Open Veterinary Journal, (2026), Vol. 16(4): 2385-2391

Case Report

10.5455/OVJ.2026.v16.i4.40

Successful management of recurrent feline hepatic lipidosis with equine placenta extract supplementation: A case report

Makoto Akiyoshi^1,2* and Masaharu Hisasue²

¹Akiyoshi Animal Clinic, Yamato City, Japan

²Laboratory of Small Animal Internal Medicine, Azabu University, Sagamihara City,Japan

*Corresponding Author: Makoto Akiyoshi. Akiyoshi Animal Clinic, Yamato City, Japan.
Email: makotoaoi1109 [at] yahoo.co.jp

Submitted: 18/11/2025 Revised: 27/02/2026 Accepted: 14/03/2026 Published: 30/04/2026

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ABSTRACT

Background: Hepatic lipidosis (HL) is a common and life-threatening hepatopathy in cats, for which novel therapeutic options remain limited.

Case Description: A 14-year-old neutered male Egyptian Mau cat presented with a 1-week history of anorexia, intermittent vomiting, and jaundice. Plasma biochemistry revealed markedly elevated levels of alanine aminotransferase (ALT: 7270 U/L), aspartate aminotransferase (AST: 2754 U/L), and total bilirubin (5.5 mg/dl). Histopathological examination revealed multifocal hepatocellular vacuolar degeneration and random hepatocellular necrosis, consistent with HL, potentially associated with chronic enteropathy and a suspected early neoplastic lymphoid process. Standard therapy with hepatoprotective agents and nutritional support led to limited improvement; therefore, 2 ml of equine placental extract (EPE; Japan Bio Products Co., Ltd., Japan) was administered orally once daily. The cat remained clinically stable with continued administration of EPE and ursodeoxycholic acid.

Conclusion: EPE may represent a potential novel adjunctive therapy for feline hepatic lipidosis and was temporally associated with biochemical improvement, indicating hepatocellular recovery and appetite restoration in this case.

Keywords: Cholangitis, Hepatocellular necrosis, Hepatocellular vacuolar degeneration, Lymphoplasmacytic enteritis, Small cell lymphoma.

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Introduction

In cats, the term “hepatic lipidosis” refers to a clinicopathological syndrome characterized by severe hepatic triglyceride accumulation associated with anorexia, whereas “hepatic steatosis” is used as a histopathological descriptor of lipid accumulation within hepatocytes. Feline hepatic lipidosis (HL) remains one of the most common causes of hepatic failure and icterus in cats, characterised by triglyceride accumulation within hepatocytes, leading to acute liver dysfunction (Center et al., 1993). Despite advances in supportive care, the mainstay of treatment—nutritional support and hepatoprotective drugs, such as ursodeoxycholic acid, S-adenosylmethionine, and silymarin—has remained unchanged. Mortality rates of 38%–45% have been reported, even with intensive therapy (Armstrong et al., 2009; Kuzi et al., 2017; Wallace et al., 2024).

Recently, placenta-derived biological extracts have attracted interest owing to their regenerative and hepatoprotective properties (Neo et al., 2009; Akiyoshi et al., 2017; Kakabadze et al., 2018). In vitro studies have demonstrated that placental extracts can induce the differentiation of bone marrow-derived cells into hepatocyte-like cells, suggesting a direct role in hepatic regeneration (Neo et al., 2009). Furthermore, in feline clinical settings, parenteral administration of placental extract has been reported to facilitate clinical recovery and normalization of elevated liver enzyme activities in cats with hepatic lipidosis, supporting its potential therapeutic relevance in vivo (Akiyoshi et al., 2017). In human medicine, placental extract promotes hepatocyte regeneration and accelerates recovery from hepatic failure (Kakabadze et al., 2018). Similarly, the equine placental extract (EPE) has demonstrated beneficial effects on canine immune-mediated and gastrointestinal disorders (Amano et al., 2022; Fukushima et al., 2022; Kotoku et al., 2023; Nakagaki et al., 2024). However, evidence for novel adjunctive therapies that can accelerate biochemical recovery and improve appetite in feline hepatic lipidosis remains scarce. Herein, we describe a case of acute hepatic lipidosis that showed clinical and biochemical improvement following EPE administration, suggesting its potential as a novel adjunctive hepatoprotective treatment in cats.

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Case Details

A 14-year-old neutered male Egyptian Mau cat presented with a 1-week history of reduced appetite, intermittent vomiting, and mild dehydration. The cat had been diagnosed with lymphoplasmacytic enteritis (LPE) and biliary sludge 6 years earlier and had remained clinically stable under long-term therapy with ursodeoxycholic acid [10 mg/kg, bis in die (BID)] and prednisolone [0.15 mg/kg, semel in die (SID)]. Routine blood tests and abdominal ultrasonography performed 1 month prior were unremarkable.

On day 1, the cat developed jaundice and mild dehydration (Fig. 1). A complete blood count revealed mild anaemia [packed cell volume (PCV): 27%] and leukocytosis (white blood cells: 23,940/μl). Serum biochemistry indicated marked hepatocellular injury [alanine aminotransferase (ALT): 7,270 U/l, aspartate aminotransferase (AST): 2,754 U/L] and hyperbilirubinemia [total bilirubin (T-Bil): 5.5 mg/dl, total bile acids (TBA): 88.8 μmol/l] (Table 1). Ultrasonography revealed diffuse hyperechogenic hepatic parenchyma, mildly thickened duodenal walls (4.5 mm), and accumulation of biliary sludge. Fine-needle aspiration cytology revealed HL (Fig. 1). Endoscopic examination, esophageal feeding tube placement, and surgical hepatic biopsy were performed under general anesthesia. Histopathological examination revealed multifocal hepatocellular vacuolar degeneration and random hepatocellular necrosis without inflammatory infiltration or hepatic lymphoma, compatible with hepatic lipidosis within the clinical context. Duodenal sections showed moderate LPE with small areas of intraepithelial lymphocytic infiltration. Immunohistochemistry for CD3, CD20, and granzyme B revealed focal anti-CD3-positive T-cell clusters, suggesting a possible early neoplastic process consistent with small cell T-cell lymphoma, although reactive lymphoid hyperplasia could not be completely excluded.

Table 1. Day 1 results of CBC and blood chemistry.

Fig. 1. Photomicrographs of cytological smears from hepatocytes obtained during the first episode of hepatic lipidosis. Hepatocytes show mild to moderate cytoplasmic vacuolar degeneration with variably sized clear vacuoles, consistent with lipid accumulation. Occasional hepatocytes exhibit cellular swelling and indistinct cytoplasmic borders, indicating hepatocellular injury. No significant infiltration of inflammatory cells was observed (Wright Giemsa stain, bar=20 µm, ×400).

Therefore, the cat was diagnosed with hepatic lipidosis, potentially associated with chronic enteropathy and suspected early neoplastic lymphoid process. Prednisolone was discontinued, and ursodeoxycholic acid (10 mg/kg/BID), silymarin (1 tablet/BID), monoammonium glycyrrhizinate–glycine–DL-methionine (1 tablet/day), and trepibutone (1 mg/kg/BID) were administered with enteral nutrition via the feeding tube. Despite temporary stabilization, bilirubin levels increased again on day 7. Oral equine placental extract (EPE; Japan Bio Products Co., Ltd.) was administered (2 ml/day/SID). By day 9, bilirubin normalized, and chlorambucil (2 mg/cat, three times weekly) with prednisolone (0.5 mg/kg/SID) was introduced. Liver enzymes decreased progressively, and by day 26, ALT, AST, ALP, and GGT levels were within reference intervals. EPE was discontinued on day 26 (Fig. 2). Vomiting and nausea resolved, duodenal wall thickness normalized, and prednisolone and chlorambucil doses were gradually tapered and stopped by days 61 and 82, respectively. However, there was no improvement in appetite; the cat was unable to feed independently, necessitating tube feeding for nutritional support.

Fig. 2. Clinical representation of the first episode of hepatic lipidosis in this case. The graph shows the transition between ALT and T-Bil.

On day 147, HL recurred after the accidental removal of the feeding tube, likely due to transient starvation. Biochemical analysis showed ALT 1,197 U/L, AST 220 U/L, and T-Bil 5.2 mg/dl (Table 2). Cytological examination revealed HL (Fig. 3). The feeding tube was reinserted, and EPE therapy (2 ml/SID) was resumed. On day 150, bilirubin normalized, EPE therapy was continued without termination, and voluntary appetite progressively improved, allowing for tube removal on day 200 (Fig. 4). Thereafter, the hepatoprotective agents were sequentially withdrawn, and the cat was maintained on ursodeoxycholic acid and EPE alone. On day 1,115, the cat remained clinically stable with normal hepatic values and no recurrence of HL.

Table 2. Day 147 results of CBC and blood chemistry.

Fig. 3. Photomicrographs of cytologic smears from the second episode of hepatic lipidosis recurrence. Hepatocytes exhibit multifocal cytoplasmic vacuolar degeneration with randomly distributed clear vacuoles. Compared with the first episode, vacuolar change appears similarly mild without diffuse massive lipid accumulation. These findings are compatible with cholestasis-associated vacuolar degeneration within the clinicopathological context of feline hepatic lipidosis. (Wright Giemsa stain, bar=20 µm, × 400).

Fig. 4. Clinical representation of the case’s second episode of hepatic lipidosis. The graph shows the transition between ALT and T-Bil.

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Discussion

This case report presents the first documented feline case in which oral EPE was temporally associated with rapid and sustained remission of hepatic lipidosis. The cat experienced two biochemically confirmed HL episodes: one potentially associated with a suspected early intestinal lymphoid neoplastic process and the other with idiopathic relapse. In both episodes, EPE administration was temporally associated with rapid normalization of bilirubin and liver enzymes, including ALT, AST, ALP, and GGT. The temporal relationship observed in both episodes raises the possibility that EPE contributed to the clinical course.

Feline hepatic lipidosis is characterized by triglyceride accumulation within hepatocytes, inducing severe metabolic and oxidative stress. Despite aggressive nutritional support, hepatic regeneration is often slow and incomplete, leading to prolonged hospitalization and frequent relapses (Center et al., 1993). Even with intensive care, mortality remains at 30%–45%, underscoring the need for adjunctive therapies that enhance hepatocellular recovery and accelerate functional restoration (Armstrong et al., 2009; Kuzi et al., 2017; Wallace et al., 2024).

Placenta-derived extracts, including EPE, contain a rich mixture of growth factors, peptides, cytokines, and amino acids with regenerative, antioxidant, and anti-inflammatory properties (Neo et al., 2009; Akiyoshi et al., 2017; Kakabadze et al., 2018). In humans, placenta extracts have been shown to promote hepatocyte proliferation and accelerate recovery from acute hepatic injury. In veterinary medicine, EPE has shown benefits in dogs with immune-mediated haemolytic anemia, protein-losing enteropathy, and corneal wounds (Fukushima et al., 2022; Kotoku et al., 2023; Nakagaki et al., 2024). Collectively, these studies suggest that placental extracts support hepatocellular recovery through multifactorial mechanisms beyond simple regeneration. However, in this cat, the histological features were atypical of classical hepatic lipidosis. The observed vacuolar changes were mild and randomly distributed, with isolated hepatocellular necrosis but without diffuse triglyceride accumulation, typical of HL. Furthermore, these histological findings may reflect vacuolar degeneration secondary to cholestasis, a consequence of inflammatory changes in the gallbladder or bile ducts. This alternative interpretation implies that the benefits of EPE may not arise solely from regenerative stimulation but also from its anti-inflammatory modulation of the biliary and intestinal microenvironments.

EPE’s reported components include hepatocyte growth factor, epidermal growth factor, and transforming growth factor-β, which can promote hepatocyte proliferation. Simultaneously, it contains bioactive molecules that reduce oxidative stress and inflammatory cytokine signalling, potentially mitigating cholestatic hepatocellular injury. Given the rapid biochemical recovery in this cat, within 2–3 days of EPE initiation, it is plausible that EPE’s anti-inflammatory and antioxidant properties, rather than de novo hepatocyte proliferation alone, played a major role in the early clinical improvement. These observations suggest that the clinical benefit of EPE in this case may be mediated predominantly through anti-inflammatory and antioxidative mechanisms affecting the hepatobiliary and enterohepatic axis, rather than through direct hepatocyte regeneration alone. This mechanism aligns with human and canine studies demonstrating that placental extracts attenuate cytokine release, stabilize cellular membranes, and improve microcirculatory flow within the hepatic tissue. In addition to its hepatic effects, EPE may also exert systemic anti-inflammatory effects on the biliary tract and intestinal mucosa. The cat’s pre-existing chronic enteropathy and biliary sludge suggested a chronic inflammatory state involving the enterohepatic axis. By modulating local inflammation in the duodenum and bile ducts, EPE may reduce secondary cholestatic stress on hepatocytes, thereby accelerating the normalization of liver enzymes and bilirubin levels. This hypothesis may explain why biochemical improvement preceded full nutritional recovery during both episodes.

Interestingly, a clear difference in appetite restoration was observed between the two HL episodes. During the first episode, EPE was administered for 26 days and was discontinued after biochemical normalisation. Although the hepatic parameters stabilized, spontaneous food intake did not recover, and tube feeding continued. In contrast, during the second episode, EPE was maintained long-term, and a gradual return of voluntary appetite was documented, ultimately permitting the removal of the feeding tube. This temporal relationship suggests a possible appetite-enhancing effect of EPE, potentially mediated by improved systemic inflammation or modulation of gut–liver–brain signalling. Although speculative, this observation warrants further investigation, as appetite stimulation is a key prognostic factor for feline HL recovery. Compared with standard supportive care alone, nutritional support and hepatoprotectant-EPE supplementation appeared to considerably shorten the recovery timeline. In cats with HL, bilirubin normalization often requires 2–4 weeks of aggressive therapy (Armstrong and Blanchard, 2009; Wallace et al., 2024). In the present case, normalisation occurred within 3 days of both episodes following EPE initiation, enabling earlier resumption of chemotherapy and improved overall clinical stability, although the individual contribution of EPE cannot be separated from concurrent therapies. These findings suggest EPE as an adjunct therapy during the critical early phase of HL to enhance the efficacy of conventional management. During long-term follow-up, no clinical progression of the suspected intestinal lymphoid process was observed. The cat remained clinically stable without gastrointestinal deterioration under low-intensity chemotherapy, suggesting that this lymphoid process remained indolent during the observation period.

This study has some limitations. First, the contribution of concurrent therapies, such as chlorambucil and prednisolone, to sustained remission cannot be completely excluded. Second, the histopathological findings may represent cholestatic vacuolar degeneration rather than true lipid accumulation, complicating the classification of this case as typical HL. Third, spontaneous fluctuations or delayed effects of the nutritional therapy cannot be ruled out. Despite these constraints, the consistent biochemical response to EPE during two independent episodes, along with its long-term clinical stability, provides meaningful support for its therapeutic potential. Furthermore, because the hepatic lipidosis in this case was considered secondary to chronic enteropathy and a suspected lymphoid process rather than typical idiopathic HL, extrapolation of these findings to the broader feline HL population should be made with caution. Future studies should investigate the dose–response relationships, safety, and molecular mechanisms of EPE in feline hepatopathies. Controlled clinical trials and mechanistic studies, particularly those examining inflammatory markers, oxidative stress indices, and appetite-regulating hormones, could clarify whether EPE’s benefits are primarily hepatocellular, anti-inflammatory, or metabolic. The interaction between EPE and the gut or biliary inflammation, as suggested in this case, is a potentially important therapeutic pathway for hepatic and intestinal diseases. To the best of our knowledge, this is the first feline case demonstrating a reproducible temporal association between EPE administration and biochemical improvement of hepatic lipidosis associated with equine placenta extract supplementation. This reproducibility, along with the observed appetite recovery and long-term stability, highlights EPE’s potential as a novel adjunct in feline hepatology.

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Conclusion

This case demonstrated that oral EPE supplementation is temporally associated with rapid biochemical recovery, improved appetite, and long-term stability in a cat with recurrent hepatic lipidosis. Although a reproducible dechallenge–rechallenge pattern was observed, causality cannot be definitively established because of concurrent supportive and immunomodulatory therapies. EPE may represent a promising adjunctive therapy for feline hepatopathies, including the atypical or cholestatic forms of hepatic lipidosis. However, controlled studies are required to clarify the therapeutic contribution of EPE.

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Acknowledgments

This study was conducted under a research writing contract commissioned by Japan Bio Products Co., Ltd. The authors express their gratitude to Japan Bio Products Co., Ltd., for their support in facilitating this study. The authors thank Midori Goto Asakawa for the diagnoses of histopathology. The authors thank Masami Akiyoshi and the animal care staff at the Akiyoshi Animal Clinic.

Conflicts of interest

Makoto Akiyoshi was contracted by the Japan Bio Products Co., Ltd., for the preparation of this manuscript. Masaharu Hisasue has an academic advisory agreement with Japan Bio Products Co., Ltd., but has received no financial compensation.

Funding

Japan Bio Products Co., Ltd., provided funding for the preparation of this manuscript under a contract with Makoto Akiyoshi. Masaharu Hisasue did not receive any financial support for this study.

Authors' contributions

MA conceived and designed the clinical study, analysed and interpreted the data, and wrote the manuscript. MH analysed and interpreted the data.

Data availability

All data were provided in the manuscript.

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References

Akiyoshi, M., Hisasue, M. and Akiyoshi, M. 2017. Human placenta extract therapy for feline hepatic lipidosis. J. Azabu Univ. 29, 5–10.

Amano, T., Ikeda, T., Yamaguchi, M., Kakehi, N., Hanada, K., Watanabe, T., Tahara, K. and Hirano, E. 2022. Equine placental extract supplement as a night barking remedy in dogs with cognitive dysfunction syndrome. Vet. Med. Sci. 8(5), 1887–1892.

Armstrong, P.J. and Blanchard, G. 2009. Hepatic lipidosis in cats. Vet. Clin. North Am. Small Anim. Pract. 39(3), 599–616.

Center, S.A., Crawford, M.A., Guida, L., Erb, H.N. and King, J. 1993. A retrospective study of 77 cats with severe hepatic lipidosis: 1975–1990. J. Vet. Intern. Med. 7(6), 349–359.

Fukusima, N., Kakehi, N., Tahara, K., Watanabe, T. and Hirano, E. 2022. Successful treatment of ascites accumulation and diarrhea associated with protein-losing enteropathy with oral equine placenta extract supplementation in a dog: a case report. Open. Vet. J. 12(5), 774–781.

Kakabadze, Z., Kakabadze, A., Chakhunashvili, D., Karalashvili, L., Berishvili, E., Sharma, Y. and Gupta, S. 2018. Decellularized human placenta supports hepatic tissue and allows rescue in acute liver failure. Hepatology 67(5), 1956–1969.

Kotoku, S., Tahara, K. and Hirano, E. 2023. Successful steroid tapering and partial treatment of suspected immune-mediated haemolytic anaemia in a dog with equine placenta extract supplementation: a case report. Open Vet. J. 13(5), 668–676.

Kuzi, S., Segev, G., Kedar, S., Yas, E. and Aroch, I. 2017. Prognostic markers in feline hepatic lipidosis: a retrospective study of 71 cats. Vet. Rec. 181(19), 512.

Nakagaki, T., Nakari, M., Tahara, K. and Hirano, E. 2024. Supplementation of equine placenta extract on corneal wound in two dogs: case report. Open Vet. J. 14(6), 1503–1508.

Neo, S., Ishikawa, T., Ogiwara, K., Kansaku, N., Nakamura, M., Watanabe, M., Hisasue, M., Tsuchiya, R. and Yamada, T. 2009. Canine bone marrow cells differentiate into hepatocyte-like cells and placental hydrolysate is a potential inducer. Res. Vet. Sci. 87(1), 1–6.

Wallace, O.P., Jablonski, S.A., Thomas, J.S., Bock, J.H. and Langlois, D.K. 2024. Association of time to start of enteral nutrition and outcome in cats with hepatic lipidosis. J. Vet. Intern. Med. 38(6), 3144–3152.