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J Gastroenterol Dig Dis 2017 | Volume 2, Issue 3

World Gastroenterological &

Gastroenterology and Endoscopy

October 30-31, 2017 | Toronto, Canada

World Congress on

Phytotherapy-induced hepatocytotoxicity

Manuela Neuman, Yaacov Maor, Marius Braun, Ana Tobar, Ehud Melzer

and

Stephen Malnick

University of Toronto, Canada

Background & Aims:

Herbal medicine is frequently

integrated with conventional medicine. We report a case of

severe-herbal-induced liver injury (HILI) due to Herbalife tea

and protein-shake. We present both clinical and laboratory

evidence implicating an immune response leading to a

hypersensitivity reaction.

Methods:

A 65 year old lady was hospitalized due to

progressive jaundice and hepatocellular injury. 6 months

previously she noted lassitude and disturbed liver enzymes

were detected. Due to the appearance of deep jaundice

she was hospitalized. On repeated history ingestion of

Herbalife tea and protein-shake was noted. Liver biopsy

revealed necrotizing granulomatous hepatitis, apoptotic

cells. PAS diastase stain was showing cluster of foamy

macrophages with ceroid pigment, characteristic of toxicity.

Immunohistochemistry demonstrated and bile duct loss

(attached). Discontinuation of the Herbalife, and treatment

with both prednisone and urso-deoxycholic acid resulted

in slow resolution of her complaints (the ALT decreased

from 1096 U/L to 69U/L and the GGT decreased from 899

to 218 U/L, but relapsed on 10 mg daily of prednisone (ALT

increased to 246). Retreatment with both prednisone and

azathioprine resulted in remission (ALT 41 and GGT 49 U/L).

A lymphocyte toxicity assay (LTA) was performed. LTA %

toxicity was: protein alone 20; tea alone 44; protein+ tea 66.

The proinflammatory cytokines and chemokine (x control)

in serum were elevated as follow: TNF (tumor necrosis

factor alpha) x40; IL1 (interleukin) 12; IL6-x1.2; IL13-x3;

IL8-x5. Vascular endothelial growth factor was 5106 pg/

mL (x46). Mitochondrial markers M30 and M65 revealed

a predominant level of necrosis process versus apoptosis.

The severe HILI resulting from the protein and herbal tea is

consistent with a cholestatic picture. This is the first report

of the cytokine disturbances associated with HILI from the

combination of tea and shake protein (Herbalife). Moreover

this is a clear demonstration of hypersensitivity-induced

lymphocyte death linked to the same product combination.

Conclusions:

In susceptible individuals protein and herbal

tea might produce a strong T1 response leading to HILI. This

finding is consistent with the majority of reports of Herbalife

toxicity in the literature being due to the combination of

protein shake and tea consumption.

Speaker Biography

Manuela Neuman teaches clinical and experiment al toxicology and pharmacology

at the University of Toronto, Medical School, Canada. Dr. Neuman supervised

several

M.Sc

., and Ph.D. theses as well as post-doc fellows and research projects for

Medical Physicians. She is also in charge with Ph.D. international students (Cuba,

Israel, Romania, France, Australia, South Africa) as well with Pharmacy and Medicine

exchange

M.Sc

., international students from France and Medical fellows from Israel,

Brazil, Cuba, Romania and Argentina.She is the founder of the In Vitro Drug Safety

and Biotechnology. She is the head of In Vitro and of the biomarkers platforms at

the University of Toronto.The role of micro quantitative liver function based upon

mitochondrial activities; non-invasive biomarkers of fibrosis, inflammation and repair,

immuno-pharmaco-genetics are subject of her research. She also explores biomarkers

such as immuno-genomics and metabolomics as individual variation in personalized

medicine approaches. Neuman studies the role of microbiota in the development of

non-alcoholic liver disease as well as in severity of inflammation and its possible repair.

This includes translational research that characterize, obesity, non-alcoholic fatty liver

disease and non-alcoholic steatohepatitis. The recognition of the key role played by

lipotoxicity in cellular injury and stimulation of the inflammatory responses leading to

fibrogenesis is key for therapies.

e:

m_neuman@rogers.com