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Treatment of hepatiоanemia syndrome in dogs

The animals are mostly found combined internal pathology, which scientists joined in syndromes. Among the latter often 
appears anemic syndrome. This is due, primarily, to the metabolic organs: kidneys (they synthesized erythropoietin) and liver 
directly supervise and regulate state erytrotsytopoez. So scientists for anemia in kidney damage combined nefroanemic syn-
drome, and for liver disease in hepatoanemic. 
In  the  literature  there  are  reports  on  the  development  and  nefroanemic  hepatoanemic  syndrome  in  different  species. 
However, methods of correction hepatoanemic syndrome in dogs is not covered. Therefore chosen research topic is relevant. 
The aim of the work was not estimate in developing treatment regimes for dogs hepatoanemic syndrome nutritional origin 
using hepavikel and brovaferan-100. 
The study used dogs 2−8 years of age German Shepherd and Rottweiler breeds in which the survey found anemic con-
junctiva. In the blood of dogs - oligotsytemiya, oligohromemiya, hypoalbuminemia, AST and ALT hyperenzymemia. The 
animals were kept in cages. Feeding carried out twice a day using barley, wheat and oat groats and bone meal. There were no 
meat products in the diet of dogs. That dog diet is not balanced for nutrients. The animals were clinically examined, meas-
ured body temperature; determined fatness, constitution, temperament, body position. 
To study the effectiveness and hepavikelu brovaferanu 100 dogs were divided into two groups: experimental (n=7) and 
control (n=8). Dogs in experimental group used hepavikel (subcutaneously at a dose of 5 mL, three times at intervals of 5 
days) and brovaferan 100 (3 mL intramuscularly three times in 5 days). The animals in the control group suyiferrovit used in 
doses of 5 ml (intramuscular injection three times at intervals of 5 days). 
The general condition of dogs was satisfactory, normal body temperature (37,8−38,7 ° C), a lively temperament, natural 
posture, delicate constitution, dense, degree of muscle skeletal medium, anemic conjunctiva. In animals, from the experi-
mental group the average number of red blood cells was 4,8±0,15 Т/l. Oligotsytemiya found in 57,1% of dogs. In control 
dogs number of red averaged 5,4±0,24 Т/l. Oligotsytemiya found in 37,5% of dogs. 
The content of hemoglobin in dogs in both groups was low and 131,1±3,50 and 127,0 ± 2,95 g / l respectively. Oli-
gohromemiya found in 87,5 and 85,7% of dogs in control and experimental groups. Index "red" blood - МСН was 85,7% 
higher in experimental animals and in 37.5% of the control group. Obviously, increasing the МСН indicates the metabolism 
of cobalt, iron, cyanocobalamin, folic acid because their metabolism is dependent on the functional state of the liver. 
Hematocrit value of all dogs in the experimental group was low – 30−36 %. In dogs controls set low hematocrit value of 
75% of the animals. In dogs MСV both groups was within physiological fluctuations. Consequently, most dogs (60%) for 
hepatoanemic syndrome manifested normocytic anemia hyperchromic. 
For a more detailed assessment erytrotsytopoez determines the state transferrіnum-iron complex. Markert is, above all, 
the content of iron in the blood transfusion because it provides oxygen and carboacid in tissues. The content of iron in animal 
research 57,1 % and 75 % of the animals of the control groups was low. Hyposyderemiya in animals caused apparently by 
feeding cereal forages that have a large amount of phytic acid. Last inhibits the resorption and absorption of iron. TIBC (indi-
cates the amount of iron bound to transferrin) in dogs in the control group averaged 72,9±3,14 mmol/l in the experimental − 
62,3±2,93 mmol/l. That TIBC values did not differ from clinically healthy dogs (62,5−83,2 mmol/l) [], ferrum, and transfer-
rinum 
UIBC (evidence of unbound iron to transferrin pull) in the experimental group dogs to treatment averaged 37,8±2,78 
mmol/l. In control animals markers of iron values were higher (52,7±,42 mmol/l, p<0.05). In 87,5% of the animals UIBC 
index was greater than 50 mmol/l, which is evidence of the accumulation of toxic iron and transferrin low capacity of iron. 
The content of transferrin in dog serum of experimental and control groups was 2,78±0,130 and 3,26±0,140 g/l, respec-
tively, that is no different from the quantities clinically visual dogs. 
If the content of transferrin in the blood of dogs by hepatoanemic syndrome compared with healthy probably no different 
then its iron saturation within both groups had some differences. This is primarily the control group, as in 75% of dogs iron 
saturation was lower  minimum rate (33,3%), which obviously indicates a slow synthesis in hepatocytes,  which results in 
slowing the transport of iron to the marrow. 
In assessing the functional status of liver aminotransferases set hyperenzymemia AST and ALT in 57,1% of dogs as ex-
perimental and control groups. In dogs found hypoalbuminemia. It is found in all animals of both groups. In 42,9% of dogs 
and 57,1 experimental and control groups found low quantities of urea in blood serum. 
In the treatment improved the general condition of the animals from the 11th day. They appeared luster wool, 85,7% of 
dogs in the experimental group was conjunctiva from pale pink to pink color (in control only 37,5%). The body temperature 
in all dogs was normal (38,2−38,9 
o
C). 
Number of red blood cells and hemoglobin in animal experimental group increased by 28,6 and 21,3%, respectively 
(p <0,01) in control − no different from the values of the beginning of the experiment (p<0,5), although 50 % of the animals 
found an increase in hemoglobin 1,6−14,5 %. MCH in experimental animals 42,9% increased compared with initial values on 
10,4-12,3%. In the index fell 57,1% to physiological values − 21,6−24,7 pg. In control MCH different from the initial values. 
The value of hematocrit in dogs after treatment in experimental group increased by 23,3% (p <0.01). In dogs of the control 
group, this figure has not changed in comparison with the values to treatment. 
The content of iron in the blood serum of dogs after treatment in experimental group was 30,6±2,32 mmol/l, increased 
by 24,9% compared with initial values. In control animals the average iron content had only tended to increase (p <0.2). 
TIBC dogs in the experimental group after the proposed treatment regimes hepatoanemic syndrome tended to decline com-
pared with the values of the beginning of the experiment (p <0.2). A similar trend found in dogs of control group. 
An indication of the accumulation of free iron ions is UIBC that in animal experiments in comparison with the beginning 
of the experiment, decreased to 26,2±3,57 mmol/l (30,7 %; p <0,05); in control − had only a downward trend (p<0,2). Trans-
ferrin saturation percentage of iron in the experimental dogs after treatment increased by 14,9%, in control, this ratio has not 
changed significantly. 

After treatment of hepavikel brovaferanom 100 improved functional status of the liver. In particular, the animals of ex-
perimental  group  increased  albumin  content  in  serum  by  32.1%).  In  control  -  protein  content  changed.  AST  activity  de-
creased  by  32.8%  compared  with  the  values  before  treatment  (p<0,05).  ALT  activity  decreased  by  24%  and  averaged 
268,6±11,13 nkat/l, which is 28,8 % less than in dogs in the control group (p<0,05). 
Thus, the combined use of hepavikel brovaferan 100 to dogs for hepatoanemic syndrome have positive impact on ery-
trotsytopoez and functional status of hepatocytes. This is due to the presence of thiamine, pyridoxine (improves the body use 
of fatty acids, improves metabolism of bile acids through synthesis of taurine from cysteine and methionine), vitamin E (reg-
ulates  cellular  respiration,  carbohydrate  and  lipid  metabolism),  cyanocobalamin  (involved  in  the synthesis  of  methionine, 
acetate, deoxyribonucleotides, metabolism of nucleic acids and proteins). 
Key  words:  dogs,  hepatitis  anemic  syndrome  hepavikel,  suyiferrovit,  brovaferan  100,  hepatocytes,  erythrocytes, 
hemoglobin, hematocrit value, iron, TIBC, UIBC, factor transferrin saturation with iron, albumiy, urea, AST, ALT. 

1.  Levchenko  V.I. Polimorbidnist'  patologii'  u  vysokoproduktyvnyh  koriv  /  V.I.  Levchenko,  V.V.  Sahnjuk  //  Visnyk 
Bilocerkiv. derzh. agrar. un-tu: zb. nauk. prac'. – Bila Cerkva, 1997. – Vyp. 3, ch. 1. – S. 89–92. 
2. Golovaha V.I. Gepatorenal'nyj syndrom u sobak sluzhbovyh porid / V.I. Golovaha, O.A. Dykyj // Naukovi doslidzhennja v 
galuzi vet. medycyny: materialy mizhnar. nauk.-prakt. konf. molodyh vchenyh, 1– 2 kvit. 1997 r. – Harkiv, 1997. – S. 17–18. 
3. Kondrahin I.P. Izuchenie sochetannyh vnutrennih boleznej – prioritetnoe nauchnoe napravlenie / I.P. Kondrahin // 
Veterinarija. – 2005. – № 11. – S. 48–50. 
4. Sahnjuk V.V. Hvoroby vysokoi' produktyvnosti / V.V. Sahnjuk // Zdorov’ja tvaryn i liky, 2015. – S.17–19. 
5.  Metody  veterinarnoj  klinicheskoj  laboratornoj  diagnostiki:  spravochnik  /  I.P.  Kondrahin,  A.V.  Arhipov, 
V.I. Levchenko i dr.; pod red. I.P. Kondrahina. – M.: Kolos, 2004. – 520 s. 
6. Slivins'ka L.G. Nefrotychnyj syndrom pry hronichnij gematurii' velykoi' rogatoi' hudoby / L.G. Slivins'ka // Visnyk 
Sum. nac. agrar. un-tu: serija «Vet. medycyna». – Sumy, 2005. – Vyp. 1–2 (13–14). – S. 130–133. 
7.  Levchenko  V.I.  Nefro-  i  gepatoanemichnyj  syndromy  u  sobak  (rozpovsjudzhennja  i patogenez)  /  V.I.  Levchenko, 
V.P. Fasolja // Visnyk Bilocerkiv. derzh. agrar. un-tu: zb. nauk. prac'. – Bila Cerkva, 2008. – Vyp. 56. – S. 106–110. 
8.  Zminy  biohimichnogo  spektra  krovi  u  konej  za  latentnogo  perebigu  nefroanemichnogo  syndromu  /  [Piddub- 
njak O.V., Golovaha V.I., Vovkotrub N.V. ta in.] // Nauk. visnyk vet. medycyny: zb. nauk. prac'. – Bila Cerkva, 2009. – Vyp. 
2 (68). – S. 52–56.  
9. Golovaha V.I. Zminy pokaznykiv gemopoezu u kobyl z oznakamy gepatopatii' / V.I. Golovaha, O.V. Piddubnjak // 
Visnyk Bilocerkiv. derzh. agrar. un-tu: zb. nauk. prac'. – Bila Cerkva, 2007. – Vyp. 48. – S. 33–36. 
10. Anderson B.F. Hepatic iron metabolism / B.F. Anderson, D.M. Frazer // Semin. Liver Dis. – 2005. – Vol. 25, № 4. – 
P. 420–432. 
11. Cronic hepcidin induction causes hyposideremia and alters the pattern of cellular iron accumulation in hemochroma-
totic mice / [Viatte L., Nicolas G., Lou D-Q. et al.] // Blood. – 2006. −Vol. 107, № 7. – P. 2952–2958. 
12. Gans T. Iron imports IV. Hepcidin and regulation of body iron metabolism / T. Gans, E. Nemerh // Am. J. Physiol. 
Gastrointest. Liver Phisiol. – 2006. – Vol. 290. –P. 199−203.  
13. Gans T. Hepcidin-a key regulator of iron metabolism and mediator of anemia inflammation / T. Gans // Blood. – 
2003. – Vol. 102. – P. 783–788. 
14. Fleming R.E. The iron sensor: macrophage, hepatocyte, both / R.E. Fleming // Blood. – 2005. – Vol. 106, № 6. – 
P. 1893–1894. 
15. Anf'orova M.V. Zminy erytrocytopoezu u sobak z oznakamy gepatopatii' / M.V. Anf'orova // Nauk. visnyk L'viv. nac. un-tu 
vet. medycyny ta biotehnologij im. S.Z.Gzhyc'kogo. – L'viv, 2015. – Serija «Veterynarni nauky». – T. 17, № 2 (62). – S. 3–7.