A Diagnostic Challenge: Uncovering Autoimmune Hepatitis Masked by Choledocholithiasis and Unsupervised Ivermectin Use

Abstract

Autoimmune hepatitis (AIH) is a chronic immune-mediated liver disease diagnosed by the clustering of compatible biochemical, serological, and histological features after exclusion of competing causes. Concurrent biliary obstruction or drug-induced injury can obscure the underlying autoimmune process and misdirect the initial diagnosis toward a purely obstructive or toxic cause.

A 65-year-old woman with a remote cholecystectomy presented with one week of painless jaundice, dark urine, fatigue, and pruritus on a background of a year of slowly progressive aminotransferase elevation. She had also completed an unprescribed two-week course of oral ivermectin shortly before presentation. Admission studies showed marked hepatocellular injury (aspartate aminotransferase (AST): 2,109 U/L, alanine aminotransferase (ALT): 1,652 U/L), conjugated hyperbilirubinemia (total bilirubin: 8.4 mg/dL), mildly elevated alkaline phosphatase (ALP) (253 U/L), hypergammaglobulinemia (globulin: 5 g/dL; subsequent immunoglobulin G (IgG): 2,925 mg/dL), and an international normalized ratio (INR) of 1.6. With a negative viral hepatitis panel, a normal acetaminophen level, and bland cross-sectional imaging, empiric intravenous corticosteroids were begun on hospital day 2. Aminotransferases and bilirubin fell briskly over the next 72 hours, before any mechanical relief of obstruction. Magnetic resonance cholangiopancreatography (MRCP) on hospital day 4 revealed a 7-mm common bile duct stone, extracted at endoscopic retrograde cholangiopancreatography on hospital day 5. Smooth muscle antibody (SMA) returned at a titer of ≥1:640, with negative antinuclear antibodies (ANA) and antimitochondrial antibodies (AMA), a profile consistent with type 1 AIH. By a simplified International Autoimmune Hepatitis Group (IAIHG) score of 6, the combination of high-titer SMA, markedly elevated IgG, and a corticosteroid response that preceded biliary decompression identified AIH as the most likely dominant driver of injury, with choledocholithiasis as a concurrent second insult and ivermectin as a possible contributor of indeterminate magnitude.

Obstructive imaging findings can anchor clinicians away from a concurrent, treatable autoimmune process, and a corticosteroid response that precedes mechanical decompression carries genuine diagnostic weight. Because histology was not obtained during the index admission, the relative contributions of the biliary stone and ivermectin cannot be fully excluded; long-term follow-up, including confirmatory biopsy and a structured trial of corticosteroid withdrawal, will clarify whether the disease is best classified as idiopathic AIH unmasked by concurrent insults or as a drug-related variant.

Introduction

Autoimmune hepatitis (AIH) is a chronic immune-mediated liver disease that affects all ages and ethnicities, with a female predominance and a clinical spectrum ranging from asymptomatic enzyme elevation to acute liver failure [1,2]. Its diagnosis rests on a constellation of supportive features: elevated aminotransferases, hypergammaglobulinemia with selective immunoglobulin G (IgG) elevation, characteristic autoantibodies (most often antinuclear antibodies (ANA) and smooth muscle antibodies (SMA)), interface hepatitis on biopsy, and exclusion of viral, hereditary, metabolic, cholestatic, and drug-induced disease [1-3]. In everyday practice, two of these carry the greatest diagnostic weight in an adult with hepatocellular injury and act as practical red flags: a high-titer SMA and an IgG more than roughly twice the upper limit of normal, either of which sharply raises the pre-test probability of AIH. The simplified 2008 International Autoimmune Hepatitis Group (IAIHG) criteria provide a practical bedside tool, with reported sensitivity of approximately 88% and specificity of 97% at a cutoff of 6 points [3]. The updated 2025 European Association for the Study of the Liver guidelines reaffirm this framework while removing prior recommendations to subclassify AIH by autoantibody profile and broadening the treatment-response assessment window [2].

In practice, this picture is often mimicked or masked, creating a triangular diagnostic problem of autoimmune, obstructive, and drug-related injury. AIH is itself under-recognized in older adults, in whom presentations are frequently insidious or atypical, and diagnosis is delayed [4]. Acute choledocholithiasis compounds the difficulty: it can drive aminotransferases above 1,000 U/L and closely mimic acute hepatitis, and the key trap is that severe hepatocellular injury does not exclude a biliary origin, nor does a demonstrated stone exclude a concurrent parenchymal process [5,6]. Drug-induced autoimmune-like hepatitis (DI-ALH) poses the mirror-image problem, as it is biochemically and histologically indistinguishable from idiopathic AIH at presentation and separated from it mainly by its course, and has been reported with more than 40 agents, including herbal and dietary supplements [7,8]. Ivermectin, historically considered hepatically benign, has occasionally been linked to drug-induced liver injury (DILI) and to corticosteroid-responsive autoimmune-like patterns, particularly with off-label and unsupervised use [9-11]. Its antiparasitic action on invertebrate glutamate-gated chloride channels is not itself hepatotoxic; the injury instead appears idiosyncratic and largely immune-mediated, which is what aligns it with the DI-ALH pattern, possibly with a dose-related component at supratherapeutic exposure.

We report a 65-year-old woman in whom AIH, choledocholithiasis, and recent unsupervised ivermectin exposure coincided. The case is instructive because the corticosteroid response preceded mechanical relief of biliary obstruction, the SMA returned at a titer of ≥1:640 with marked IgG elevation, and the overlapping findings initially anchored the clinical team toward a purely obstructive diagnosis.

Case presentation

A 65-year-old woman with a past medical history of arthritis, hypertension, hyperlipidemia, obesity, and remote laparoscopic cholecystectomy presented to an outside emergency department (ED) with one week of progressive painless jaundice, dark urine, light-colored stools, generalized pruritus, decreased appetite, and fatigue. She denied abdominal pain, fever, recent travel, alcohol or tobacco use, illicit drug use, herbal supplements, or prescribed medications other than over-the-counter cholecalciferol. Family history was notable only for cancer in her mother. She had no personal or family history of autoimmune or liver disease. In summary, the recognizable phenotype was an older woman with a year of mild, unexplained transaminitis who developed acute painless jaundice with marked hepatocellular injury (aspartate aminotransferase (AST) and alanine aminotransferase (ALT): >1,000 U/L), conjugated hyperbilirubinemia, hypergammaglobulinemia with high IgG, and a high-titer smooth muscle antibody, in the concurrent presence of a common bile duct stone and recent unsupervised ivermectin use.

Outpatient records disclosed a longstanding pattern of mildly elevated aminotransferases first noted roughly one year before presentation, attributed by her primary care physician to nonalcoholic fatty liver disease in the context of negative hepatitis A, B, and C serologies and an abdominal ultrasound performed four months prior demonstrating hepatic steatosis without intra- or extrahepatic biliary ductal dilation. She was referred to hepatology but did not establish care. Ambulatory testing five months prior to admission showed aspartate aminotransferase (AST) of 320 U/L, alanine aminotransferase (ALT) of 541 U/L, alkaline phosphatase (ALP) of 121 U/L, and total bilirubin of 0.8 mg/dL.

In the weeks preceding admission, the patient reported having self-administered an approximately two-week course of oral ivermectin, completed roughly one week before presentation. The exact dose, formulation, and source were undocumented, and no prescription was identified. She denied use of acetaminophen, nonsteroidal anti-inflammatory drugs, or other agents.

On arrival at the first ED, vital signs were stable. Physical examination showed scleral icterus and jaundiced skin without abdominal tenderness, hepatomegaly, ascites, or asterixis. Laboratory studies revealed AST of 2,109 U/L, ALT of 1,652 U/L, ALP of 253 U/L, total bilirubin of 8.4 mg/dL with direct fraction 6 mg/dL, total protein of 8.2 g/dL, albumin of 3.2 g/dL, globulin of 5 g/dL, prothrombin time of 18.1 seconds, international normalized ratio (INR) of 1.6, and activated partial thromboplastin time of 37.2 seconds (Table 1). The complete blood count, lipase, and basic metabolic panel were otherwise unremarkable. After discussion with the consulting gastroenterologist, the patient was transferred to a tertiary referral hospital.

Table 1. Laboratory study findings upon initial admission to the emergency department.

The combination of marked hepatocellular injury with only mildly elevated ALP and prominent hypergammaglobulinemia (reversed albumin-to-globulin ratio) is the bedside signature that should prompt consideration of an autoimmune process rather than uncomplicated obstruction.

AST: aspartate aminotransferase, ALT: alanine aminotransferase, ALP: alkaline phosphatase, A/G: albumin-to-globulin, INR: international normalized ratio, aPTT: activated partial thromboplastin time, CBC: complete blood count, BMP: basic metabolic panel

Parameter	Admission value	Reference range
AST	2,109 U/L	<35 U/L
ALT	1,652 U/L	8-37 U/L
ALP	253 U/L	37-135 U/L
Total bilirubin	8.4 mg/dL	0.3-1.2 mg/dL
Direct bilirubin	6 mg/dL	0.0-0.4 mg/dL
Total protein	8.2 g/dL	6.3-8.2 g/dL
Albumin	3.2 g/dL	3.5-4.9 g/dL
Globulin	5 g/dL	2.2-3.7 g/dL
Prothrombin time	18.1 seconds	11.0-13.5 seconds
INR	1.6	0.8-1.2
aPTT	37.2 seconds	25-35 seconds
CBC, lipase, BMP	Within normal limits	-

On arrival at the tertiary center, repeat testing showed AST of 1,993 U/L, ALT of 1,539 U/L, ALP of 268 U/L, and total bilirubin of 7.9 mg/dL with direct 5.7 mg/dL. The acute viral hepatitis panel was nonreactive, and serum acetaminophen was less than 3 µg/mL. Computed tomography of the abdomen and pelvis with intravenous contrast demonstrated mild intrahepatic and extrahepatic biliary dilation with a surgically absent gallbladder and no hepatic mass, pancreatic abnormality, or other acute finding.

The admitting differential included acute hepatocellular injury of viral, autoimmune, ischemic, or drug-induced origin and biliary obstruction from a retained or recurrent stone, malignancy, or stricture. Given the bland imaging, the absence of pain or fever, and the marked transaminitis disproportionate to the alkaline phosphatase elevation, the team prioritized a parenchymal process. Competing causes were excluded stepwise: viral hepatitis by a nonreactive A, B, and C panel, acetaminophen and other toxic injury by an undetectable acetaminophen level, and primary biliary cholangitis by a negative antimitochondrial antibody, while ischemic injury was unlikely given hemodynamic stability. This left an autoimmune parenchymal process as the leading diagnosis, with the retained stone regarded as a concurrent rather than sufficient explanation for the degree of hepatocellular injury. An autoimmune workup was sent (antinuclear antibody (ANA), smooth muscle antibody (SMA), antimitochondrial antibody (AMA), anti-liver-kidney microsome type 1 (anti-LKM-1), and quantitative immunoglobulin G (IgG)), and on hospital day 2, the patient was started on intravenous methylprednisolone 20 mg every 12 hours for empiric treatment of suspected autoimmune hepatitis (AIH).

The biochemical response was prompt. By hospital day 4, AST had fallen to 752 U/L, ALT to 1,095 U/L, ALP to 230 U/L, and total bilirubin to 3.6 mg/dL, representing roughly a 65% reduction in AST and a 57% reduction in total bilirubin within 72 hours of corticosteroid initiation, before any mechanical intervention on the biliary tree. ANA and AMA returned negative. Anti-LKM-1 IgG was within the normal range. Quantitative IgG, measured on hospital day 4, was markedly elevated at 2,925 mg/dL (reference: 700-1,400 mg/dL). Magnetic resonance cholangiopancreatography (MRCP), also performed on hospital day 4, disclosed a 7-mm filling defect in the common bile duct measuring 8 mm in caliber (Figure 1), with otherwise normal hepatic parenchyma. The longitudinal trajectory of the laboratory studies is shown in Figure 2 and detailed in Table 2.

Table 2. Longitudinal trajectory of liver-associated biochemical studies.

Laboratory values from outpatient baseline through hospital discharge. Methylprednisolone was initiated on HD2; ERCP was performed on HD5.

AST: aspartate aminotransferase, ALT: alanine aminotransferase, ALP: alkaline phosphatase, INR: international normalized ratio, HD: hospital day, PCP: primary care physician, DC: discharge, ERCP: endoscopic retrograde cholangiopancreatography

Parameter	Baseline (PCP)	HD1 (admit)	HD2	HD3	HD4	HD5 (pre-ERCP)	HD6 (DC)	Reference range
AST (U/L)	320	2,109	1,878	949	752	494	314	<35
ALT (U/L)	541	1,652	1,414	1,157	1,095	879	719	8-37
ALP (U/L)	121	253	238	238	230	188	159	37-135
Total bilirubin (mg/dL)	0.8	8.4	8.3	4.4	3.6	2.5	2.4	0.3-1.2
Direct bilirubin (mg/dL)	-	6.0	-	-	-	-	-	0.0-0.4
Albumin (g/dL)	4.0	3.2	2.6	2.7	2.7	2.3	2.2	3.5-4.9
Globulin (g/dL)	2.4	5.0	4.1	4.8	4.4	4.0	3.5	2.2-3.7
INR	-	1.6	-	-	-	-	-	0.8-1.2

Figure 1. MRCP demonstrating a 7-mm common bile duct stone.

Coronal heavily T2-weighted MRCP image obtained on hospital day 4. The orange arrow indicates a 7-mm filling defect within an 8-mm common bile duct, consistent with a stone. The hepatic parenchyma was otherwise unremarkable.

MRCP: magnetic resonance cholangiopancreatography

Figure 2. Trajectory of liver-associated biochemical studies from outpatient baseline through discharge.

The key teaching point is that aminotransferases and bilirubin fell substantially before decompression while ALP stayed nearly flat, a pattern that points to a corticosteroid-responsive hepatocellular process rather than a purely obstructive one. AST, ALT, and ALP are plotted on the primary axis (left); total bilirubin is plotted on a secondary axis (right, dashed line). Vertical reference lines indicate methylprednisolone initiation on HD 2 and ERCP on HD5. The 65% reduction in AST and 57% reduction in total bilirubin between HD1 and HD4 occurred prior to mechanical decompression of the biliary tree.

AST: aspartate aminotransferase, ALT: alanine aminotransferase, ALP: alkaline phosphatase, ERCP: endoscopic retrograde cholangiopancreatography, HD: hospital day

On hospital day 5, the patient underwent endoscopic ultrasound followed by endoscopic retrograde cholangiopancreatography (ERCP). Endoscopic ultrasound confirmed a stone within the common bile duct without pancreatic mass. ERCP was performed with first-pass cannulation of the major papilla, sphincterotomy, extraction of a 7- to 8-mm stone and biliary sludge from a dilated common bile duct (9-10 mm), and deployment of a 10-French by 7-cm plastic biliary stent across the papilla (Figure 3). There were no procedural complications.

Figure 3. ERCP fluoroscopy images before and after stone extraction and biliary stent placement.

Endoscopic retrograde cholangiopancreatography fluoroscopy images obtained on hospital day 5. (A) Pre-extraction view: contrast opacifies a dilated common bile duct (9-10 mm) with a discrete teardrop filling defect at the distal end, corresponding to the stone identified on prior MRCP. (B) Post-procedure view following sphincterotomy, stone extraction, and deployment of a 10-French by 7-cm plastic biliary stent across the papilla, with successful biliary decompression.

ERCP: endoscopic retrograde cholangiopancreatography, MRCP: magnetic resonance cholangiopancreatography

The serological capstone arrived on hospital day 6: SMA returned at a titer of ≥1:640, an order of magnitude above the 1:80 threshold the simplified International Autoimmune Hepatitis Group (IAIHG) criteria recognize as supportive of AIH and well into the range generally regarded as highly specific for type 1 disease [12,13]. Combined with polyclonal hypergammaglobulinemia (admission globulin: 5 g/dL with selective IgG elevation to 2,925 mg/dL), negative viral and competing autoimmune serologies, and the documented corticosteroid response, the diagnosis of AIH was strongly supported. Application of the simplified IAIHG criteria yields a score of 6 (Table 3), at the threshold for probable AIH even without a confirmatory biopsy.

Table 3. Application of the simplified IAIHG criteria.

Component scoring of the simplified IAIHG criteria as applied to the patient [3]. A total of ≥6 points indicates probable AIH; ≥7 indicates definite AIH. The patient’s score reaches the probable threshold without the additional 1-2 points that a compatible or typical biopsy would contribute.

ANA: antinuclear antibody, SMA: smooth muscle antibody, ULN: upper limit of normal, HAV: hepatitis A virus, HBsAg: hepatitis B surface antigen, anti-HBc: hepatitis B core antibody, anti-HCV: hepatitis C antibody, AIH: autoimmune hepatitis, IAIHG: International Autoimmune Hepatitis Group

Variable	Patient finding	Cutoff met	Points
ANA or SMA ≥ 1:40	SMA ≥ 1:640	≥1:80 (2 points)	2
IgG above ULN (700-1,400 mg/dL)	IgG: 2,925 mg/dL (>1.10× ULN)	>1.10× ULN (2 points)	2
Liver histology	Not performed during admission	-	0
Absence of viral hepatitis	HAV IgM, HBsAg, anti-HBc IgM, anti-HCV all nonreactive	Yes (2 points)	2
Total (cutoff ≥6 = probable AIH; ≥7 = definite AIH)	6

By the morning of hospital day 6, AST had fallen to 314 U/L, ALT to 719 U/L, ALP to 159 U/L, and total bilirubin to 2.4 mg/dL. Jaundice and pruritus had resolved. The patient was discharged on her preadmission cholecalciferol with planned outpatient gastroenterology follow-up in one week for stent removal and a hepatology referral for confirmatory liver biopsy and initiation of long-term immunosuppression.

Discussion

This case illustrates an occult but biochemically active AIH that was simultaneously masked and unmasked by a concurrent obstructing common bile duct stone, with recent unsupervised ivermectin use as an additional variable of uncertain weight. The central message is straightforward: although choledocholithiasis was present and could account for part of the enzyme elevation, the combination of very high-titer SMA, markedly elevated IgG, a year-long history of unexplained aminotransferase elevation, and a brisk corticosteroid response that preceded biliary decompression points to underlying AIH as the dominant process. By convention, AIH is divided into three serologic types: type 1 (ANA and/or SMA), type 2 (anti-LKM-1 and/or anti-LC1), and a historically described type 3 (anti-SLA/LP) [12]. The SMA-positive, ANA- and anti-LKM-1-negative profile in this patient places the disease firmly within type 1.

Disambiguating overlapping injuries

Acute choledocholithiasis can produce mixed laboratory profiles; in a meta-analysis of more than 1,300 patients, approximately 7.8% presented with AST or ALT greater than 1,000 U/L and roughly one-third (pooled frequency: 33.1%) with elevations greater than 500 U/L, which typically reverse rapidly after biliary decompression [5,6]. Quantitatively, the injury was unambiguously hepatocellular: the R factor at admission, calculated using the equation defined by Danan and Teschke as (ALT ÷ ULN) ÷ (ALP ÷ ULN), was (1,652/37) ÷ (253/135) ≈ 24, far above the value of 5 that defines a hepatocellular pattern and arguing against a predominantly cholestatic, stone-driven process [14]. Two features of the present case argued against a purely obstructive process. First is the temporal pattern: hepatocellular enzyme elevation had been documented roughly one year before admission, progressing from AST of 320 U/L and ALT of 541 U/L five months prior to AST of 2,109 and ALT of 1,652 U/L on admission, without pain, fever, or biliary dilation on the ultrasound four months prior. Second, the magnitude of the IgG elevation (2,925 mg/dL, more than twice the upper limit of normal) and the elevated globulin fraction (5 g/dL; albumin-to-globulin ratio: 0.7) are characteristic of an immune-mediated parenchymal process rather than uncomplicated choledocholithiasis [1,2].

Corticosteroid response preceding mechanical decompression

The most informative observation was the temporal sequence of treatment effects. Methylprednisolone was initiated on hospital day 2, whereas ERCP was not performed until hospital day 5; by hospital day 4, AST had fallen from 2,109 to 752 U/L (65% reduction) and total bilirubin from 8.4 to 3.6 mg/dL (57% reduction), while alkaline phosphatase moved slightly (253 to 230 U/L). Biliary obstruction can fluctuate, and spontaneous passage or partial decompression of a stone can transiently improve liver chemistries; however, the absence of marked pain, the bland cross-sectional imaging, and the magnitude and timing of improvement after corticosteroids together favor an inflammatory hepatocellular process as the principal contributor. Early aminotransferase response to corticosteroids has been proposed as a feature that helps distinguish immune-mediated injury from idiosyncratic DILI, with brisk improvement more characteristic of the former [15]; the response in our patient was consistent with AIH, although this inference remains probabilistic in the absence of histology, and a contribution from transient partial biliary decompression cannot be entirely excluded.

The same corticosteroid response that carried diagnostic weight also guided the treatment plan. First-line therapy for AIH pairs corticosteroid induction with a steroid-sparing agent for maintenance, classically azathioprine, with mycophenolate mofetil now also endorsed as a first-line maintenance alternative; budesonide is generally limited to non-cirrhotic patients and is no longer favored as initial therapy, and calcineurin inhibitors are reserved for refractory disease [1,2]. Current guidance advises deferring azathioprine until the serum bilirubin falls below 6 mg/dL so that drug-induced hepatotoxicity is not mistaken for treatment failure [2]. Accordingly, high-dose intravenous methylprednisolone was used for induction given the severity of presentation and the coagulopathy, and because the admission bilirubin was 8.4 mg/dL, the steroid-sparing agent was deferred to the outpatient setting once cholestasis resolved, with azathioprine planned as first-line maintenance and mycophenolate mofetil as the alternative.

Diagnostic weight of high-titer SMA and IgG elevation

SMA, particularly in the F-actin pattern, is detected in up to 85% of patients with type 1 AIH and is among the most specific conventional autoantibody markers, with pooled specificity near 92% [13]. Low-titer SMA (1:40 to 1:80) occurs in viral hepatitis, malignancy, and other conditions, but persistently elevated titers above 1:160 are considered highly suggestive of type 1 AIH [12,13]. Our patient’s titer of ≥1:640, together with an IgG more than twice the upper limit of normal in a non-cirrhotic patient with marked hepatocellular injury, is difficult to attribute to incidental autoimmunity from biliary obstruction or transient drug exposure and constitutes a specific serological signature [2,16].

Role of ivermectin

The patient’s self-administered two-week course of oral ivermectin, completed roughly one week before symptom onset, is best regarded as an extenuating factor that may have influenced the degree of enzyme elevation rather than as the primary driver. Because the dose, formulation, and source were undocumented, its contribution cannot be quantified. Ivermectin has historically been considered hepatically benign, but isolated reports describe severe hepatitis and, since its off-label promotion during the COVID-19 era, corticosteroid-responsive autoimmune-like injury and an increasing pharmacovigilance signal [9-11,17]. Drug-induced autoimmune-like hepatitis (DI-ALH) is biochemically and histologically indistinguishable from idiopathic AIH at presentation but characteristically does not relapse after withdrawal of the agent and a finite corticosteroid course, whereas idiopathic AIH typically relapses without ongoing immunosuppression [7,8]. More than 40 agents have been implicated in DI-ALH, most commonly nitrofurantoin, minocycline, methyldopa, hydralazine, and infliximab, along with statins, interferons, other anti-tumor necrosis factor agents, and herbal or dietary supplements [7,8]. In this patient, the year-long antecedent enzyme elevation predating any ivermectin exposure, the very high SMA titer, and the marked IgG elevation favor idiopathic AIH as the dominant process, with ivermectin and choledocholithiasis as concurrent contributors. Long-term follow-up will be definitive: sustained remission after a finite corticosteroid course would suggest a drug-related component, whereas relapse off immunosuppression would confirm idiopathic AIH.

Limitations

Several limitations are worth noting. A confirmatory liver biopsy was not performed during the index admission; biopsy was recommended but deferred at the patient’s preference. The simplified IAIHG score of 6 reaches the threshold for probable rather than definite AIH precisely because the histology variable is absent, and a compatible biopsy would both raise the score and help discriminate AIH from DI-ALH [3,18]. In addition, the undocumented ivermectin exposure precluded formal Roussel Uclaf Causality Assessment Method scoring [14], and the SMA was reported as a screening titer without sub-pattern characterization, which would have further refined specificity [13].

Conclusions

We describe a 65-year-old woman in whom a previously undiagnosed AIH was the most likely dominant contributor to an acute hepatitis unmasked in the setting of concurrent choledocholithiasis and recent unsupervised ivermectin use. The diagnostic key was the early and substantial corticosteroid response that preceded mechanical biliary decompression, supported by an SMA titer of ≥1:640, an IgG of 2,925 mg/dL, negative viral and competing autoimmune serologies, and a year-long antecedent history of unexplained enzyme elevation. The case highlights three practical points: biliary imaging findings should not anchor the differential away from a concurrent autoimmune process; the temporal trajectory of corticosteroid response carries diagnostic weight; and unsupervised ivermectin use warrants awareness as a possible contributor to hepatic injury, even when its precise role cannot be quantified. Long-term follow-up, including a confirmatory biopsy and a structured trial of corticosteroid withdrawal once remission is achieved, will clarify whether the disease is best classified as idiopathic AIH unmasked by concurrent insults or as a drug-related variant. Because no histology was obtained during the acute episode, the individual contributions of transient biliary obstruction and possible drug-related injury cannot be fully excluded or quantified, and the diagnosis rests on the probable AIH threshold pending confirmatory biopsy. In either case, the diagnostic logic that brought her to immunosuppression preserved hepatic function in a window where delay would likely have been costly.