant difference of data was analyzed by using statistical package of social sciences (SPSS) version 25. The parametric t-test and paired t-test were performed and considered p-value = 0.05 as statistical significant. Results: Baseline demographics, clinical features of diabetes, levels of liver enzymes, liver function test, renal function test, lipid profile, and urinalysis of randomized patients were similar in both treatment groups by showing p = 0.05. Followed by the initiation of the respective treatment, the baseline change of mean FBG and hemoglobin A1c levels with dapagliflozinmetformin combination was shown significantly reduce more compared to glimepiride-metformin combination (p = 0.05). Conclusion: Dapagliflozin-metformin combination therapy was superior and well-tolerated to regulate glycemic control as compare to glimepiride-metformin combination

Pro-inflammatory cytokines gene expression in liver and kidneys of rats exposed to a sub-lethal dose of Bitis arietans snake venom.

Bitis arietans (Puff adder) is a poisonous snake and its bite causes pain, edema, blistering, tissue damage and neutrophilia. There are limited studies on inflammatory process involved in Bitis arietans envenomation. We therefore investigated the role of proinflammatory cytokines in Bitis arietans venom (BAV)-induced liver and kidney toxicities in rats. Adult male Sprague Dawley rats were treated with BAV (0.5 mg/kg) and were sacrificed after specific time intervals (2 h, 24 h, 1 week). Blood samples were collected for liver and renal function tests and tissues were collected for histopathology and gene expression analysis of IL-1β, IL-6, and TNF-α in liver and kidneys. There was no significant difference in serum ALT activities among different treatment groups. Serum AST was significantly increased at 24 h following BAV injection. In both organs, injection of BAV resulted in mild inflammatory cell infiltration at 2 h post-dosing which normalized after 1 week. In liver, there was a significant increase in IL-1β expression in BAV-treated rats at 2 and 24 h post-dosing that reduced after one week. Significant increases in IL-6 and TNF-α were observed at 24 h and 1 week after BAV exposure. In kidneys, there were significant increases in IL-1β and TNF-α expression at 24 h that subsided after 1 week. In conclusion, a single sub-lethal dose of BAV caused an acute phase inflammation in liver and kidneys. It is most probable that a higher dose of BAV may result in greater and irreversible damage to these organs.

Screening of the most common cardiometabolic diseases based on risk factor assessment among military personnel

Objective — to assess the prevalence of major cardiometabolic diseases by identifying their risk factors and comparing them with metabolic disorders and stress indicators in military personnel. Materials and methods. The study included 74 male military personnel with an average age of 43.4 [31.4; 50.6] years. Among all the participants, the proportion of individuals with hypertension (HTN) was 51.4%, with dyslipidemia (DLP) — 75.7%, with metabolic­associated steatotic liver disease (MASLD) — 48.6%, and with overweight or obesity — 51.4%. The participants were divided into groups based on the number of cardiometabolic diseases: group 1 (comparison) consisted of military personnel without HTN, DLP, or MASLD (n=14, 18.9%), group 2 — personnel with 1—2 of the above­mentioned cardiometabolic diseases (n=32, 43.2%), and group 3 — military personnel with comorbid pathology, including HTN, DLP, and MASLD (n=28, 37.8%). All participants were assessed for anthropometric profile, traditional clinical and biochemical indicators. Stress indicators included dehydroepiandrosterone sulfate (DHEA­S), cortisol, and oxidative stress marker 8­OH­deoxyguanosine (8­OH­DG), which were measured in the blood using immunoassay methods. Results. Among military personnel with HTN, overweight/obesity was twice as common (p=0.003, χ2=9.110), MASLD was 3.3 times more frequent (p=0.0001, χ2=19.598), and DLP was 1.7 times more frequent (p=0.0001, χ2=15.418). Among military personnel with MASLD, overweight/obesity was observed three times more frequently (p=0.0001, χ2=19.598), and dyslipidemia was 1.6 times more common (p=0.0001, χ2=13.416). Personnel with more cardiometabolic diseases were significantly older (p=0.003). In group 3, 21.4% had a normal BMI, while in group 1, 28.6% were overweight or had obesity (p=0.001). The increase in the number of cardiometabolic diseases between groups was accompanied by a significant reduction in skeletal muscle percentage (p=0.039 for group 1 vs group 2; p=0.001 for group 1 vs group 3; p=0.001 for group 2 vs group 3). Military personnel in group 3 had significantly higher BMI, waist circumference (WC), total fat percentage, and lower skeletal muscle percentage compared to groups 1 and 2 (p=0.001 for all comparisons). The highest levels of aspartate aminotransferase (AST), alanine aminotransferase (ALT), uric acid (UA), and the lowest AST/ALT ratio were observed in group 3 compared to group 1 (p=0.002; p=0.0001; p=0.001; p=0.0001) and group 2 (p=0.0001; p=0.0001; p=0.0001; p=0.0001), respectively. Alkaline phosphatase levels were significantly lower in group 3 compared to group 1 (p=0.048). Lipid profile deterioration was observed with an increase in the number of cardiometabolic diseases: total cholesterol (TC), triglycerides (TG), very low­density lipoprotein cholesterol (VLDL­C), and low­density lipoprotein cholesterol (LDL­C) levels were significantly higher in group 3 compared to group 1 (p=0.0001; p=0.0001; p=0.0001; p=0.007) and group 2 (p=0.0001; p=0.024; p=0.002; p=0.005), respectively. In group 2, only TG (p=0.0001) and VLDL­C (p=0.0001) levels were higher compared to group 1. DHEA­S levels were significantly lower in group 3 compared to group 1 (p=0.019), but no differences in cortisol levels were found. 8­OH­DG levels were significantly lower in groups 2 (p=0.003) and 3 (p=0.019) compared to group 1. Correlation analysis revealed that stress hormone levels were inversely associated with WC (p=0.016), AST (p=0.004), ALT (p=0.021), total bilirubin (p=0.033), UA (p=0.002), glycated haemoglobin (HbA1с) (p=0.024), TC (p=0.002), TG (p=0.001), and VLDL­C (p=0.001). Conclusions. Cardiometabolic diseases are highly prevalent among military personnel, and comorbidity is a frequent phenomenon that contributes to a significant increase in cardiovascular risk and highlights the need for optimized preventive and therapeutic strategies. The increase in the number of cardiometabolic diseases is associated with older age, worsened anthropometric status, liver function tests, increased uric acid levels, and deteriorating lipid profile. DHEA­S can be considered a marker of chronic stress in individuals with cardiometabolic comorbidity. Monitoring and timely correction of WC, AST, ALT, total bilirubin, UA, HbA1с, TC, TG, and VLDL­C levels among military personnel are necessary, as these indicators are related to stress and can improve cardiometabolic disease prevention.

ROLE OF BIOCHEMICAL MARKERS AMONG COVID-19 PATIENTS AND THEIR ASSOCIATION WITH SEVERITY OF DISEASE

Objectives: The present study was aimed to evaluate the levels of biomarkers (D-dimer, Procalcitonin [PCT], lactate dehydrogenase [LDH], interleukin [IL]-6, and C-reactive protein [CRP]) among coronavirus disease 2019 (COVID-19) patients visiting/admitted in Government Medical College Jammu and analyze their association with the severity of disease. Methods: The study was conducted on 100 COVID-19-positive patients 18–75 years of age of either sex, visiting/admitted in Government Medical College Jammu, for a period of 6 months. The serum glucose levels, creatine phosphokinase, LDH, liver function tests, renal function tests, and various biochemical COVID-19 markers such as CRP, serum ferritin, IL-6, D-dimer, and PCT were analyzed. Results: In the present study, it was observed that when patients were divided according to the severity of disease, there was a significant difference in the mean levels of total bilirubin, serum sodium, serum potassium, D-dimer, SpO2, and duration of symptoms in a mild and severe group of patients, while there was no significant difference in the parameters such as IL-6, ferritin, CRP, PCT, LDH, and other routine biochemistry parameters. When a comparison was done between both the groups according to SpO2, only the mean levels of serum total bilirubin were significant. Conclusion: Thus, it is concluded that serum bilirubin was significantly elevated in mild, moderate, and severe groups of patients. Further research should be conducted to find some biomarkers which are specific to COVID-19 only.

Assessment of IV albumin and ringer lactate on the acute oral toxicity of acetylsalicylic acid in albino rats

BackgroundDespite the frequent inclusion of fluid therapy in the treatment of many conditions, there are limited studies available to provide an evidence-based specific recommendation for fluid therapy in acute drug toxicity. Salicylate toxicity is considered one of the common clinical problems. It is commonly associated with fatal complications and even can lead to death. The study was designed to investigate the effects of various IV fluid types as isotonic saline (NaCl 0.9%), Ringer lactate (RL), and albumin and their impact on acetyl salicylic acid (ASA) toxicity outcome in a rat model of acute salicylate toxicity.Sixty male Albino rats were divided into 10 groups of 6 rats each. The first four groups were the control, saline, RL, and albumin groups. The fifth group received two doses of ASA solution orally, and the next five groups were treated with IV fluids as follows: saline-ASA, RL-ASA, albumin-ASA, RL + albumin-ASA, and saline + albumin-ASA. Upon completion of the study, spirometry, arterial blood gas analysis (ABG), and serum liver and kidney function tests were done on all groups. Furthermore, quantitative real-time polymerase chain reaction (PCR) was used to assess interleukin-6 (IL6), nuclear factor kappa beta (NF-kβ), and beta-actin mRNA gene expression of histopathology and immunohistochemistry assessments were also performed on liver and kidney tissues.ResultsThe results revealed the ASA group showed marked deterioration across all the investigated parameters. The groups that received saline and RL showed improvements in the following: respiratory rates, ABG, liver and kidney function, and histopathological findings.The RL + albumin group did not show any improvements. The albumin group and the saline + albumin group showed variable responses, ranging from mild improvement to no improvement.ConclusionsThe saline and RL groups showed positive results; however, the RL + albumin group showed the worst outcomes. The inclusion of albumin did not appear to provide any extra benefits and produced varying results.

Liver ultrasound evaluation of acutely increased liver function tests of COVID-19 hospitalized patients.

The incidence of hepatic abnormalities has been notably higher following the coronavirus disease 2019 (COVID-19) infection, attributed to the virus's entry into cells via angiotensin-converting enzyme 2 (ACE2) surface expression. The gastrointestinal tract's significant ACE2 expression, alongside a lesser degree in the biliary epithelium, has been implicated in gastrointestinal symptoms and liver injury. The aim of this study was to determine whether specific ultrasonographic findings in the liver correlate with acute increases in liver function tests (LFTs) among hospitalized patients. A retrospective analysis was conducted on hospitalized COVID-19 patients at Hazem Mebaireek General Hospital in Qatar, from March 1, 2020, to June 30, 2020. The study focused on patients who experienced acute increases in LFTs, excluding those with chronic liver disease. Ultrasound imaging and patient records were reviewed to gather data. Out of 223 ultrasound studies of COVID-19 patients, 158 met the inclusion criteria. The majority were male, with a mean age of 47.76 ± 13.76 years. Ultrasound results showed 43.7% normal liver parenchyma, while 56.3% exhibited nonspecific abnormalities such as diffuse liver hyperechogenicity (39.2%), enlargement with diffuse hyperechogenicity (12.7%), and other findings (4.4%). The biliary tree was predominantly normal (96.2%), with 3.8% showing abnormalities, including intrahepatic (2.5%) and extrahepatic (1.3%) dilatation. Gallbladder evaluations were normal in 60.1% of cases, with 39.9% showing abnormalities like stones (6.3%), stones with sludge (13.3%), polyps (6.3%), wall thickening (1.9%), and other conditions (12%). A significant correlation was found between abnormal liver parenchyma findings and elevated levels of bilirubin (total and direct) and alkaline phosphatase, with p-values < 0.05. Only aspartate aminotransferase levels showed a significant correlation with biliary tree abnormalities. The most common ultrasonographic finding associated with acute increases in LFTs among hospitalized COVID-19 patients was diffuse liver hyperechogenicity, with or without enlargement. These findings suggest a nonspecific yet significant association with liver function anomalies in the context of COVID-19.

6898 A Case Report Of Drug-Induced Liver Injury Secondary To Sublingual Estradiol In A Transgender Woman

Abstract Disclosure: F. Manas: None. E. Davydov: None. A. Caines: None. K. Estrada: None. J.E. Shill: None. Drug-induced liver injury (DILI), the leading cause of acute liver failure in the United States, occurs in response to a medication or natural compound. Estrogens can lead to idiosyncratic DILI. According to LiverTox [livertox.nih.gov], estrogen has a likelihood score of A (highly likely) to cause DILI, whereas spironolactone has a likelihood score of D (rare). The current formulations of estrogens usually produce a mixed or cholestatic pattern of liver enzyme elevations, however very early, the ALT levels can be markedly elevated (5- to 20-fold). One can be asymptomatic. Often the liver injury resolves after removing the offending agent. We present a case of DILI with elevations of both alanine transferase (ALT) and aspartate transferase (AST), secondary to sublingual estradiol (E2). A 23-year-old transgender female presented for feminizing gender-affirming care. She was started on sublingual E2 2 mg once daily and spironolactone 100 mg orally twice daily. Approximately 14 weeks later, sublingual E2 was increased to 2 mg twice daily for a below-target E2 level, and spironolactone was decreased to 50 mg twice daily due to gas and nausea. Routine blood work three weeks later showed elevated liver function tests (LFTs) in a hepatocellular pattern with ALT of 216 IU/L (normal:&amp;lt;52IU/L), AST of 223 IU/L (normal:&amp;lt;35 IU/L), with normal total bilirubin and alkaline phosphatase. LFTs were normal six months prior. At the time of liver injury, she had consumed six alcoholic beverages in the previous fourteen days, and two doses of acetaminophen. She had no personal history of autoimmunity and no family history of liver disease. Acute hepatitis screen was normal. Abdominal US with liver Doppler was unremarkable. E2 and spironolactone were discontinued. Evaluation by hepatology lead to a diagnosis of DILI from sublingual E2, based on the temporal relationship between initiation of E2 and LFT elevation. Other potential causes of elevated LFTs were excluded. Although she reported alcohol use, the AST/ALT elevation was not in a classic 2:1 pattern. Three weeks after cessation of E2 and spironolactone, her LFTs normalized. Spironolactone was resumed along with E2 by patch, but due to skin-adherence issues she was transitioned to injectable E2 valerate. Her LFTs have remained normal since. This case illustrates a rare but potentially dangerous adverse event of DILI secondary to sublingual E2. Due to the low incidence of liver injury in various studies of individuals with gender incongruence on hormone therapy, current evidence does not support routine liver enzyme monitoring. Clinicians should be aware of the potential risk of liver injury and counsel patients accordingly. As in this case, patients may be successfully rechallenged with the offending DILI medication. Further studies on different formulations of hormone therapy and their effects on the liver would be beneficial in this unique population. Presentation: 6/2/2024

8481 A 32 Year Old Male With Recurrent Acute Pancreatits and Severe Hypertriglyceridemia: Importance of Considering Genetic Variants

Abstract Disclosure: M.F. Salazar Zelaya: None. J.D. Sibaja Jiménez: None. Background : Hypertriglyceridemia is a common medical scenario in daily practice, causing a variety of symptoms including recurrent episodes of acute pancreatits, which can be severe. Multiple genetic variants can lead to different spectrums of the disease. CLINICAL CASE: A 32 year old male police officer presented to our Endocrinology Outpatient Clinic with a history of long standing hypertriglyceridemia and six previous episodes of acute pancreatits, two in the last twelve months. Familiy history was negative for lipid disorders. The patient had adecuate adherence to diet and exercise as well to prescribed medications, which included Fenofibrate 250 mgs/day and Rosuvastatin 40 mgs/day. The patient denied consumption of alcoholic beverages. Recent abdominal ultrasound was reported without abnormalities. His lipid panel reported elevated triglycerides at 5831 mg/dl (n&amp;lt;150 mg/dl), Total Cholesterol normal at 147 (n&amp;lt;200 mg/dl), low HDL levels at 12 mg/dl (range 12-92 mg/dl) and direct LDL Cholesterol at 120 mg/dl. His TSH value was normal at 1.02 uUI/mL (range 0.55-4.78 uUI/mL). Creatinine level was normal at 0.81 mg/dl (range 0.7-1.3 mg/dl). Liver function tests were normal with AST level at 25 IU/L (range 13-39 IU/L) ALT levels at 22 IU/L (range 7-52 IU/L) and alcaline phosphatase at 62 IU/L (range 34-104 IU/L).His fasting glucose level were normal at 82 mg/dl (n&amp;lt;100 mg/dl). Due to a high Familial Chylomicronemia Syndrome clinical score (13 points) we proceeded with genetic analysis of this patient. Next Generation Sequencing for genes related with chylomicronemia (APOA5, APOC2, GPIHBP1,LMFI, LPL) was performed to determine gene sequence plus copy number variation.Two heterocigote variants were reported, both in the LPL gene. The first one: LPL (NM 000237.3) c.644&amp;gt;A;p.Gly215Glu heterozygous is a missense variant already reported in the literature, registered in ClinVar (ID 1522) and the Leiden Open Variation Database. This variant is classified as pathogenic according to criteria PS3, PM1, PP3, PP5 of the American College of Medical Genetics and Genomics. The second one: LPL (nm 000237.3): c.383C&amp;gt;A;p.Thr128Asn;heterozygous is also a missense variant which to the extent of our knowledge has previously been reported only once in the literature: ClinVar (ID 1520537). This variant is classified currently as of unknown clinical significance according to PM2 criteria. There is however and entry reported (PMID: 8778602) of another variant affecting the same codon (p.Thr128AIa) that is associated to chylomicronemia syndrome. Conclusion: In cases of severe hypertriglyceridemia, suspicion and determination of gene variants are of great importance nowadays as they could eventually guide treatment, given the availability in some countries (and currently pending FDA approval) of new pharmacological therapies such as apo C-III inhibitors. Presentation: 6/2/2024

6849 Insulin Edema in newly diagnosed T1DM Pediatric Patient

Abstract Disclosure: A. Ansar: None. K. McNerney: None. Background: Insulin edema is a rare complication of insulin therapy, especially in the pediatric populations. The pathogenesis is not fully understood but has been linked to Insulin’s role in renal sodium handling and vascular permeability. It has been seen with the initiation of insulin in newly diagnosed patients or the intensification of insulin therapy in those with poor glycemic control.Clinical Case: A previously healthy 12 year old girl presented to the ED with polyuria, polydipsia and fatigue. She was alert and oriented but had kussmaul breathing. She was tachycardic but all other vitals were appropriate. Lab work up showed that she was in DKA with pH 7.07 and bicarbonate 7 mmol/L. Her corrected sodium and electrolytes were normal. Her HbA1C was elevated at 11.7% (4.0-5.6%). Initial fluid resuscitation was performed with 20 mL/kg NS fluids. She was transferred to our Pediatric ICU and was started on the DKA protocol consisting of intravenous insulin infusion at 0.1 unit/kg per hour and 2-bags of dextrose and non-dextrose containing intravenous fluids. She was given a new diagnosis of Type 1 Diabetes. She was transitioned to subcutaneous insulin 22 hours later with multiple daily injections with insulin lispro and glargine, with total dose of insulin at 0.7 unit/kg per day. She was transferred to the general care floor and received diabetes education while in the hospital. On the fifth day after discharge, patient started complaining of leg tightness, puffiness around her eyes and generalized swelling of both feet. She returned to the ED, where she was found to be hemodynamically stable and normotensive with a blood pressure of 113/54 mmHg. Her weight had increased 8.8 kg from the weight at discharge. Her physical exam was notable facial and bilateral periorbital edema, abdominal distension, and 2+ bilateral non-pitting non-tender edema of both legs extending to her medial malleolus. Neurologic exam was performed which was unremarkable. Work up was performed to rule out other causes of edema, including a complete blood count, electrolytes, kidney and liver function tests, all of which were normal. She received 20 mg of furosemide and was instructed to perform fluid restriction to 1 L/m2/day and sodium restriction to &amp;lt;2 grams per day at home. She followed up in clinic 3 days after her ED visit where her weight had decreased by 4.2 kg and her edema had mostly resolved with only 1+ bilateral non-pitting edema. Her total dose of insulin remained at 0.7 unit/kg per day, with acceptable blood glucose levels at home. Her fluid restriction was discontinued and patient was instructed to follow up as usual, and she had no further edema in follow-up. Conclusion: This was a rare case of a newly diagnosed pediatric patient presenting with Insulin edema, which is essential for clinicians to recognize, so they can identify patients presenting with this uncommon side effect to rule out conditions that may present in a similar manner. Presentation: 6/2/2024

8243 Euglycemic Diabetic Ketoacidosis Unveiled: Delayed Presentation and Complications of SGLT-2 Inhibitor Therapy in a Multimorbid Patient - A Case Report

Abstract Disclosure: T. Amin: None. A.K. Bala: None. M.A. Jones: None. M.S. Akula: None. K. Chalasani: None. M. Patel: None. J. Cheng: None. Introduction: Normal serum glucose levels (&amp;lt;200 mg/dL) in euglycemic diabetic ketoacidosis (EDKA) can complicate the typical clinical presentation of diabetic ketoacidosis (DKA), posing a diagnostic challenge. SGLT-2 inhibitors, a class of antihyperglycemic drugs, have been rarely but significantly associated with EDKA. These inhibitors enhance renal glucose clearance by preventing glucose reabsorption via sodium-glucose cotransport. The increased renal clearance may contribute to the euglycemic picture, potentially leading to an underestimation of required insulin dosage, thereby precipitating ketoacidosis in EDKA. Although the mechanisms of EDKA are not fully understood, the association with SGLT-2 inhibitors is becoming increasingly evident. Case A 53-year-old male with a medical history of type 2 Diabetes Mellitus, coronary artery disease, chronic kidney disease, hyperlipidemia, was admitted to the trauma bay after a fall. Medications included empagliflozin, metformin, aspirin, amlodipine, spironolactone, and carvedilol. Upon presentation, he had a brief loss of consciousness, complained of headache and chest pain, and was found to have an epidural hematoma with regional brain compression on the CT head. Admission labs showed a blood glucose level of 172, an unremarkable anion gap, and normal renal and liver function tests. Due to traumatic brain injury, he was admitted to the ICU for neurological monitoring. Despite remaining neurologically stable, he developed hypoxia, necessitating intubation. After successful extubation, he exhibited worsening metabolic acidosis on the fourth day, with an elevated anion gap of 22 and a blood glucose level of 174. Arterial blood gas analysis revealed a pH of 7.3 (and elevated beta-hydroxybutyrate (&amp;gt;4), while lactic acid levels remained normal. Urine analysis showed elevated blood glucose (&amp;gt;1000) and ketones (&amp;gt;40). Home medications, metformin, and empagliflozin were appropriately withheld, but euglycemic DKA attributed to empagliflozin was diagnosed. Treatment included intravenous fluid resuscitation and insulin infusion, leading to resolution of acidosis and improved mentation within 24 hours. Conclusion: EDKA is a diagnosis of exclusion often overlooked in ICU patients due to diverse causes of high-anion gap metabolic acidosis. Typical cases occur while the patient is using the drug, often associated with triggers like illness, alcohol use, surgery, or starvation. SGLT2 inhibitors, such as empagliflozin, with a half-life of 12.4 hours, are expected to clear the bloodstream in about 48 hours, yet this case suggests an association with EDKA both during use and after drug cessation. This delayed presentation highlights additional risk considerations associated with SGLT2 inhibitors, guiding future clinical diagnoses of EDKA even several days post discontinuation. Presentation: 6/3/2024

5074 Licorice Root Supplement As A Cause Of Hypokalemic Hypertension

Abstract Disclosure: G. Gill: None. S.M. Harman: None. L.A. Robles: None. A 67-year-old female Veteran presented to an emergency room with a one-day history of high blood pressure, chest tightness, and exertional dyspnea. Her blood pressure was 162/90 mm Hg, pulse regular at 71 BPM, and pain level 5/10. She had a history of hypertension, stable on hydrochlorothiazide alone, hyperlipidemia, anxiety, and depression. Physical exam was benign. EKG revealed normal sinus rhythm at 60 BPM, normal axis, a prolonged QT interval of 510 ms, and no ST changes. Lab evaluation showed a low potassium of 2.4 mEq/L, sodium 145 mEq/L. Other lab measurements (CBC, liver function tests and cardiac enzymes) were within laboratory reference ranges. Medications included topiramate for migraine and over-the-counter supplements for constipation, “thyroid health,” and a topical “testosterone booster” prescribed by a non-allopathic practitioner. Her hypokalemia was attributed to hydrochlorothiazide and topiramate and both were discontinued. She was started on nifedipine for blood pressure control and 40 mEq/day of potassium for hypokalemia. Within 2 weeks of discharge, she presented again with elevated blood pressure and a plasma potassium of 4.0 mMol/L. Further history revealed that her constipation supplement consisted of licorice root (glycyrrhiza glabra) extract 900 mg per capsule, of which she took 3 to 4 capsules daily. The patient was advised to discontinue all supplements. Thyroid function tests were within normal limits. Due to a suspicion of hyperaldosteronism, the ED physician requested an abdominal CT scan which showed a 1 cm, -17.5 Hounsfield unit, right adrenal nodule. Also consistent with hyperaldosteronism, plasma renin activity (PRA) was suppressed at 0.07 ng/mL/hr. However, a serum aldosterone level was less than 1 ng/dL. Her 24-hour urinary metanephrines were normal and a 24-hour urine free cortisol was 31.6 mcg/dL. Morning plasma cortisol was 5.1 mcg/dL. A tentative diagnosis of licorice-induced hyperaldosteronism was made and the patient was treated with a taper of spironolactone. After discontinuing spironolactone, blood pressure was 116/70mmHg and serum potassium was 4.5 mMol/L with a PRA of 0.66 ng/mL/hr and serum aldosterone of &amp;lt;5.0 ng/dL. The syndrome of factitious hyperaldosteronism due to licorice consumption has been well described. The mechanism, inhibition of renal (type 2) 11-beta-hydroxysteroid dehydrogenase by glycyrrhizic acid, allowing cortisol to exercise its considerable mineralocorticoid action, is well understood. Most prior reports have been in patients habitually consuming licorice candy, usually imported, since conventional licorice sold in the U.S. is artificially flavored. Our report illustrates the importance of obtaining a history of use of over-the-counter supplements and assessing their ingredients and the fact that presence of an adrenal nodule and a low PRA does not always indicate endogenous hyperaldosteronism. Presentation: 6/2/2024

6570 Treatment of Cushing’s With Levoketoconazole: A Case Series

Abstract Disclosure: N. Chamorro-Pareja: None. M. Haines: None. L.E. Dichtel: Consulting Fee; Self; Lumos Pharma. Research Investigator; Self; Recordati, NovoNordisk, Perspectum Ltd, Lumos Pharma, Pfizer, Inc.. Stock Owner; Self; Marea Therapeutics. Other; Self; Third Rock Ventures. B.M. Biller: Consulting Fee; Self; Xeris Pharmaceuticals, Recordati Rare Diseases, Sparrow, Lundbeck. Background: Endogenous Cushing’s syndrome (CS) is a rare condition of excess cortisol secretion; the most common cause is a pituitary corticotroph tumor (Cushing’s disease [CD]). Medical treatment for CD is primarily used to control hypercortisolism in patients with persistent or recurrent disease after transsphenoidal surgery (TSS). Levoketoconazole (LKCZ), a steroidogenesis inhibitor, was FDA approved in January 2022 for CS treatment. This reports 3 cases of patients who were treated with LKCZ for recurrent CS. Clinical Cases: Case 1: 44-year-old (yo) male (M) with a history of CD with urinary free cortisol (UFC) &amp;gt;26x upper limit of normal (ULN) who was treated preoperatively with ketoconazole (KCZ) 1000 mg/day with UFC improved to 6x ULN. KCZ was discontinued at TSS, and he achieved remission post-operatively. He was lost to follow-up and re-presented after several years with worsening hypertension, muscle weakness, edema, and anxiety with UFC 28x ULN and a recurrent pituitary lesion on MRI. He declined repeat TSS and underwent radiation therapy (RT) and medical treatment. LKCZ was initiated at 150 mg twice daily (BID) and increased to 300 mg BID. At LKCZ 300 mg BID, he had a low UFC and mild nausea but an adequate serum morning cortisol (10.4 ug/dL, ref:6-18.4 ug/dL); LKCZ was reduced to 150 mg BID with resolution of symptoms (sxs) and normal UFC. Case 2: 56 yo M with a history of CD (UFC &amp;gt;3x ULN) who underwent 2 TSSs and RT over 10 years prior with eventual remission, but later recurred. Sxs included brain fog and mood disturbances. He achieved control with pasireotide but discontinued due to abnormal liver function tests. He was then treated with KCZ 400 mg/day but remained hypercortisolemic (LNSC 1.1x ULN) and was interested in trying a new medication, so was switched to LKCZ 150 mg BID with significant improvement of sxs and normalization of LNSC. Case 3: 54 yo F with presumed cyclic CD (negative whole-body and octreotide scans) with UFC 1.7x ULN and LNSC 3x ULN. TSS was performed with negative pathology; she had persistent hypercortisolemia and sxs including insomnia, fatigue, and mood disturbances. She was intolerant to and/or uncontrolled on 4 medications, including KCZ at 1000 mg/day that was discontinued due to a rash. She was started on LKCZ 150 mg BID and achieved normal LNSC and UFC after about 1 month. The drug was discontinued due to the development of a rash similar to that with KCZ. Conclusion: LKCZ is a new option for the treatment of CS in patients whose disease persists after TSS. These 3 patients had improvement of sxs and normalization of cortisol levels while on LKCZ, although one patient discontinued LKCZ due to a rash that was previously experienced with KCZ. The other two patients are being carefully monitored for liver function test elevation, QTc abnormalities and adrenal insufficiency with no issues to date. To our knowledge, this is the first case series of CS patients treated clinically with LKCZ. Presentation: 6/1/2024

8197 A Captivating Case Report of Teprotumumab Induced Hyperglycemic Hyperosmolar State

Abstract Disclosure: K.M. Tuna: None. J.P. Perdomo Rodriguez: None. Introduction: Teprotumumab, a monoclonal antibody targeting the IGF-1 receptor, is increasingly utilized for moderate to severe thyroid eye disease. Initial trials noted mild hyperglycemia in patients with diabetes, while recent trials revealed a significant elevation in Hemoglobin A1c (HbA1c) among those with diabetes or pre-diabetes post-infusion. Here, we discuss a case of a patient with diet-controlled diabetes who developed hyperglycemic hyperosmolar state (HHS) two months after Teprotumumab infusion. Case Presentation: A 43-year-old male, with class III obesity, obstructive sleep apnea, dyslipidemia, coronary artery disease, and diet-controlled diabetes (HbA1c 6.5%) presented with worsening proptosis, decreased color vision, severe visual field depression. Laboratory evaluation revealed elevated TSH (6.3 mIU/ml), normal free T4 (0.67 ng/dl, ref: 0.60-1.2 ng/dl), and undetectable Thyroid Stimulating Immunoglobulin (&amp;lt;0.1 IU/L). Blood cell count, renal and liver function tests were normal. Due to high clinical suspicion of thyroid eye disease, he was treated with timolol, dorzolamide, brimonidine, and methylprednisolone 1g daily for 3 days. Glycemic control was achieved with 30 units of daily insulin while on pulse steroids. On outpatient ophthalmology follow-up, Teprotumumab was initiated and he received 2 doses. Eight weeks later, the patient was hospitalized with altered mental status caused by HHS (glucose 617 mg/dl, serum osmolality 316 osm). HbA1c was found to be significantly increased to 12% and the patient required 150 units total daily insulin and metformin upon discharge. Of note, the patient did not have significant weight changes during this time. GAD, IA2, and Zinc Transporter-8 antibodies were obtained prior to discharge and results are pending. Discussion: The IGF-1 receptor, a partial homologue of the insulin receptor, plays a pivotal role in glucose homeostasis. Inhibiting this receptor can lead to hyperglycemia. Initial randomized controlled trials (RCTs) reported a 10% incidence of mild hyperglycemia. A recent RCT from a cohort of 42 patients demonstrated a 50% incidence of hyperglycemia, in which two-thirds of the patients remained in a dysglycemic state with one patient with pre-existing prediabetes developing diabetic ketoacidosis (DKA). Our patient mirrored this scenario with no identifiable confounding factors. Conclusion: Teprotumumab-induced hyperglycemia, though rare, can lead to life-threatening complications. Baseline glycemic assessment, identification of high-risk patients, and comprehensive discussions on risks and benefits are crucial before initiating therapy. Close monitoring, especially in those with prediabetes, is recommended. Patient education plays a pivotal role in early symptom recognition, averting delayed diagnoses, and subsequent hospitalization. Presentation: 6/3/2024

7302 Efficacy And Hepatotoxicity Of Ketoconazole In Cushing’s Syndrome

Abstract Disclosure: H. Elenius: None. R. McGlotten: None. S.T. Sharma: None. L.K. Nieman: None. Medical therapy (Rx) of Cushing’s Syndrome (CS) is complicated by variable efficacy, delays to treatment goal and adverse reactions. Ketoconazole (KTZ) use is limited by hepatotoxicity. We retrospectively reviewed records of 65 inpatients receiving KTZ for CS between 2004-2023 to assess efficacy and hepatotoxicity. 24-hour urinary free cortisol (UFC), AM serum cortisol (F), liver function tests (LFTs: alanine transaminase (ALT), aspartate aminotransferase (AST) and alkaline phosphatase (ALP)) and daily doses of KTZ were noted. Patients were excluded if they received other medical Rx for CS or strong CYP3A4 inducers/inhibitors; baseline (base) or endpoint F/LFTs were unavailable; or if they received KTZ within 4 days prior to base labs. 35 patients (pts) were evaluated for efficacy. Treatment success was defined as F ≤12 mcg/dL. 17 pts (49%) achieved goal F at a median of 3 days (1-11, IQR 2.5-5.5). Compared to uncontrolled pts, there was no difference in Rx duration, base UFC or F, or initial or final KTZ doses, including when adjusted for base UFC, F, weight or body surface area. The absolute and percent dose increases and the F level prompting an increase did not differ between groups. Pts who reached goal had fewer days (d) between dose increases than uncontrolled pts (median 2 vs 4 d, p=0.025). Of 19 pts on a stable KTZ dose for ≥3 d after an increase, mean F decreased from d 0 to d +1 (-19%, p=0.01), +3 (-38%, p=0.0001) and +4 (-25%, p=0.04). D +3 F decreased from d +1 (-14%, p=0.03) and +2 (-13%, p=0.03). After d+3 no further reduction was seen (but likely biased by subsequent dose changes or discharge after d +3). 37 pts were evaluated for toxicity during KTZ Rx. Of 3 pts with a base LFT ≥3 times upper limit of normal (3ULN), LFTs rose ≥30% in 1, improved to &amp;lt;3ULN in 1 and did not change in the last pt. Of 34 pts with base LFTs &amp;lt;3ULN, a ≥30% rise of ≥1 LFT was seen in 27. Of these, 10/27 had ≥1 LFT rise to ≥3ULN after a minimum cumulative dose of 3400 mg and at least 4 days of Rx. Compared to the other 24, these 10 pts had higher means of base AST (75 vs 54% of ULN, p=0.046), cumulative KTZ doses (10080 vs 4071 mg, p=0.0015), and daily KTZ doses (927 vs 650 mg, p=0.004). AST and ALT increased by ≥30% before ALP (AST vs ALP: 4 vs 6 d, p=0.08). After KTZ was stopped or reduced, LFTs reached &amp;lt;3ULN at a median of 3 days (1-10, IQR 1.5-8.5) in 9 pts; pt 10 improved by discharge. 15/27 with an LFT rise ≥30% continued the same KTZ dose; LFTs stayed ≤ULN in 8, rose to &amp;gt;ULN in 5 and improved from base &amp;gt;ULN to ≤ULN in 2. By the end of inpt KTZ Rx (median 6 d, range 1-27, IQR 4-9), 13 pts (35%) had ≥1 LFT rise from ≤ULN to &amp;gt;ULN, 4 (11%) had ≥1 LFT improve from &amp;gt;ULN to ≤ULN. 12 stayed &amp;gt;ULN (32%); 8 (22%) stayed ≤ULN. Our data supports raising KTZ doses every 72 hours for rapid control. Base AST correlates with liver toxicity risk and tends to rise before ALP. An LFT rise ≥30% is seen in most pts and should not prompt Rx cessation if &amp;lt;3ULN. KTZ improves LFTs in a minority of pts, likely from cortisol reduction. Presentation: 6/3/2024

8016 Resolution of Refractory Hypoglycemia Following Pancreatic Solitary Fibrous Tumor Resection

Abstract Disclosure: M.E. Horowitz: None. S. Stefan: None. Introduction: Solitary fibrous tumors (SFT) are exceptionally rare mesenchymal tumors, accounting for only 3.7% of all cases of soft-tissue sarcoma with an incidence of 0.35 cases per 100,000 persons per year. SFT may arise in various anatomical locations, approximately 30% occuring in the abdomen. SFT can manifest with paraneoplastic syndromes, with the most commonly described being non-islet cell hypoglycemia. We present a case of refractory hypoglycemia which resolved following the resection of a large pancreatic SFT. Clinical Case: A 75-year-old male with a history of hypertension presented from oncology clinic with hypoglycemia. Two weeks prior, a 26cm mass of the pancreatic head was identified after he presented to the hospital for one month of abdominal pain and distention, and biopsy of the mass confirmed an SFT. The patient complained of nighttime weakness, confusion, nausea, vomiting, and urinary incontinence for two nights prior to arrival. During this time, the patient had multiple fingersticks showing hypoglycemia below 70 mg/dL, the lowest at 37 mg/dL. On arrival, fingerstick glucose was 38 mg/dL and serum glucose was 27 mg/dL, with a c-peptide level of 0.28 ng/mL (1.00-4.00 ng/mL). Despite hypoglycemia, he was asymptomatic at the time of presentation, indicating hypoglycemia unawareness. Investigation into the cause of hypoglycemia included normal morning cortisol levels, normal thyroid function tests, and normal liver and renal function tests. Further assessment for paraneoplastic disease was conducted, revealing an IGF1 level of 36 ng/dL (5-34 ng/dL) and IGF2 241 ng/dL (267-616 ng/dL), with a ratio of IGF2:IGF1 of 6.7:1. He underwent surgical removal of the large abdominal mass with distal gastrectomy and Billroth-I reconstruction. Pathology was consistent with a 34cm retroperitoneal SFT, STAT6 positivity, and negative margins. Following surgery, the patient did not experience any further hypoglycemia or related symptoms, and glucose ranged 78-135 mg/dL through discharge. Clinical Lessons: Refractory hypoglycemia resulting from a tumor's production of IGF2 is a rare paraneoplastic syndrome known as Doege-Potter Syndrome. This syndrome is observed in fewer than 5% of patients with SFT. The first documented case of hypoglycemia in a patient with "fibrous sarcoma" dates back to 1930. To establish a diagnosis, a ratio of IGF2:IGF1 exceeding 3:1 is suggestive of tumor-mediated production, while a ratio exceeding 10:1 is considered diagnostic. A positive immunohistochemical stain for STAT6 confirms the diagnosis. Patients with these tumors should be routinely monitored for hypoglycemia and related symptoms. Presentation: 6/3/2024

8113 Thyroid Storm in a Patient with Thyroid Nodule on Anticoagulation

Abstract Disclosure: R. Kulkarni: None. S.S. Krishnasamy: None. N. Mon: None. R. Downs: None. Background: There are very few case reports related to hyperthyroidism due to anticoagulation use. We describe a case, of a less common cause of hyperthyroidism due to hemorrhagic thyroiditis in a patient on anticoagulation and history of metastatic colon cancer. Clinical case: A 67-year-old white male with PMH significant for colon cancer with liver metastasis s/p exploratory laparotomy with sigmoid colectomy, end-colostomy with Hartman's pouch creation, pre-diabetes, recent left IJ &amp; axillary vein thrombus on Eliquis, and thyroid nodule; presented with complaints of shortness of breath, difficulty swallowing and dizziness. Other symptoms included weight loss, complaints of heart racing and generalized body aches. The patient had a recent admission for similar complaints and was newly diagnosed with left IJ/axillary vein thrombus and expanding hemorrhagic thyroid nodule on imaging. He was discharged on anticoagulation for the DVT with 2 week follow up for elective thyroidectomy for goiter. The patient was admitted to the ICU for worsened respiratory status needing ventilatory support and pressor support. Physical findings on admission included jaundice, sinus tachycardia, lethargy with agitation. Initial labs showed TSH 0.02 uIU/mL, FT4 4.85 ng/dL and FT3 6.8 pg/mL, LFTs &amp;gt;500 U/L. Burch-Wartofsky Point Scale score was &amp;gt;60 suggestive of thyroid storm. Imaging with PET CT was concerning for thyroid enlargement with multiple nodules with increased uptake. Thyroid US was consistent with heterogenous gland with hemorrhagic nodules. Based on clinical history, physical findings, diagnostic labs, and imaging the patient was diagnosed with severe hyperthyroidism with thyroid storm secondary to hemorrhagic thyroid nodules in the setting of anticoagulation. The patient underwent thyroid artery angiogram with particle embolization of left inferior and right superior thyroid arteries. Endocrinology started the patient on methylprednisolone, cholestyramine and propranolol. Thionamide was held since the patient had abnormal liver function tests in the setting of shock liver. The patient’s thyroid function slowly improved on current regimen to TSH 0.05 uIU/mL, FT4 1.7 ng/Dl and FT3 4.1 pg/mL on day 3. At the family interdisciplinary meeting, due to guarded prognosis, family opted for comfort care, and the patient finally succumbed to multiple co-morbidities. Conclusion: The case presented discusses diagnosis and management of less common causes of hyperthyroidism and management of thyroid storm in liver dysfunction. The patient would have needed a thyroid biopsy at a later date to rule out colonic metastasis as a cause of hemorrhage if he had survived the thyroid storm and comorbid illnesses. Presentation: 6/3/2024