Abeer K Al Ghumlas

King Saud University, Riyadh, Mintaqat ar Riyad, Saudi Arabia

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Publications (10)12.83 Total impact

  • Abeer K Al Ghumlas, Abdel Galil M Abdel Gader
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    ABSTRACT: Despite evidence of active hemostasis, camel platelets barely respond to common aggregating agents at standard doses used for human platelet aggregation. The purpose of the study was to find out whether camel platelets can be activated by high doses or combinations of aggregation agonists, and to characterize the receptor that mediates the aggregation response to adenosine diphosphate (ADP), the most potent agonist for camel platelets known so far. Aggregation studies were performed with platelet-rich plasma (PRP) in response to multiple doses or combinations of ADP, epinephrine (EPN), collagen, and arachidonic acid (AA). Aggregation responses to ADP were performed before and after the addition of the ADP receptor (P2Y12 ) antagonist Clopidogrel. Camel platelets responded to ADP at doses higher than the standard dose for human platelets, and to combinations of EPN and other agonists, while no aggregation was elicited with EPN or AA alone. Clopidogrel blocked the ADP-induced aggregation responses in a dose-dependent fashion in vitro. Camel platelet aggregation can be activated by increasing the dose of some agonists such as ADP, but not AA or EPN. Irreversible aggregation of camel platelets could also be triggered by a combination of EPN and ADP, and collagen and AA. Inhibition with clopidogrel suggests that camel platelets express the ADP receptor, P2Y12 . Understanding platelet function in camels will add to the understanding of platelet function in health and disease.
    Veterinary Clinical Pathology 08/2013; · 1.29 Impact Factor
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    ABSTRACT: The use of pnuemoperitonium to create the working environment for laproscopic cholecystectomy results in an increase in intraabdominal pressure, which exceeds the pressure of the venous-return from the legs. The resulting venous stasis may increase the risk of thrombosis formation and deep vein thrombosis in the lower limbs. However, there is no information as to whether the venous stasis will also exacerbate the coagulabililty of blood flowing out of the lower limbs. The aim of the study is to find evidence of haemostatic activation in the blood draining the lower limbs, which experience venous stasis as a result of the laparoscopic cholecystectomy (LC) procedure. In this study, we prospectively studied 25 patients who underwent LC for uncomplicated cholelithiasis; 20 were female and 5 were male, aged between 17 to 65 years. LC was carried out according to a standard procedure. After general anesthesia, the patients were laid in a 30 degrees anti-Trendelenburg position, and pnuemoperitonium was maintained during the procedure with abdominal pressure of 12 mm Hg. The mean operating time was 55 minutes (range 25 to 118 min).Blood samples were collected simultaneously from the antecubetal fossa (the upper limb) and the dorsum of the foot (the lower limb), on 4 different occasions: i. preoperative; ii. after the induction of anesthesia, and before the inflation of the abdomen; iii. at the end of surgery, before deflation of the abdomen, and iv. 24 hours after surgery. LABORATORY ASSAYS: Prothrombin time, activated partial thromboplastin time, thrombin time, and plasma fibrinogen, Plasma Protein S (total and free), Protein C, Antithrombin, tissue plasminogen activator, and plasminogen activator inhibitor (PAI-I). Platelet function was assessed by the platelet function analyser (PFA100). No significant differences were noted in all measured haemostatic parameters, including PFA100 closure times, when comparing the measurements that were taken simultaneously in the upper and lower limbs' blood. Plasma fibrinogen increased significantly 24 hours after surgery, and antithrombin levels dropped slightly, immediately after surgery, but recovered preoperative levels 24 hours after surgery. Coagulation inhibitors (total and free protein S and protein C), and fibrinolytic parameters did not show any significant fluctuations throughout the study intervals. The finding of this study is of no significant activation of coagulation in the blood flowing out of the lower limbs at the time of venous stasis, adds to the criteria of safety of the current surgical procedure used in LC, including reverse Trendelenburg position and pneumoperitoneum that unavoidably produce significant stasis in the lower limbs.
    Surgical laparoscopy, endoscopy & percutaneous techniques 04/2010; 20(2):79-83. · 0.88 Impact Factor
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    ABSTRACT: Protein S (PS), protein C (PC), and antithrombin (AT) are produced by the liver, and their levels were previously shown to be reduced in chronic as well as acute liver disease. The aim of this study was to determine whether measurement of PS, PC, and AT levels in patients would be as good as the commonly used clinical and histological parameters of liver disease in discriminating early and advanced hepatocyte dysfunction. A total of 154 patients were recruited and categorized into five groups: hepatitis B inactive carriers in group 1 (n = 29), nonalcoholic steatohepatitis patients in group 2 (n = 30), chronic hepatitis B patients with elevated liver enzymes in group 3 (n = 29), chronic hepatitis C patients with elevated liver enzymes in group 4 (n = 30), liver cirrhosis patients in group 5 (n = 36). There were significant differences between groups in the levels of PC (P = 0.0001), total PS (P = 0.0001), and free PS (P = 0.0001) and AT (P = 0.0001). These parameters were least affected in the control group, then groups 1 and 2, followed by groups 3 and 4, and most affected in group 5. No differences in these tests were detected between groups 1 and 2 and between groups 3 and 4. Univariate and multivariate analyses showed that free PS was the only predictor of significant inflammation (P = 0.0001), and AT (P = 0.001) and PC (P = 0.003) were the most important factors associated with advanced fibrosis. Both PS and PC are sensitive markers of liver disease, but PS is a sensitive marker of liver inflammation, whereas PC may be a more sensitive marker for liver fibrosis.
    Blood coagulation & fibrinolysis: an international journal in haemostasis and thrombosis 12/2009; 21(2):122-7. · 1.25 Impact Factor
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    ABSTRACT: Multiple transfusions are frequently complicated by alloimmunization. This retrospective study aims to determine whether alloimmunization could be accounted for by racial differences between donors and recipients. The development of alloantibodies were determined in 68 multi-transfused patients (thalassaemia, n=38) and (sickle cell anemia, n=30). The overall frequency of alloantibody formation in our patients is 22.06%. Thirteen patients received blood from the same ethnic group (Arab) and none developed antibodies, while of 47 patients who received multi-ethnic blood, 10 developed alloantibodies. Alloantibodies formation can be reduced by limiting the transfusion of RBC, collected from donors of the same ethnic origin.
    Transfusion and Apheresis Science 11/2008; 39(3):199-204. · 1.23 Impact Factor
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    ABSTRACT: Chronic liver disease is accompanied by derangement of hepatocyte function including the synthesis of haemostastic factors. It is, however, not known whether the improvement in liver functions as a result of interferon (IFN)-alpha therapy would be reflected in the plasma levels of these factors. To evaluate the effect of IFN-alpha therapy on the plasma levels of natural anticoagulants and on the fibrinolytic parameters, in patients with chronic viral hepatitis. Twenty one patients with chronic viral hepatitis (B and C) were treated with IFN-alpha, and were studied before commencement of therapy (first sample) 3 (second sample) and 6 months (third sample) later. The coagulation screening tests: activated partial thromboplastin time, prothrombin time, thrombin time, reptilase time and plasma fibrinogen and the natural anticoagulants: antithrombin, Protein C and free and total protein S as well as fibrinolytic parameters (tissue type plasminogen activator, plasminogen activator inhibitor type-1 and plasminogen) were measured. An increase in the levels of total protein S at 3 and 6 months after the commencement of IFN therapy was noted but the increase was statistically significant in the latter period. Reptilase time was prolonged in the first (pretreatment) and in the second samples and then began to decrease in the third sample but remained higher than the pretreatment level. Fibrinogen level increased in the second and third samples. No remarkable changes were noted in other haemostatic parameters. Total protein S level is a good marker of response to IFN therapy. IFN therapy does not affect other natural anticoagulants or fibrinolytic parameters. More detailed studies need to be done to confirm these findings.
    Blood Coagulation and Fibrinolysis 07/2008; 19(4):263-7. · 1.25 Impact Factor
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    ABSTRACT: Camels and many other desert animals are uniquely adapted to conserve water and other fluids in order to survive intense heat for long periods. Earlier studies have suggested that human platelets may be the trigger for the coagulopathy involved in heat prostration and stroke. The present study has compared the resistance of camel and human platelets to heat in order to see if they might help to protect camels from the effects of high body temperature for prolonged periods. The findings demonstrate that camel platelets are significantly less sensitive to heat than human platelets. Temperatures (43 degrees C-45 degrees C) that cause human cells to undergo marked structural alterations and lose their ability to spread and aggregate have no effect on camel platelets. Even higher temperatures (50 degrees C) that destroy human platelets have minor effects on camel cells and do not seriously compromise their function. Temperatures of 55 degrees C do destroy camel platelets and their functional capability. The resistance of camel platelets to heat may help protect camels from the effects of extreme body temperature and dehydration, which are everyday conditions in the desert.
    Platelets 06/2008; 19(3):163-71. · 2.24 Impact Factor
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    ABSTRACT: Previous studies indicated that the camel has a very active haemostatic mechanism with a short bleeding time and thrombocytosis. However, platelet function, when tested by agonist-induced aggregation and PFA 100 closure time, showed marked inhibition compared to humans. Since camels are also far more resistant to long exposure to excessive heat and high body temperature than humans, it seemed worthwhile to explore fundamental morphological differences between human and camel platelets and those from other species. The present study has examined the ultrastructure of camel platelets and compared them with the fine structures of human, bovine and equine thrombocytes. Camel platelets, like bovine and equine cells, are discoid in shape and about two-thirds the size of human platelets. A circumferential coil of microtubular supports the disk-like form of camel platelets. Their cytoplasm, like bovine and equine platelets, is filled with alpha granule twice as large as those in human platelets, but lacking the organized matrix of equine alpha granules. Dense bodies are present in camel platelets with whip-like extensions not present on bovine or equine thrombocytes, but found on occasional human platelet dense bodies. Camel platelets, like bovine and equine thrombocytes, lack an open canalicular system (OCS) and must secrete granule products by fusion with the cell wall rather than an OCS. Future studies will determine if the differences in ultrastructural anatomy protect camel platelets from heat more than human thrombocytes.
    Platelets 03/2008; 19(1):51-8. · 2.24 Impact Factor
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    ABSTRACT: Despite the very active coagulation system in camels, there are no previous studies on camel platelet functions. It is our aim to study camel platelet function using aggregometry, Platelet Function Analyzer (PFA100), and flow cytometry. A total of 103 camels, 19 males and 84 females, were studied. Their ages ranged from 5 to 20 years (mean±SD: 6.4±4.4 years). The results obtained were compared with healthy humans. Platelet aggregometry was undertaken in platelet-rich plasma in response to adenosine diphosphate (ADP), adrenaline, collagen, arachidonic acid, and ristocetin. Camel platelet function in whole blood was also tested using the PFA-100 and by flow cytometry using three human monoclonal antibodies (CD42, CD61, and CD62). Camel platelets failed to respond to arachidonic acid, adrenaline, and ristocetin. However, responses to ADP and collagen were obtained but were less than the human values. The addition of human plasma caused some enhancement of the aggregation responses to adrenaline and collagen but not ristocetin or arachidonic acid. However, the presence of human serum or heparin resulted in a very marked enhancement of the camel platelet aggregation responses to all agonists, except arachidonic acid. PFA-100 closure times of the collagen–ADP and the collagen–epinephrine cartridges were markedly longer than in humans. In the flow cytometry studies, camel platelets failed to respond to any of the human monoclonal antibodies with or without activation by ADP, thrombin, human plasma, or serum. This first study on camel platelet functions uncovered the distinction between camel and human platelet functions. The lack of platelet responses to certain aggregating agonists, their enhancement with human plasma and serum, as well as the prolongation of the PFA-100 closure times, add other unique characteristics to the biology of this interesting creature.
    Comparative Clinical Pathology 01/2006; 15(1):31-37.
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    ABSTRACT: The liver plays a central role in haemostasis, being the site of synthesis of most of the clotting factors, coagulation inhibitors and fibrinolytic parameters, in addition to its clearance of activated clotting and fibrinolytic factors. Nonetheless, no haemostatic test(s) is included among the routine liver function tests and this study aims to probe this possibility. The liver disease group (n=258) included acute hepatitis (n=25), chronic viral hepatitis (n=128), hepatitis B (HB) carriers (n=25), liver cirrhosis (n=67), and hepatocellular carcinoma (HCC) (n=13). The prothrombin time was significantly prolonged in acute hepatitis, liver cirrhosis and HCC. However, the reptilase time was prolonged in all the groups except in HB carriers, while the thrombin time was prolonged only in the HCC group. Antithrombin III and protein C levels exhibited significant reduction in acute hepatitis, liver cirrhosis and HCC. On the other hand, protein S levels (total and free) were reduced significantly in all the patients groups, including HB carriers when compared with healthy controls. Derangement of haemostatic tests is a common feature in liver disease, being most significant in acute hepatitis, liver cirrhosis and hepatocellular carcinoma. The most sensitive markers of hepatocyte malfunction are protein S (total and free) and the reptilase time as they were abnormal, in the mildest liver affections, when other biochemical tests as well as other haemostatic tests were normal. Further studies are needed to see whether these two tests qualify for inclusion among the routine liver function tests.
    Blood Coagulation and Fibrinolysis 08/2005; 16(5):329-35. · 1.25 Impact Factor
  • Abeer Khalid Al Ghumlas, Abdel Galil Mohammed AbdelGader
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    ABSTRACT: The liver plays a central role in the control of haemostasis being the site of synthesis of most of the coagulation factors and natural anticoagulants, as well as fibrinolytic factors except the main activators of the fibrinolytic system (t-PA and u-PA). The liver also clears many of the activated clotting and fibrinolytic factors, as well as haemostatic activation complexes (TAT and PAP) and end product of fibrin degradation, FDP. Therefore, liver disease results in a complex and multifactorial pattern of defects in haemostatic function in the form of: (i) decreased synthesis of coagulation factors (ii) Abnormal protein synthesis e.g. dysfibrinogen (iii) Deficiency of natural anticoagulants (iv) Enhanced fibrinolytic activity (v) Quantitative and qualitative platelet defects (vi) Consumptive coagulopathy as in advanced liver disease. These abnormalities of haemostasis, which often occurs in the form of multiple defects, underlie the haemorrhagic diathesis, which often complicates liver disease. In the same manner, measurement of various haemostatic factors can be employed to reflect the degree of liver damage.
    Saudi Journal of Gastroenterology 05/2003; 9(2):59-68. · 1.22 Impact Factor