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研究生:陳聖怡
研究生(外文):Sheng-Yi Chen
論文名稱:兔出血熱病之病理生理學研究--血液學、血清生化學、電解質及甲型胎兒蛋白質之變化
論文名稱(外文):Pathophysiological Studies of Rabbit Hemorrhagic Disease: Changes in Hematology, Serum Chemistry, Electrolyte Balances and Alpha-fetoprotein Levels
指導教授:黃鴻堅
學位類別:博士
校院名稱:國立中興大學
系所名稱:獸醫學系暨研究所
學門:獸醫學門
學類:獸醫學類
論文種類:學術論文
論文出版年:2008
畢業學年度:96
語文別:英文
論文頁數:100
中文關鍵詞:兔出血熱病血液學血清生化學電解質甲型胎兒蛋白質
外文關鍵詞:Rabbit Hemorrhagic DiseaseHematologySerum ChemistryElectrolyte BalancesAlpha-fetoprotein
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兔出血熱病(rabbit hemorrhagic disease; RHD)屬於必須通報世界動物衛生組織的兔科疾病,本病最早於1984年在中國大陸爆發,隨後橫掃歐洲、中東及亞洲。台灣於1994年首次發生RHD疫情,當時由呂榮修博士藉由血清學檢查證實,其後數年內RHD重創整個台灣的養兔事業與生物製劑業。本試驗之研究目的是藉由詳細的血清生化變化與病理學檢查來了解與釐清兔出血熱病毒之致病機轉,同時找出最適合做為早期篩檢猛爆型肝炎病兔與病程監控之指標,供做後續研究之依據。
兔出血熱病主要引起急性致死的壞死性病毒性肝炎,2月齡以上的成兔於染病後36-72小時間即暴斃,其致死率高達85%。在第一個試驗中,15週齡的紐西蘭白兔經接種兔出血熱病毒(rabbit hemorrhagic disease virus; RHDV)後,血清中天門冬酸鹽轉氨酶(AST)、氨基丙酸轉氨酶(ALT)、乳酸鹽脫氫酶 (LDH)、加瑪麩氨基酸轉換酶(r-GT)及鹼磷酶(ALP)的上升均達極顯著水準(p<0.0001)。在配對血清(paired serum sampling)檢測方面,接種18小時後立即分別有95%、89%與61%的接種兔呈現血清中AST、ALT與LDH等漏出性酵素增加的現象。與平均正常值比較時發現,接種18小時後,血清中AST為正常值之16倍,ALT為正常值之4倍,而LDH則為正常值之1.3倍;而接種後42小時的值達最高點,其中AST為正常值之47倍,ALT為正常值之11倍,而LDH則為正常值之8倍。
不同於前述3種酵素,ALP一直到接種24小時後,才開始逐漸上升,顯著上升則在接種後第30小時開始出現。最大值(691.92 IU/L)出現在接種後第42小時,是平均正常值的5倍。r-GT的變化則更遲且更緩慢,顯著性的上升一直到接種後第36小時才出現;直到接種後第42小時,才有83%的接種兔出現血清r-GT檢測值高於正常值上限(14.4 IU/L)的情形,此時血清中之檢測值達其最高平均值(59.85±34.02IU/L),為平均正常值的7.8倍。而r-GT/ALT比,於接種後30小時內先呈下降趨勢,待36小時起方呈增加現象,但試驗期間所有的r-GT/ALT比值均低於正常值;這顯示接種後42小時內,血清中ALT與r-GT的增加主因肝細胞的損傷而非膽道阻塞所致。對死亡RHDV接種兔的肝臟進行病理學檢查發現,其病理變化隨著肝血清酵素的增加而加劇。這種種結果顯示血清中肝細胞酵素之持續上升代表RHDV的感染導致快速且嚴重之肝損害,而血清中呈對數性上升的AST及ALT則為預測RHD趨向猛爆性的最佳指標。
在測定血清中腎功能與電解質等相關成分的試驗中,血清中尿素氮(BUN)、肌酸酐(CREA)及鈉(Na+)的上升與低血糖的發展均達極顯著差異(p<0.0001);而鉀(K+)的上升亦達顯著差異(p<0.05)。有5隻兔子於血糖低於20 mg/dl後的2小時內死亡。血清中BUN與CREA的値與正常値相比較,其差異顯著性(p<0.05 vs. baseline)分別出現於接種後第36與42小時。雖然死亡兔子的BUN與CREA均較平均正常値高,但是3隻於58小時後犧牲的兔子其犧牲前最後一次採血之血清BUN與CREA之平均値均較前者更高。同樣的情形也出現在平均滲透壓(osmolality),死亡兔子的平均值顯著(p<0.05)低於存活超過58小時者。RHDV對腎功能的傷害由接種後36小時才開始逐漸上揚的BUN與CREA的表現可知,其功能不足的情形隨著病情的惡化逐漸加重;而血清中電解質的顯著變化,使胞外液滲透壓上升,擾亂體液的流動方向,進而導致細胞恆定的破壞。因此逃過急性猛爆期後的病兔,其腎功能的下降與電解質的不平衡仍是這些倖存者莫大的威脅。
隨著血清中AST、ALT和r-GT的顯著上升(p<0.0001),三酸酸甘油脂(triglyceride; TG)與膽固醇(cholesterol; CHOL)的升高也達顯著水準(ptriglyceride <0.0001,p cholesterol =0.0003),其中又以三酸酸甘油脂的上升速率呈對數性最為顯著。RHDV接種30小時後發生的高血脂(hyperlipidemia)現象顯示,RHDV的感染會損害脂肪代謝反應的運作。
RHDV接種後24小時起,血清甲型胎兒蛋白(Alpha-fetoprotein;AFP)的濃度也隨著AST、ALT、r-GT和ALP的顯著上升而逐漸攀升(P AFP=0.0082)。接種RHDV而死亡的兔子,死前最後一次AFP値的平均值,高達4.22± 1.61 ng/ml (n=6)。相關性統計分析(correlation analysis)的結果顯示AFP的變化與ALP變化的相關性高於r-GT,但與AST和ALT的變化的相關性卻未達顯著水準。這樣的結果顯示造成AFP上升的主因是隨著肝細胞漏出性酵素上升後,肝細胞嚴重壞死後所釋出。
綜合以上結果,RHDV首先引起大範圍的肝細胞壞死,而嚴重的低血糖導致急性期病兔的死亡。隨著病情的惡化,腎功能的運作、電解質的平衡及脂肪的代謝逐漸受到影響而威脅著病兔的存活。雖然再生指數AFP也隨後上升,但由於缺乏健康活細胞來因應再生以修補肝損害,病兔仍可能因隨後而來的全身性的功能衰竭而死亡。猛暴型肝病是以肝臟損害為中心所引起的全身性功能衰竭。因此,對於猛暴型病毒性肝炎治療期間病程的監控,除了例行的肝功能指數的檢測外,腎功能、電解質及脂肪代謝等指數之監控亦必須同等重視。
Rabbit hemorrhagic disease (RHD), a notifiable disease for OIE, was first reported in 1984 in China and dispersed into Europe, the Middle East and Asia. In Taiwan, RHD was first reported by Dr. Y. S. Lu by serological tests in 1994 and severely damaged the rabbit-raising industry and the bio-products industry in the following years. The purpose of this study is to use serum biochemistry tests along with histopathological examination to construct the pathogenesis of rabbit hemorrhagic disease virus (RHDV) as a useful index for medical treatment in fulminant viral hepatitis in human and animals.
RHD infection has been characterized as an acute fatal necrotic viral hepatitis in up to 85% adult (older than 2 months) rabbits died within 36 to 72 hours after infection. In the first study, after RHDV inoculation, highly significant elevations in serum aspartate aminotransferase (AST), alanine aminotransferase (ALT), lactate dehydrogenase (LDH), r-glutamyltransferase (r-GT) and alkaline phosphatase (ALP) (p<0.0001) were noted. In comparison with baseline values (pair serum comparison), rabbits with leakage enzymes elevated immediately at 18 HPI were 95%, 89% and 61% for AST, ALT and LDH, respectively. In comparisons with the means of baseline, the changes were about 16 times, 4 times and 1.3 times at 18 HPI for AST, ALT and LDH, respectively. The maximal values appeared at 42HPI, there were 47 times, 11 times and 8 times for AST, ALT and LDH, respectively.
Differently from parameters above, the ALP was not elevated until 24HPI. Significant increasing observed later at 30 HPI. The means peaked at 42 HPI with a value of 691.92 IU/ L which was about 5 times of the baseline mean. The elevation of r-GT was even more gradual and later by time proceeded, it significantly increased at 36 HPI in comparison with baseline value. The frequency distribution revealed that only 83% tested samples had values over the upper limit (14.4 IU/L) at 42HPI. The peak mean appeared at 42 HPI (59.85±34.02IU/L) which was 7.8 times of the base line mean. The r-GT /ALT ratios tended to decreasing from baseline to 30HPI and then increasing from 36HPI to 42HPI, but all mean ratios after infection were lower than baseline one. This indicated that the increase of serum ALT and r-GT were mainly from hepatocellular disease instead of biliary tract disease in the first 42 hours. Histopathological findings of the liver from the dead rabbits correlated well chronologically with the release of the liver enzymes into the serum. Our results suggested that profound changes in serum liver enzymes implicated the damage in liver is fast and severe, and the exponential elevations in AST and ALT would be a strong prediction of the fulminant consequence in RHD.
The investigation on the damage of renal function and electrolyte balance found after virus inoculation, serum blood urea nitrogen (BUN), creatinine (CREA) and sodium (Na+) were elevated to a highly significant level (p<0.0001), whereas serum potassium (K+) was moderately elevated to a significant level (p<0.05). Hypoglycemia developed highly significantly (p<0.0001). The rabbits would die within 2 hr when the glucose level was lower than 20 mg/dl (in 5 rabbits). Significant elevation in serum BUN and CREA (p<0.05 vs. baseline) appeared at 30 HPI and 36 HPI, respectively. Although the means of BUN and CREA were higher than the baseline in rabbits prior to death, the surviving 3 rabbits (survived over 58 HPI) had even higher means prior to sacrifice. The mean osmolality value of surviving rabbits was higher than the dead ones. The dying rabbits had significantly lower values than the surviving ones. Renal insufficiency progressed from 30 hr, as indicated by the increases in BUN and CREA; significant changes in electrolytes resulting in the increased osmolality of extracellular fluid that induced flow disturbance which consequently destroy the homeostasis in cells. Therefore, the later impairments in renal function and electrolyte balance following liver injury might be an important threat for rabbits which might have survived from acute fulminant hepatitis in RHD.
On the study of lipid metabolism, hyperlipidemia was observed (p triglyceride <0.0001, p cholesterol =0.0003) along with significant increases in serum AST, ALT and r-GT (p<0.0001) after RHDV inoculation. An exponential increase in serum triglyceride was also seen. Thus, the presence of hyperlipidemia (from 30 hours post-inoculation) in the infected rabbits points to impairment in lipid metabolism.
Serum alpha-fetoprotein (AFP) elevated significantly (p=0.0082) from 24 HPI together with significantly elevated AST, ALT, r-GT and ALP after RHDV inoculation. Rabbits that died tend to have high AFP values prior to death, the mean value being 4.22± 1.61 ng/ml (n=6). By correlation analysis, AFP significantly correlated more strongly to ALP than r-GT, but insignificantly with AST and ALT suggested that the elevation in AFP was later released from severer hepatic necrosis following the leakage of cytoplasmic enzymes.
In conclusion, the results above showed that RHDV mainly caused massively necrosis in liver first. The severe hypoglycemia caused the death of the rabbits in the acute phases. Following the progression of the disease, renal function, electrolyte balance and lipid metabolism were all impaired and threatened the life of the survivals. Although the AFP was elevated later, the lack of normal hepatocytes for regeneration could not save the infected rabbits from systemic failures. Fulminant liver disease is regarded as a group of systemic diseases with the main focus of illness in the liver. Therefore, the measurements of renal function, electrolytes balance, serum glucose level and lipid metabolism as well as liver functional parameters for monitoring the progression in a fulminant viral hepatitis as index for medical treatment are necessary.
CONTENTS
Content Page No.
Chinese Abstract(中文摘要) i
English Abstract(英文摘要) v
Contents(目錄) ix
Table Contents(表目錄) xi
Figure Contents(圖目錄) xii
Chapter I. INTRODUCTION 1
Chapter II. LITERATURE REVIEW 5
Chapter III. KINETICS OF THE SERUM LIVER ENZYMES IN RABBITS EXPERIMENTALLY INFECTED WITH RABBIT HEMORRHAGIC DISEASE VIRUS
Abstract 15
3.1 Introduction 16
3.2 Materials and Methods 17
3.3 Results 19
3.4 Discussion 21

Chapter IV. IMPAIRMENT OF RENAL FUNCTION AND ELECTROLYTE BALANCE IN RABBIT HEMORRHAGIC DISEASE
Abstract 36
4.1 Introduction 37
4.2 Materials and Methods 39
4.3 Results 41
4.4 Discussion 45

Chapter V. HYPERLIPIDEMIA IN RABBIT HEMORRHAIC DISEASE
Abstract 65
5.1 Introduction 65
5.2 Materials and Methods 66
5.3 Results 68
5.4 Discussion 69

Chapter VI. CHANGE IN SERUM ALPHA-FETOPROTEIN IN RABBITS EXPERIMENTALLY INFECTED WITH RABBIT HEMORRHAGIC DISEASE VIRUS
Abstract 75
6.1 Introduction 75
6.2 Materials and Methods 76
6.3 Results 79
6.4 Discussion 80

Chapter VII. CONCLUSION 86
Chapter VIII. REFERENCE 92
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