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�<I��vJi�Yzi�.x}[�������FURTHER INSIGHTS INTO THE CLINICAL ASPECTS OF ANGIOSTRONGYLUS VASORUM NATURAL INFECTION IN SYMPTOMATIC AND ASYMPTOMATIC DOGS 
Antonio Capognaa, Mariateresa Sasanellia, Riccardo Paolo Liab, Piera Paola Spagnoloa, Paola Paradiesa *


aDepartment of Emergency and Organ Transplantation (DETO), Faculty of Veterinary Medicine, Strada Provinciale per Casamassima Km 3, CAP 70010 Valenzano, Bari, Italy
bDepartment of Public Health and Animal Science (DISPEZ), Faculty of Veterinary Medicine, Strada Provinciale per Casamassima Km 3, CAP 70010 Valenzano, Bari, Italy


*	Corresponding author. Tel.: +39 0804679847; fax: 0039-80-4679889
	Email address:  HYPERLINK "mailto:paola.paradies@uniba.it" paola.paradies@uniba.it; pparadies@veterinaria.uniba.it (P. Paradies) HYPERLINK "mailto:" .
ABSTRACT
Canine angiostrongylosis is a cardiopulmonary disease emerging in Europe which can be fatal if left untreated. An early diagnosis and appropriate treatment is auspicable not only in symptomatic dogs because it may lead to a complete clinical resolution but also in asymptomatic dogs to reduce the risk of parasite importation in new areas suitable for parasite establishment. The aim of the present work is to investigate the different clinical and paraclinical findings in both symptomatic and asymptomatic dogs naturally infected by Angiostrongylus vasorum. Twelve dogs were included in the study. Diagnosis was made by means of larval morphological identification on faecal samples. Pathological paraclinical findings were registered both in symptomatic and asymptomatic dogs. In particular, the increase in ( globulin fraction at serum protein electrophoresis and radiographic alterations were reported as usefull findings to increase the suspicion of infection in asymptomatic dogs. 
KEY WORDS: angiostrongylosis, asymptomatic infection, dogs, clinical pictures, paraclinical findings.INTRODUCTION
Canine angiostrongylosis is an emerging disease whose expansion is probably due to climatic factors, to the presence of foxes in urban areas that have facilitated the spread of the parasite, or more simply, to more accurate diagnostic methods [1]. In Italy data on the prevalence of canine angiostrongylosis are scant [2], however recent cases [3-6] suggest a spread of the infection.
Despite the parasite Angiostrongylus vasorum defined the "great imitator" [7] is responsible for very different clinical pictures, it is generally associated with respiratory, neurological and coagulative disorders [1]. The severity of symptoms can greatly vary ranging from severe to asymptomatic forms [7]. The identification of asymptomatic dogs is an important task to reduce the risk of parasite importation in new areas suitable for parasite establishment [8].
Laboratory [9, 10], radiographic [11, 12], echocardiographic [13-15], and thoracic computer tomographic [16, 17] abnormalities are not-specific. The gold standard to achieve the diagnosis still remain the first-stage larvae (L1) detection using the Baermann technique in faecal samples preferably collected on three consecutive days despite serological and biomolecular tests have been recently developed [18]. As treatment milbemycin oxime and a combination of moxidectin with imidacloprid in a spot-on formulation (Im/Mox) are licensed while fenbendazole which is widely used in naturally infected dogs and appears to be effective is unlicensed [19].
It is known that the infections with A. vasorum are of great importance in veterinary medicine (potentially fatal if left untreated) thus any additional information that may provide clues to an early diagnosis may be of value. On this view the aim of the present work is to investigate the clinical and paraclinical changes of twelve naturally A. vasorum infected symptomatic and asymptomatic dogs. Furthermore the reverse to normal of clinical and paraclinical findings after therapy are reported when available.
MATERIALS AND METHODS 
Dogs were referred to the Clinical Unit of the Veterinary Faculty of Bari (Southern Italy). Diagnosis was reached by means of A. vasorum L1 detection in faecal samples on direct smears or using Baermann test; in one dog larvae were also found in pleural effusion (case 1). Identification was possible following the morphological and morphometric parameters [20]. Asymptomatic dogs were revealed because Baermann test was introduced as routin test during clinical practice. Dogs were also tested for Dirofilaria immitis infection resulting negative.
A blood sample was collected for haematology, blood coagulation profile, biochemical analysis and serum protein electrophoresis in all animals. Thoracic radiographs and echocardiography were performed. 
Specific therapy was administered choosing fenbendazole (Panacur, Intervet, Animal Health) and/or Im/Mox (Advocate spot-on, Bayer) according to the severity of symptoms. Fenbendazole was used in monotherapy as previously reported (50mg/kg, PO daily) [21] in case of severe clinical symptoms (i.e. dyspnea) while Im/Mox was used in monotherapy with three applications at 15 days interval in asymptomatic/paucisymptomatic (i.e. sporadic coughing) dogs or in combination with fenbendazole at 25mg/kg, PO, once a day.
According to owner availability clinical and paraclinical changes were monitored till normalization of clinical-pathological alteration and/or till the end of treatment.
The animals were be kept under their usual housing conditions, they were be handled and sampled with the owners� consent and with the approval of the Ethical Committee of the Faculty of Veterinary Medicine of the University of Bari.
RESULTS
Dogs described in this study (Table 1) were aged between nine months and 12 years. All dogs were from central-southern Italy and never moved from. Presenting complaint was heterogeneous (Table 1) and five cases were presented for routine control visit and one case for eye examination to investigate a long lasting reduction of visus. Thoracic auscultation was normal in seven cases, while in the other animals muffling of heart sounds (2/12), rales (3/12), wheezing (1/12), and loud bronchovescicular sounds(2/12) were detected (Table 1).
The complete blood count showed anemia (5/12), leukocytosis (4/5), eosinophilia (6/12) and basophilia (3/12) (Table 2). Serum protein electrophoresis showed a variable increase in � globulin fraction (Figure 1) in all animals except for two dogs (Table 2). The biochemical examination showed non-specific and non-uniform alterations but in four cases an increase in phospho-creatine kinase (CK) was found. Primary hemostasis disorders characterized by thrombocytopenia were detected in three cases, associated or not to alterations of clotting profile that were registered in 6 cases.
Thoracic radiographs showed pathological findings in both symptomatic and asymptomatic dogs except for one asymptomatic dog (table 1). In particular in four asymptomatic dogs thick radiodense circles or S shaped radiodensities were observed on radiographs (Figure 2-3). Among symptomatic dogs a variable pulmonary pattern was registered (Table 1). Enlargement of the right heart was observed in two cases associated to dilatation of pulmonary artery trunks in one of them. The echocardiographic examination was normal in all dogs except for 2 cases 3 where signs of mild and severe pulmonary hypertension were registered respectively.
All dogs were treated; fenbendazole was administered in monotherapy in five cases; the Im/Mox was administered in monotherapy in five cases and in combination with fenbendazole (25mg/kg, PO, once a day, for 21 days) in other two cases (table 1).
Clinical pictures significantly improved in all symptomatic dogs after 1-2 weeks of treatment (Table 1). The radiographic monitoring showed an improvement in quite all dogs while the reverse to normal of radiographic abnormalities, when reached, was registered at different times (Table 1). The radiodensities of asymptomatic dogs were no longer visible after two months of treatment in two cases. In cases 3 and 6 radiographic controls were available only at the end of treatment and in other two cases (case 4, 5) radiographic controls were totally unavailable. The laboratory monitoring after treatment was available in 6 out of 12 dogs and it is reported in Table 2.
DISCUSSION
In this study different clinical presentations were associated with the presence of A. vasorum in dogs ranging from asymptomatic to severe forms. The occasional detection of L1 (Figure 4) in the feces of five dogs referred for a routine control visit suggests that faecal samples can reveal asymptomatic subjects [7]. The identification of those subjects that could act as diffusor of infection is an important task to break the cycle of the parasite by using successfull therapy. From data of this study pathological paraclinical findings have been registered both in symptomatic and asymptomatic dogs. In particular the increase in ( globulin fraction at serum protein electrophoresis and the serpiginous/circular areas of radiopacity on thoracic radiographs were documented as usefull findings that may help to reveal asymptomatic infections.
Angiostrongylosis is characterized by a highly variable clinical picture and the absence of characteristic findings on clinical examination. In this study the hemothorax (case 1), the hemoptysis associated to the formation of a large jugular hematoma after blood collection (case 4) and the uilateral hyphema may be caused by the primary and secondary hemostasis alterations [22-24] and it has been suggested that the presence of haemostasis alterations is associated to high parasite burden and poor prognosis [25]. Causes of the coagulopathy associated with angiostrongylosis are not fully known, but chronic disseminated intravascular coagulation (DIC) as well as an immune-mediated thrombocytopenia have been proposed as possible mechanisms [26]. It is important to note that angiostrongylosis should be included in the differential diagnosis when alterations of haemostasis are registered at the clinical examination. The abdominal effusion of case 3 is the consequence of the severe pulmonary hypertension probably caused by the presence of adult worms responsable for thrombosis of the pulmonary vessels [13].
Abnormalities in complete blood count and serum biochemistry have frequently been described but are not specific. The most common clinico-pathologic changes are hyperglobulinemia, eosinophilia and anemia [21]. Chapman and colleagues (2004) reports of 70% with an increase in serum globulin and this is very similar to the report in this study. Anyway the report of the � globulin fraction increase in this study is more specific than previously reported and it s interesting to note that this pathological finding has been quite constantly registered also in asymptomatic dogs (4/5). Eosinophilia, observed in six cases, should increase the suspicion of the disease, but eosinophils values in the reference range, as observed in the other cases, does not exclude the diagnosis [27]. An increase in CK has been registered in four cases; this finding is reported as an alteration in kinase-myocardial band isoenzyme (CK-MB) possibly related to acute cardiac injury [9]. Thoracic radiographic findings are largely described in the course of angiostrongylosis [11, 12, 21] with the possibility of abnormalities also in asymptomatic dogs [11]. The particular aspect of the serpiginous/circular areas of radiodensities described in asymptomatic dogs (Figure 5) could be attributed to fistulas created during larval migration from the pulmonary capillaries into the alveoli or to bronchiectasis with bronchial walls markedly thickened and misshapen. The latter hypotesis was not supported by the typical aspect of bronchiectasis (i.e. loss of the normal tapering of the bronchial walls) on lateral radiographic view. A not better defined bronchial pattern has been documented in 60% of dogs in natural condition [12], differently in a recent work no bronchial changes have been documented by using computer tomography under experimental conditions [16], but it is assumed that experimental infection is not identical to natural infection. Furthermore, the association with asymptomatic cases suggest the possibility that these findings represent the earliest changing on thoracic radiographs before the onset of clinical disease and the disappearance of these alterations after treatment in two dogs support the correlation with canine angiostrongylosis.
The persistence of some paraclinical alterations after therapy (eosinophilia and a mild increase in � fraction apparently persisted in three dogs; reverse to normal of radiographic findings was not available in all dogs) probably depends on the variability of follow up. On the other hand studies have not definitively shown wheter any of the specific used medications completely clear infection [28], thus the persistence of some alteration is possible.
The detection of L1 in a dog of 12 years reveals the receptivity to infection also in old dogs, although a greater risk of infection is reported in young subjects because of their high predation activity that facilitate the ingestion of the intermediate host [21]. In one dog L1 were found also in the pleural effusion; it was assumed that L1 passed from lung tissue to the thoracic cavity following lung rupture occurred concurrently with acute respiratory distress observed by the owners [3].
A. vasorum infection can be fatal, thus an early diagnosis and appropriate treatment is auspicable to avoid the onset of potentially lethal lesions. Although none of clinico-pathological findings are specific, a combination of these findings could increase the index of suspicion also in asymptomatic dogs. In this view the increase in ( globulin fraction at serum protein electrophoresis and the circular areas of radiopacity on thoracic radiographs could be usefull findings. Given the geographical difference between the previously reported case series from Italy [6] this study also documents the apparent spread of disease in Italy.
CONFLICT OF INTEREST
None of the authors of this paper has a financial or personal relationship with other people or organizations that could inappropriately influence or bias the content of the paper
ACKNOWLEDGEMENTS
The authors thank Dr. Guido Filomarino, Dr. Marcella Rosato and Dr. Michele Lattanzi for their contribution.
REFERENCES
1. Helm JR, Morgan ER, Jackson MW, Wotton P, Bell R (2010) Canine angiostrongylosis: an emerging disease in Europe. Journal of Veterinary Emergency and Critical Care 20: 98-109.
2. Di Cesare A, Castagna G, Meloni S, Milillo P, Latrofa, S et al. (2011) Canine and feline infection by cardiopulmonary nematodes in central and southern Italy. Parasitology Research 109: 87-96.
3. Sasanelli M, Paradies P, Otranto D, de Caprariis D (2008) Haemothorax associated with Angiostrongylus vasorum infection in a dog. Journal of Small Animal Practice 49: 417-420.
4. Traversa D, Torbidone A, Malatesta D, Guglielmini C (2008) Occurrence of fatal canine Angiostrongylus vasorum infection in Italy. Veterinary Parasitology 152: 162-166.
5. Lepri E, Veronesi F, Traversa D, Conti MB, Marchesi MC et al (2011) Disseminated angiostrongylosis with massive cardiac and cerebral involvement in a dog from Italy. Parasitology Research 109: 505-508.
6. Tieri E, Pomilio F, Di Francesco G, Saletti MA, Totaro P et al (2011) Angiostrongylus vasorum in 20 dogs in the province of Chieti, Italy. Veterinaria Italiana 47: 65-76.
7. Koch J and Willesen JL (2009) Canine pulmonary angiostrongylosis: an update. The Veterinary Journal 179: 348-359.
8. Morgan ER, Jefferies R, van Otterdijk L, McEniry RB, Allen F et al (2010) Angiostrongylus vasorum infection in dogs: Presentation and risk factors. Veterinary Parasitology 173: 255-261.
9. Cury MC, Guimar�es MP, Lima WS, Caldeira MC, Couto TR et al. (2005) HYPERLINK "http://www.ncbi.nlm.nih.gov/pubmed?term=%22Cury%20MC%22%5BAuthor%5D"  Biochemical serum profiles in dogs experimentally infected with Angiostrongylus vasorum (Baillet, 1866).Veterinary Parasitology 128: 121-127.
10. Willesen JL, Jensen AL, Kristensen AT, Koch J (2009) Haematological and biochemical changes in dogs naturally infected with Angiostrongylus vasorum before and after treatment. The Veterinary Journal 180: 106-111.
11. Boag AK, Lamb CR, Chapman PS, Boswood A (2004) Radiographic findigs in 16 dogs infected with Angiostrongylus vasorum. The Veterinary Record 154: 426-430.
12. Willesen JL, Kristensen AT, Jensen AL, Heine J, Koch J (2007) Efficacy and safety of imidacloprid/moxidectin spot-on solution and fenbendazole in the treatment of dogs naturally infected with Angiostrongylus vasorum (Baillet, 1866). Veterinary Parasitology 147: 258-264.
13. Esteves I, Tessier D, Dandrieux J, Polack B, Carlos C et al. (2006) Reversible pulmonary hypertension presenting simultaneously with an atrial septal defect and angiostrongylosis in a dog. Journal of Small Animal Practice 45: 206-209.
14. Nicolle AP, Chetboul V, Tessier-Vetzel D, Carlos Sampedrano C, Aletti E et al (2006) Severe pulmonary arterial hypertension due to Angiostrongylus vasorum in a dog. The Canadian Veterinary Journal 47: 792-795.
15. Kranjc A, Schnyder M, Dennler M, Fahrion A, Makara M et al (2010) Pulmonary artery thrombosis in experimental Angiostrongylus vasorum infection does not result in pulmonary hypertension and echocardiographic right ventricular changes. Journal of Veterinary Internal Medicine 24: 855-862.
16. Dennler M, Makara M, Kranjc A, Schnyder M, Ossent P et al (2011) Thoracic computed tomography findings in dogs experimentally infected with Angiostrongylus vasorum. Veterinary Radiology & Ultrasound 52: 289-294.
17. Zarelli M, Shiel R, Gallagher B, Skelly C, Cahalan S et al (2011) CT findings in a dog with intracranial hemorrhage secondary to angiostrongylosis Veterinary Radiology & Ultrasound 52: 289-294.
18. Traversa D, Di Cesare A, Conboy G (2010) Canine and feline cardiopulmonary parasitic nematodes in Europe: emerging and underestimated. Parasites and Vectors 3: 623-22.
19. Morgan ER and Shaw SE (2010) Angiostrongylus vasorum infection in dogs: continuing spread and developments in diagnosis and treatment. Journal of Small Animal Practice 15: 616-621.
20. McGarry JW and Morgan ER (2009) Differential identification of first stage larvae of canine metastrongyles. The Veterinary Record 165: 258-261.
21. Chapman PS, Boag AK, Guitian J, Boswood A (2004) Angiostrongylus vasorum infection in 23 dogs (1999-2002). Journal of Small Animal Practice 45: 435-440.
22. Schelling CG, Greene CE, Prestwood AK, Tsang VC (1986) Coagulation abnormalities associated with acute Angiostrongylus vasorum in dogs. American Journal of Veterinary Research 31: 131-143.
23. Cury MC, Lima WS, Guimar�es MP (2002) Hematological and coagulation profiles in dogs experimentally infected with Angiostrongylus vasorum (Baillet, 1866). Veterinary Parasitology 104: 139-149.
24. Whitley NT, Corzo-Menendez N, Carmichael NG, McGarry JW (2005) Cerebral and conjunctival haemorrhages associated with von Willebrand factor deficiency and canine angiostrongylosis. Journal of Small Animal Practice 46: 75-78.
25. Gredal H, Willesen JL, Jensen HE, Nielsen OL, Kristensen AT et al (2011) Acute neurological signs as the predominant clinical manifestation in four dogs with Angiostrongylus vasorum infections in Denmark. Acta Veterinaria Scandinavica 53: 43.
26. O�Neill E, Acke E, Tobin E, McCarthy G HYPERLINK "http://www.ncbi.nlm.nih.gov/pubmed?term=%22Jo%27neill%20E%22%5BAuthor%5D"  (2010) Immuno-mediate trombocitopenia associated with Angiostrongylus vasorum infection in Jack Russel terrier. Irish Veterinary Journal 63: 434-440.
27. Schnyder M, Fahrion A, Riond B, Ossent P, Webster P et al (2010) Clinical, laboratory and pathological findings in dogs experimentally infected with Angiostrongylus vasorum. Parasitology Research 107: 1471-1480.
28. Bourque AC, Conboy G, Miller LM, Whitney H (2008) Pathological findings in dogs naturally infected with Angiostrongylus vasorum in Newfoundland and labrador, Canada. Journal of Veterinary Diagnostic Investigation 20: 11-20.
FIGURE LEGENDS
Figure 1 �Serum protein electrophoresis showing a severe increase in (2, �1 and �2 globulin fraction (case 9).
Figure 2 - Thoracic radiograph of case 7, dorsoventral view. Circular/serpiginous areas of radiopacity.
Figure 3 - Thoracic radiograph of case 11, dorsoventral view. Circular/serpiginous areas of radiopacity.
Figure 4 - A. vasorum L1 larvae in faecal samples of infected dog (Baermann test).
Table 1 � Caseload of A. vasorum naturally infected dogs enrolled in the study 
12Male
2 years German Shepherd
32 KgRoutine
visitNormalNormalNormalL1 with Baermann testIm/Mox every 15 days for 3 times///11Male
4 years Mixed breed
31 KgRoutine visitNormalNormalCircular areas of radiopacityL1 with Baermann testIm/Mox every 15 days for 3 times/2months2 months10Famale 6.5years Labrador 29KgRoutine
visitNormalNormalCircular areas of radiopacityL1 on direct fecal smearIm/Mox every 15 days for 3 times/2 months2 months9Male
9 months
Mixed breed
15 KgEpistaxis, hemoptysis cough and depression of 2 months duration+ inappetence and unilateral hyphema Unilateral hyphema +
Pale mucous membranaeNormalDiffuse interstitial-bronchial pulmonary pattern L1 on direct fecal smearFenbendazole
25 mg/Kg, PO, twice a day for 21 days1 week.
(ocular problems solved in 2 months)N.K.1 month 
4 months: persistence of mild 
interstitial-bronchial pulmonary pattern8Female sterilized 12years Mixed breed 26 KgRoutine visit 
NormalNormal     Circular areas
   of radiopacityL1 with Baermann testIm/Mox every 15 days for 3 timesOccasional cough2 months2 months
3 months
6 months7Female sterilized
4 years Mixed breed
31 KgRoutine visitNormalNormalCircular areas of radiopacityL1 with Baermann testIm/Mox every 15 days for 3 times-/2 months2 months6Male
3 years
Spinone
36 KgGradual redution of visus+
sporadic coughCough induced after stimulationRales on stimulation of cough + loud bronchovescicularDiffuse interstitial pulmonary patternL1 with Baermann testFenbendazole
25 mg/kg, PO twice a day for 21 daysAfret 2 weeks-N.K.1 month:
persistence of diffuse interstitial pulmonary pattern5Female
2 years
Mixed breed
22 KgSevere cough from
2 monthsCough induced after stimulationNormalDiffuse interstitial pulmonary patternL1 on direct fecal smearFenbendazole
25mg/kg, PO once a day for 21 days + Im/Mox every 15 days for 3 times/N.K.N.A.4Male
1 year
Mixed breed
12 KgCapricious appetite and cough
from 2-3. months + HaemoptysisFever +polypnea + +hematoma after blood collectionMuffling of the heart sounds in the left cardiac areaAlveolar pattern in the diaphragmatic left lobe L1 on direct fecal smearFenbendazole
25mg/kg, PO,  once a day for 21 days + Im/Mox every 15 days for 3 timesAfter 1 weekN.K.N.A.3Female sterilized
3 years
Mixed breed
14 KgCough for 5 months + Progressive abdomen distention from 2 monthsAbdominal
effusionFew rales Diffuse interstitial-bronchial pulmonary pattern+ pulmonary artery trunks + Dilatation of the right heartL1 on direct fecal smearFenbendazole
25 mg/kg, PO twice a day for 21 daysAfter 2 weeks-N.KThree weeks: persistence of a interstitial pulmonary pattern2Female
1 year
�pagneul breton 18 KgExercise intolerance and cough of 2 months durationExpiratory dyspneaRales and wheezingDiffuse bronchial-interstitial pulmonary pattern+ Dilatation of the right heartL1 with Baermann testFenbendazole
25 mg/kg, PO twice a day for 21 daysAfter 1 week5 months1 month
2 months
5 months1Male Castrated 1year
Mixed breed
26 KgCough, fever, depression, and inappetence of 1 month duration+ Respiratory crisis in the last 2 daysDyspnea +fever (hemotorax)Muffling of the heart sounds + loud bronchovescicular soundsModerate bilateral pleural effusion + Diffuse interstitial pulmonary pattern + Alveolar pattern in the cranial left lobeL1 in the pleural effusion and in faecesFenbendazole
25 mg/kg, PO twice a day for 21 daysAfter 1 weekN.K.Two weeks:
persistence of interstitial pulmonary patternCaseSignalingHistory and
clinical complaintClinical
findingsThoracic auscultationThoracic
radiographyDiagnosisTherapyClinical recoveryRemission of radiography signsRadiographyfollow upTable 2 � Abnormal laboratory findings registered at diagnosis and in follow up post treatment in the 12 dogs included in the study.
Complete blood countBiochemicalGlobulin fraction increasedClotting
profileCASE
1T0(RBC - (Hgb - (Hct - (WBC (NEU - (EOS - (BAS - (PLT(Pt - (AST - (CK - (LDH - (Amylase - (Globulins - (A/G((2 - ( �2(PT - (AT - (FDPs - (FibrinogenT28(EOSNot evaluatedNot evaluatedNot evaluatedCASE
2T0(RBC - ( Hgb - (Hct - (WBC - (EOS - (LYM(AST - (CK - (Glu(�1 - ( �2Not evaluated-Not evaluatedCASE
3T0( Hgb - (Hct (WBC -(NEU(GGT - (Urea - (Chlorides((2 - (�2Not evaluatedT21(WBC - (NEU - (EOS(Urea(�2Not evaluatedCASE
4T0(EOS  - (PLT(Pt - (A/G - (Prot C(�1+ �2(AT - (FDPs - (D-D (Fibrinogen-Not evaluatedCASE
5T0(RBC - (Hct -
(EOS - (BAS(ALT(�1Normal-Not evaluatedCASE
6T0(Hct
(BAS(Pt  - (Glob - (A/G - (Urea - (Crea - (LDH - (Amylase(�1Not evaluated-Not evaluatedCASE 7T0(EOSNormal(�1+ �2(aPTT -
(D-DT53(EOS - (PLTNormal(�1Not evaluatedCASE
8T0(WBC
(NEU(Mg
(Crea((2 - (�1+�2(AT - (FibrinogenT48(WBC(ALP - (LDH - (Chlorides((2Not evaluatedT90normalNot evaluatedNot evaluatedNot evaluatedCASE
9T0(RBC - (Hgb - (Hct - (PLT(Pt - (A/G - (CK - (P((2 - (�1 - (�2(aPTT - (PT - (AT - (FDPs - (D-D - (FibrinogenT35Normal(ALP((2 - (�2NormalCASE
10T0NormalNormalNormalNot evaluatedT45NormalNot evaluatedNormalNot evaluatedT152Normal(ALP((1 -((2(D-DCASE
11T0NormalNormal((NormalT45NormalNot evaluated((Not evaluatedCASE
12T0(WBC - (NEU - (EOS(CK(�1+�2(FDPs - (D-D-Not evaluatedRBC = Red Blood Cells. Hgb = Hemoglobin. Hct = Hematocrit. WBC = White Blood Cells. NEU = Neutrophils. EOS = Eosinophils. BAS = Basophils. LYM = Lymphocytes. PLT = Platelets. Pt = Total Protein. AST = Aspartate Aminotransferase. CK = Creatine Kinase. LDH = Lactate Dehydrogenase. A/G = Albumin Globulin ratio. Glu = Glucose. GGT = Gamma-Glutamyl Transpeptidase. Prot C = Protein C. ALT = Alanine Aminotransferase. Crea = Creatinine. Mg = Magnesium. ALP = Alkaline Phosphatise. PT = Prothrombin Time. AT = Antithrombin III. aPTT = activated Partial Thromboplastin Time. FDPs = Fibrin Degradation Products. D-D = D-Dimer.








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