Table 2.

Suspected TB DILI characteristics.

Pat. N	Symptoms	Jaundice	Management AE	AST U/L	ALT U/L	ALP U/L	Severity Grading WHO	RUCAM Value	Pattern	DILI Causality Assessment	Hystology Findings	4 DILI-Favoring Features	Diagnosis
1	fatigue, nausea, lost of appetite	no	suspension	316	749	156	4	12.5	hepatocellular	3, possible	Mild necroinflammatory activity, and portal fibrosis (Ishak Grade 5 and Stage 2)	2	Chronic viral hepatitis HCV correlated
2	fatigue, nausea, lost of appetite	no	suspension	287	403	271	3	8.4	hepatocellular	4, possible	Portal tracts enlarged due to edema and fibrosis and containing inflammatory infiltrate of mild/moderate density, consisting mainly of lymphocytes, sometimes aggregated to form follicles, more than occasional plasma cells and some PASD+ macrophages. This inflammatory infiltrate sometimes surrounds the native bile duct with phenomena of lymphocytic cholangitis. The interlobular bile ducts demonstrate features of cholangiocyte senescence. In the acinar site there is an inflammatory intracinar lymphomonocytic infiltrate with spotty necrosis, some apoptotic bodies and hypertrophy of Küppfer cells with PASD+ pigment. Some areas appear regenerative in appearance. (Ishak Grade 9 Stage 4).	3	Chronic viral hepatitis, HCV correlated
3	fatigue, nausea, lost of appetite	no	suspension	137	407	139	3	12.5	hepatocellular	1, unlikely	Portal tracts containing minimal inflammatory lymphocytic infiltrate with some PASD+ macrophages and occasional neutrophilic granulocytes. Interlobular bile ducts always visible. Diffuse steatosis with large and medium-sized vesicles is observed in the parenchymal area, greater than 66%. There is a mixed inflammatory infiltrate with foci of mediational and perivenular necrosis (spotty) and some lipogranulomas. Küppfer cells appear hypertrophic and contain PASD+ pigment. Iron deposit of the type with weak and diffuse staining (ferritin) of the type and of the small granule type at the level of the hepatocytes in zones 1 and 2 and of the non-confluent granule type at the level of the Küppfer cells. Minimal increase in collagen density in some portal tracts.	0	Non-alcoholic steatohepatitis (nash). Secondary iron overload
4	fatigue, nausea, lost of appetite	no	suspension	440	426	152	3	8.4	hepatocellular	8, probable	inflammatory infiltrate consisting mainly of lymphocytes with some plasma cells neutrophils granulocytes and PASD+ macrophages. In the lobular area, the inflammatory lymphomonocytic infiltrate is moderate with spotty necrosis, sometimes confluent; in the lumen of the sinusoids the resident macrophages are hypertrophic/hyperplastic and several stellate cells (HSC) are also evident.	4	TB-DILI (acute)
5	fatigue, nausea, lost of appetite	yes	suspension	2134	1180	542	4	11.6	hepatocellular	4, possible	Inflammatory infiltrate of mild to moderate density consisting predominantly of lymphocytes that shows no propensity to pass the lamina. In the parenchymal site various aspects of hepatocellular suffering are observed associated with pictures of dysarray of the acinus and lymphohistiocytic infiltration with the participation of neutrophils. Sinusoids reduced in amplitude also due to the presence of numerous macrophages. Mono- and polymorphonuclear inflammatory cells are dispersed in the sinusoids.	3	TB DILI (acute)
6	fatigue, nausea, lost of appetite	no	suspension	472	480	161	3	8.2	hepatocellular	4, possible	Portal spaces containing mild inflammatory infiltrate consisting of lymphocytes, PASD+ macrophages, and occasional eosinophilic granulocytes. Minimal and focal involvement of the portoparenchymal limiting plate. The bile ducts are visible in most of the portal tracts, and rarely any lymphocytes permeate the basement membrane. At the periportal level, some intermediate immunophenotype cells are observed. The ductular reaction is absent. Spotty necrosis foci are observed in the parenchyma with a prevalence of macrophages with PASD+ pigment, often grouped in clusters. Minimal portal fibrosis.	4	TB-DILI (partial resolution)
7	fatigue, nausea, lost of appetite	no	suspension	256	330	321	3	14.1	hepatocellular	5, possible	mild macrovesicular steatosis, focal microvesicular steatosis. With the aid of histochemical stains for the reticulum, PAS-D and Perls Iron staining, we also note: dilatation of the sinusoids with Küpffer cell hyperplasia with some inflammatory cells represented by lymphocytes and clusters of phagocytosing macrophages pigment partly referable to ceroid (PAS-D+) and partly refractive and slightly bluish with iron staining (Perls) as for hemosiderin. Mild biliary phenotype of perivenular and periportal hepatocytes is observed on immunohistochemical staining for cytokeratin 19. Mild perivenular and sinusoidal fibrosis	3	TB-DILI (partial resolution)
8	fatigue, nausea, lost of appetite	no	suspension	189	220	115	3	4.6	mixed	5, possible	needle bioptic fragments of liver with preserved structure characterized by mild inflammatory infiltrate of the portal spaces consisting of rare lymphocytes and rare macrophages with PAS-D+ pigment, minimal macrovacuolar steatosis (<5% of the liver parenchyma). Rare acidophilic bodies, focus of spotty necrosis. Rare glycogenated nuclei in the lobule. No iron deposits are observed. Fibrous expansion of some portal spaces (F0-F1 sec Metavir)	2	minimal non-specific hepatitis
9	fatigue, nausea, lost of appetite	no	suspension	152	270	469	3	1.2	cholestatic	8, probable	necrotizing granulomatous inflammation. A single bacillary formation ZN+ is found, which can be referred to an acid-fast bacillus	1	TB granulomatous hepatitis
10	fatigue, nausea, lost of appetite	no	suspension	98	298	100	3	16.9	hepatocellular	4, possible	mild and focal portal inflammatory infiltrate consisting of neutrophil granulocytes, eosinophils, PASD+ macrophages and rare lymphocytes. ductular proliferation spotty necrosis, hepatocyte rosettes	4	TB-DILI