Arpita Bera1 and Chandan Lodh2
1M.V.Sc. Student, 2Professor, Department of Veterinary Medicine, Ethics and Jurisprudence, Faculty of
Veterinary Science & A.H., WBUAFS, Kolkata-700037, (W.B.) India.
[Received: 05.11.2018; Accepted: 27.5.2019]
{DOI 10.29005/IJCP.2019.11.1.005-010}

Cajanus cajan (Arhar pulse) is a legume crop. The present study was designed to show the efficacy of
methanol extract of leaves of Cajanus cajan as a hepatoprotective agent in dogs with chronic hepatic disorder. The
main clinical signs observed in dogs with liver disorders are diarrhoea, constipation, vomition, anorexia, jaundice,
polyuria, polydipsia, ascites, dehydration, pain on abdominal palpation and different colour of conjunctival mucous
membrane like pink, congested, pale, severely pale and icteric. Levels of mean values of Hb, PCV, TEC, total protein,
albumin, A/G ratio, glucose, cholesterol decreased when compared to healthy control group and parameters like AST,
ALT, ALP, BUN, creatinine and TLC increased significantly than healthy control group which significantly changed
after treatment with methanol extract of Cajanus cajan leaves along with conservative therapy.
Keywords: Antioxidant, Cajanus cajan, Dogs, Hepatic disorders, Jaundice, Polyuria, Polydipsia.

Hepatic affections in dog are associated with variable clinical signs and thus frequently observed in dog which poses
a challenge in accurate diagnosis and treatment. Hepatic disorder in dogs, either drug induced or sequelae to infectious diseases is sometimes encountered during pet animal practice. Early and accurate identification of hepatic disorders is important to improve the long term outcome. Cajanus cajan (L.) Millsp (Leguminosae)
also known as pigeon pea, congo pea, toor dal or Arahar dal. Leaf extract of pigeon pea has protective action against liver damage. Antioxidant properties of the leaves of pigeon pea due to their chemical constituents viz.
flavonoids and stilbenes. Keeping the above facts the present study was designed to evaluate the efficacy of Cajanus cajan methanol extract as adjunct therapy of hepatic disorder in dogs.

Materials and Methods
Clinical, haemato-biochemical and ultrasound examinations were undertaken in the dogs presented in the Teaching Veterinary Clinical Complex for diagnosis of hepatic disorder in dogs. The dogs presented with diarrhoea, constipation, vomition, anorexia, jaundice polyuria, polydipsia, ascites, dehydration, pain on abdominal palpation and colour changes of conjunctival mucous membrane were considered as clinical signs of liver disorder and such cases were selected for further investigation. About 3 ml of blood was collected from recurrent tarsal vein into
vials containing EDTA for haematology and 2 ml blood into vials containing sodium fluoride for blood glucose estimation. Another 5 ml of blood was drawn in a sterilized serum separating tube without any anticoagulant for biochemical estimation. Blood was centrifuged at 3000 rpm for 3-4 minutes to separate the plasma and stored the
plasma at -200C for further use. Haematological parameters viz. Haemoglobin (Hb), packed cell volume
(PCV), total erythrocyte count (TEC), total leukocyte count (TLC), differential leukocytic count (DLC) were estimated by using standard technique. The biochemical parameters viz. Total protein, ALT, AST, ALP, albumin, globulin, A/G ratio, bilirubin, BUN, creatinine, cholesterol and glucose were estimated in semi automatic analyzer
following protocols mentioned in the supplied kits. Liver disorders were also diagnosed with the help of radiography and ultrasonography. For radiographical examination the ailing dogs were restrained in dorsal recumbency
for ventro-dorsal view and left/right lateral recumbency for lateral view of the abdomen. Ultrasonographical examination was carried out by using standard technique with the help of Mindray machine using 5MHz transducer. A total number of 18 dogs aged between 3-7 years of different signalment were screened
and included in the therapeutic studies. The dogs were diagnosed as acute hepatitis and chronic hepatitis based on
haematobiochemical alterations, radiographical and ultrasonographical changes. The chronic hepatic animals were
divided into two groups namely Gr.C1 & Gr.C2 having six animals in each group. Gr.C1 treated with Inj. Dextrose10% @ 10-15 ml/Kg BW daily intravenously for 5 days, Tab Frusemide-Spironolactone @ 0.5 mg/Kg
BW daily for 14 days, Cap. Amoxicillin @ 10 mg/Kg BW thrice daily for 7 days, Followed by liver tonics, orally for 30 days, Astymin liquid @ 5ml bid for 30 days. Gr.C2 treated similarly as Gr.C1 along with methanol extract of Cajanus cajan leaves (100 mg/kg BW).

Results and Discussion
Out of 18 animals diarrhoea was observed in 12 (66.66%) animals, constipation was observed in 2(11.11%)animals and remaining 4(22.22%) animals had normal defecation status. Vomiting was seen in 7(38.89%) animals. Anorexia with weight loss was a predominant sign in 8(44.44%) animals. 6(33.33%) suffered from inappetance and 4(22.22%) dogs have normal appetite. Water intake was normal in most of the animals but there was signs of polydipsia in 3(16.67%) animals and polyuria in 2((11.11%) animals. Jaundice was seen in 6(33.33%) animals. Ascites was observed in 4(22.22%) dogs in which 1(5.55%) haveacute hepatitis and 3(16.67%) were having
chronic hepatitis. 3(16.67%) dogs have mild dehydration, 10(55.55%) dogs were moderately dehydrated, 3(16.67%) dogs were severely dehydrated and dehydration was not detected in rest of 2(11.11%) animals. Conjunctiva was pinkish in 2(11.11%) animals, congested in 1(5.55%) animals, pale in 5(27.78%) animals severely pale in
3(16.67%) animals and icteric in 7(38.89%) animals. Pain on abdominal palpation was observed in 8(44.44%) dogs. The clinical manifestations observed in the present investigation depicted in table-1.

Therapeutic efficacy will be assessed based on the clinical recovery and alteration of haematobiochemical parameters.

Assessment of clinical score in dogs given in table-2. After a week of treatment animals of both the groups showed clinical improvement in terms of reduced discoloration of mucous membrane, disappearance of clinical signs like vomition, diarrhoea and regaining the appetite. In the third week of treatment the animals showed moderately pink conjunctival mucous membrane, improvement of jaundice, ascites, polyuria, polydipsia. Improvement of jaundice was seen in Gr.C2 after four week of treatment and the animals showed total recovery and become alert and active.
Haematobiochemical studies (before treatment and after treatment) in dogs with hepatitis depicted in table-3.

Haematological findings in dogs with hepatic disorder revealed anaemia which showed fall in Hb, PCV and TEC in hepatic disorder in Gr.C1 and Gr.C2 (pre treatment) which improved after treatment. Decreased in Hb level may be due to increased degradation of erythrocytes which was attributed by increased transit time to spleen because of
reduced portal blood flow or increased fragility of erythrocytes due to elevated bile acid content as also reported by Rothuizen and Meyer (2000). Dogs with hepatic disorder showed neutrophilic leukocytosis in chronic liver disease of dogs might be due to an inflammatory response to acute phase stimulation and/or as a stress response. Serum biochemical analysis showed elevated hepatic enzymes ALT, AST and ALP level before treatment which
subsequently reduced after treatment (Table- 3). Aminotransferases are commonly elevated in hepatocellular disease, hepatitis, hepatic trauma, anaemia, toxaemia. The magnitude of elevation of ALT enzyme is roughly
proportional to the number of injured hepatocytes as also reported by Rothuizen and Meyer (2000). Elevation in ALP is subsequent to accelerate production stimulated by bile retention. Mean total bilirubin value in the affected dogs revealed significant elevation. Presence of hyperbilirubinaemia with equal amount of direct and indirect bilirubin as seen in icteric  dogs was an indicative of hepatocellular damage. Hyperbilirubinaemia was due to
disturbances of the balance between rate of production of bilirubin, metabolism and excretion of bilirubin. In the present study increased might be as a result of diminished excretion due to extensive hepatocytes damage or biliary obstruction or combination thereof. This finding is in agreement with the report of Vijayakumar et al. (2001).
Hypoproteinemia and hypoalbuminaemia was observed in the dogs with hepatic disorder (Table-3). Low serum protein and albumins could be attributed to decreased production from liver besides anorexia and inappetance.
Liver is the main site of synthesis and degradation of most of the proteins. Hyperglobulinemia in chronic liver disease as observed in present study could be due to increased synthesis of gamma globulin fraction associated with enhanced systemic immune reactivity against portal antigens or secondary to antibody production. The present findings are in agreement with Jacob and Swan (1995). There was a significant decrease in the plasma glucose level in the present study. Significant hypoglycaemia was observed in chronic hepatitis might be due to inappetance and anorexia complemented by malabsorption from intestine. Blood urea nitrogen (BUN) increased significantly in
chronic hepatitis and unsignificantly in acute hepatitis. Protein substrates produced from haemolysis require deamination and consequently lead to hyperammonaemia as also reported by Tantary et al. (2014). Creatinine increased significantly in dogs with chronic hepatitis as also mentioned by Elhiblu et al. (2015). There was  ignificant decrease in cholesterol level. Hypocholesterolemia may be attributed to decrease in synthesis or  bsorption from the gut or excessive conversion of cholesterol into bile acids as also reported by Hall

Cajanus cajan posses significant free radical scavenging property which confer potential cytoprotective activity against this marker enzyme in the serum which increase in hepatic disorder. Beside this it helps to maintain the structural integrity of the hepatocellular membrane. This further buttressed the assertion that natural antioxidant molecules impact stabilisation to cell membrane depending on their degree of intensity of free radical scavenging capability. In this way methanol extract of Cajanus cajan leaves prolonged the viability of the cell membrane against the damage by causative factors as also reported by Sarkar et al. (2013). The effect of Frusemide-Spironolactone against ascites in caninepopulation has also been reported with successful results of Varshney and Hoque (2002) and Saravanan et al. (2013). Diuretics remove excess amount of water from body system resulting the relief of portal venous pressure thus helping to regain the efficacy. Amoxicillin group of antibiotic has been used by many authors as it is considered as safest and good choice of antibiotic for hepatic disorder. A liver tonic containing Ursodeoxycholic acid derived originally from bile of black beer which later commercialised as a synthetic product used to treat cholangiohepatitis and competitively replaces endogenous bile acids that accumulate in
Cholestatis hepatic disorder and prevent the cell membrane damage, induction of apoptosis and necrosis of liver. It is also used as a powerful cholerectic agent to treat sludged bile and cholelithiasis as also mentioned by Pillai et al. (2009) and Bhardwaj et al. (2014). Astymin contained amino acid preparations which are known for its pathogenic and liver protective effect has been tried in dogs with hepatic disorder to assess its efficacy along with the combination of other drugs mentioned in groups. Methionine is a lipotropic agent contain in Astymin reduces fat accumulation in liver by increasing the mobilisation of hepatic lipids. Liver protection as well as abdominal fluid
retention was possible through this combination therapy. In the present investigation the drugs
like Inj. Dextrose10%, Tab. Frusemide- Spironolactone, Cap. Amoxicilin, Liver tonics (herbal preparation) and
(ursodeoxycholic acid), Astymin (amino acid preparation) and methanol extract of leaves of Cajanus cajan (Arahar dal) used and showed good clinical recovery in dogs with chronic hepatic disorder which were in agreement to
the reports of Saravanan et al. (2013); Tantary et al. (2014) and Bhardwaj et al. (2014).

Bhardwaj, R.K., Gupta, A.K., J.S. and Singh,  R. (2014). Diagnosis and treatment of cholangiohepatitis with ursodeoxycholic acid in a dog. Indian J. Canine Practice, 6(1): 13-15.

Elhiblu, M.A., Dua, K., Mohindroo, J., Mahajan, S.K., Sood, N.K. and Dhaliwal, P.S. (2015). Clinico haemato biochemical profile of dogs with liver cirrhosis. Veterinary World, 8(4): 487-491.

Hall, R.L. (1985). Laboratory evaluation of liver disease. Vet. Clin. North Am. Small Anim. Prac., 15(1): 3-19.

Jacob, L.S. and Swan, G.E. (1995). Supportive treatment of canine babesiosis. J. S. Afri. Vet. Assoc., 66(2): 95-105.

Pillai, U.N., Jabina, M.P., Pandian, S.J.V., Premni, E. and Baby, P.G. (2009). Ursodeoxycholic acid treatment of
cholangiohepatitis in a dog. Indian Vet. J., 86(5): 506-507.

Rothuizen, J. and Meyer, H.P. (2000). History, physical examination and signs of liver disease In: Text book of
veterinary internal medicine, Ettinger S.J. and Feldman E.C. (Eds.). 5th edn., W.B. Saunders Co, Philadelphia, U.S.A. Pp.1272-1276.

Saravanan, M., Sarma, K., Kumar, M., Mahendran, K. and Mondal, D.B. (2013). Therapeutic management of ascites in dogs. Indian Vet. J., 90(2): 110-111. Sarkar, R., Hazra, B. And Mandal, N. (2013). Anti oxidative protection against iron overload-induced liver damage in mice by Cajanus cajan (L.) Millsp. Leaf extract. Indian J. Exp. Biology, 51(2): 65-173. Tantary, H.A., Soodan, J.S., Chirag, S., Ansari, M.M., Kumar, Sandeep and Imtiyaz,
T. (2014). Diagnostic studies in dogs with hepatic disorders. Inter. J. Vet. Sci., 3(4): 210-215.

Varshney, J.P. and Hoque, M. (2002). Clinico-pathological and ultrasonographic observations in canine  hepatopathies. Ind. J. Anim. Sci., 72: 423 427.

Vijayakumar, G., Thirunavukkarasu, P.S. and Subramanian, M. (2001). Cholecystitis in a dog –ultrasonographic diagnosis. Indian Vet. J., 78: 840-841.

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