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Panax Ginseng Induces Toxic Hepatitis and Acute Kidney Injury Jeong Ho Lee

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Letters to the Editor

www.cmj.ac.kr

https://doi.org/10.4068/cmj.2017.53.2.168

Chonnam Medical Journal, 2017 Chonnam Med J 2017;53:168-169

Corresponding Author:

Eun Hui Bae

Department of Internal Medicine, Chonnam National University Medical School, 42 Jebong-ro, Dong-gu, Gwangju 61469, Korea

Tel: +82-62-220-6503, Fax: +82-62-225-8578, E-mail: [email protected]

Article History:

Received February 9, 2017 Revised March 5, 2017 Accepted March 7, 2017 FIG. 1. Microscopic image shows interstitial mononuclear cell in- filtrate with edema (hematoxyline and eosin stain, magnification 200×).

Panax Ginseng Induces Toxic Hepatitis and Acute Kidney Injury

Jeong Ho Lee

1

, Jung Hwan Yoon

1

, Sung Sun Kim

2

, Seong Kwon Ma

1

, Soo Wan Kim

1

, and Eun Hui Bae

1,

*

Departments of 1Internal Medicine, 2Pathology, Chonnam National University Medical School, Gwangju, Korea

Ginseng is a slow-growing, perennial plant with fleshy roots, belonging to the genus Panax of the family Araliaceae.1 Ginseng is one of the most widely prescribed and intensively studied herbal medicines. Several studies have indicated benefits of ginseng in the treatment of renal damage2,3 and hepatotoxicity.4 However, acute kidney in- jury as an adverse effect has not been reported.

A 43-year-old woman who had consumed 3 roots of gin- seng with alcohol some days before, was transferred to our hospital because of general weakness, myalgia, and oligouria. She had been taking hypertension medication for 1 year, and had undergone surgery for early gastric can- cer 3 years ago. She was in an oliguric state (150 mL/day) when she was admitted to the other hospital, and therefore, massive hydration (3 L/day) was administered. However, it did not increase her urine output, and she was referred to our hospital. A blood test showed elevation of aspartate aminotransferase (AST, 5,241 IU/L [normal range, 10-37]), alanine transaminase (ALT, 721 IU/L [normal range, 10-37]), and lactate dehydrogenase, 1,560 IU/L (normal range, 218-472) levels. Blood urea nitrogen (BUN) and creatinine (Cr) levels were 41.0 mg/dL (normal range, 8-23) and 4.3 mg/dL (normal range, 0.5-1.3), respectively.

The fractional excretion of sodium into urine (FENa) was 6.6%. IgE levels increased to 921 IU/mL (normal range, 0-100). Complete blood count, white blood cell count was 5,500/mm3 (Neutrophil 4570/mm3, Lymphocyte 600/mm3, monocyte 280/mm3, basophil 10/mm3, and Eosinophil 90/mm3), hemoglobin was 11.3g/dL and platelet was 101,000/mm3. There was no eosinophilia when she stayed in hospital. On urinalysis, the color of urine was dark yellow. The pH was 8.5, protein 3+ (300 mg/dL), Red blood cell was 2+ (80/uL), white blood cell 3+ (500/uL). We diag- nosed acute kidney injury and toxic hepatitis due to gin- seng ingestion. She was administered hepatotonics and physiologic saline 80 mL/h. Her liver function improved, but oliguria, general oedema, and renal function (BUN 34.4 mg/dL, Cr 7.7 mg/dL) worsened the next day. We decided to perform haemodialysis and conducted a renal biopsy.

In the biopsy, we found interstitial mononuclear cell in- filtration and oedema, which were compatible with acute interstitial nephritis (Fig. 1). After 5 rounds of haemodial- ysis, oliguria and oedema also improved. She was dis- charged from the hospital when she showed normal AST and ALT levels (16 IU/L and 26 IU/L, respectively), im- proved renal function (BUN: 48.3 mg/dL, Cr: 3.4 mg/dL), and increased urine output (2,930 mL/day). She visited the outpatient clinic after a week. Her renal function test showed completely normal results (BUN: 17.5 mg/dL, Cr:

1.0 mg/dL). Although the pathogenesis of Panax gin- seng-induced toxic hepatitis and acute kidney injury re- mained unknown, several factors might be involved. The patient ingested ginseng with alcohol and she was dehydrated. It could be hypothesized that dehydration and alcohol consumption resulted in higher susceptibility to kidney and liver damage.

This is the first reported case of acute kidney injury asso- ciated with ingestion of ginseng. We emphasize that de-

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169

Jeong Ho Lee, et al

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/

by-nc/4.0) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

spite the known benefits of ginseng, it is necessary to ingest it in sufficiently hydrated condition, without concurrent consumption of harmful agents.

CONFLICT OF INTEREST STATEMENT None declared.

REFERENCES

1. Pace R, Martinelli EM, Sardone N, DE Combarieu E.

Metabolomic evaluation of ginsenosides distribution in Panax genus (Panax ginseng and Panax quinquefolius) using multi-

variate statistical analysis. Fitoterapia 2015;101:80-91.

2. Han MS, Han IH, Lee D, An JM, Kim SN, Shin MS, et al.

Beneficial effects of fermented black ginseng and its ginsenoside 20(S)-Rg3 against cisplatin-induced nephrotoxicity in LLC-PK1 cells. J Ginseng Res 2016;40:135-40.

3. Park JY, Choi P, Kim T, Ko H, Kim HK, Kang KS, et al. Protective effects of processed ginseng and its active ginsenosides on cispla- tin-induced nephrotoxicity: in vitro and in vivo studies. J Agric Food Chem 2015;63:5964-9.

4. Kim SJ, Choi HS, Cho HI, Jin YW, Lee EK, Ahn JY, et al.

Protective effect of wild ginseng cambial meristematic cells on d-galactosamine-induced hepatotoxicity in rats. J Ginseng Res 2015;39:376-83.

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