Did Jesus Christ die of pulmonary embolism? - Wiley Online Library

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Hemopericardium [6,7], free wall cardiac rupture, fatal cardiac arrhythmia ... + 972 4 6495139; fax: + 972 4 6495127; e-
Journal of Thrombosis and Haemostasis, 4: 891–924

LETTERS TO THE EDITOR

Did Jesus Christ die of pulmonary embolism? W. R. SALIBA Department of Internal Medicine C, Hae’meK Medical Center, Affiliated to the Technion-Israel Institute of Technology, Faculty of Medicine, Haifa, Israel

To cite this article: Saliba WR. Did Jesus Christ die of pulmonary embolism? J Thromb Haemost 2006; 4: 891–2. See also Brenner B. Did Jesus Christ die of pulmonary embolism? J Thromb Haemost 2005; 3: 2130–1; ur Rehman HU. Did Jesus Christ die of pulmonary embolism? a rebuttal. J Thromb Haemost 2005; 3: 2131–3.

I have read with great interest the Letter to the Editor ÔDid Jesus Christ die of pulmonary embolism?Õ by Brenner [1]. Brenner emphasizes the fact that the death of Jesus was sudden, because it occurred 3–6 h after crucifixion, favoring the diagnosis of pulmonary embolism. However, we must not forget that Jesus was tortured and severely scourged, certainly not to be compared with the suffering of the others crucified along with him. Before crucifixion Jesus had to carry the patibulum of the cross over his shoulders (weighing 34–57 kg) for about 600 m to the Golgotha [2], leading to a further dehydration. It follows that Jesus suffered more serious trauma and appreciable blood and fluid loss leading to a preshock state even before crucifixion [3]. This may have contributed to JesusÕ earlier death. In fact, the extent of blood loss may well have determined how long the victim would survive on the cross [4]. Brenner states Ôit is clear that his death was sudden and that a Roman soldier made a stabbing on his right chest after his deathÕ. The New Testament states that this caused Ôa sudden flow of blood and waterÕ [5]. This may suggests that Jesus suffered from a hemothorax before stabbing his chest. The development of hemothorax in combination with the preexisting preshock state resulted in further aggravation of JesusÕ circulatory and respiratory condition, which may certainly explain his sudden death. This thesis seems to be more reasonable than pulmonary embolism, keeping in mind that the time from crucifixion to death was insufficient for the development of deep venous thrombosis, and thereafter, pulmonary embolism. There are many other potential causes that may have contributed to JesusÕ death. Hemopericardium [6,7], free wall cardiac rupture, fatal cardiac arrhythmia [3], and postural asphyxia [8] have all been suggested. Scourging and crucifixion may also be associated with renal failure, acid base balance Correspondence: Walid R. Saliba, Department of Internal Medicine C, Hae’meK Medical Center, Afula 18101, Haifa, Israel. Tel.: + 972 4 6495139; fax: + 972 4 6495127; e-mail: [email protected] Received 30 June 2005, accepted 11 July 2005  2006 International Society on Thrombosis and Haemostasis

disturbances, rahbdomyolysis, and lung atelectasis, as has been recently suggested by Rehman [9]. Thus, it is more likely that JesusÕ death was multi-factorial and finally resulted from severe circulatory and cardiopulmonary compromise. Moreover, it is stated the soldiers broke the legs of the two thieves, but when they came to Jesus and saw that he was already dead, they did not break his legs [5]. At this point JesusÕ cardiopulmonary and circulatory status was severely compromised and possibly caused a state of coma. His impaired consciousness status may have confused the soldiers, making them think that he was dead. Stabbing his chest may have directly led to death. Thus, whether JesusÕ death occurred before or after stabbing his chest remains questionable from a medical point of view. Brenner states ÔJesus was born in Israel to a Jewish family. It is not unlikely that he had inherited a hypercoagulable state, as thrombophilia is common in Israel, especially in people residing in the Galilee areaÕ. This theory does not necessarily fit reality at the time of Jesus (2000 years ago) especially because thrombophilia is genetically and not environmentally related. In fact, the demographic characteristics and the genetic profile of the people residing today in Israel are very heterogeneous, and have been submitted to enormous changes from the time of Jesus. Recently, another letter dealing with the same subject was reported by Rehman [9]. The author focused his discussion primarily on the Turin shroud and brought several proofs, which support the authenticity of the shroud. Rehman states Ôan analysis of the Turin shroud confirmed that the man did not die on the cross and was buried aliveÕ and he concluded his paper with the state ÔJesus would have failed in the task he had been given to save the lost tribes of Israel, if he did not survive the crossÕ. These two thesis are poorly motivated and not supported by literature, in addition they do not take into consideration the biblical account of the event. Dr Robert Bucklin, a forensic pathologist, who was an avid shroud researcher and a member of the STURP (Shroud of Turin Research Project), reported a clear and expert medical interpretation of the man depicted on the cloth [8,10,11], upon examining the chest he concluded that the blood has all the

892 Letters to the Editor

characteristics of a postmortem type flow from a body cavity or from an organ such as the heart, which is clear evidence that Jesus was buried dead. Regarding the second thesis, it is the sufferance, the death, and the resurrection all together made JesusÕ task successful [5]. References 1 Brenner B. Did Jesus Christ die of pulmonary embolism. J Thromb Haemost 2005; 3: 2130–1. 2 Pfeiffer CF, Vos HF, Rea J, eds. Wycliffe Bible Encyclopedia. Chicago: Chicago Moody Press, 1975: 404–5, 713–23, 1173–4, 1520–3. 3 Edwards WD, Gabel WJ, Hosmer FE. On the physical death of Jesus Christ. JAMA 1986; 255: 1455–63. 4 Tenney SM. On death by crucifixion. Am Heart J 1964; 68: 286–7.

5 Matthew 26:17–26:61, Mark 14:12–15:47, Luke 22:7–23:56, John 13:1–19:42. The Holy Bible (New International Version). Michigan: Grand Rapids, Mich, Zondervan Bible Publishers, 1978. 6 Bucklin R. The legal and medical aspects of the trial and death of Christ. Med Sci Law 1970; 10: 14–26. 7 Davis CT. The crucifixion of Jesus: the passion of Christ a medical point of view. Ariz Med 1965; 22: 183–7. 8 Bucklin R. An Autopsy on the Man of the Shroud. International Scientific Symposium On the Shroud of Turin. France Symposium: The Nice, 1997. 9 Rehman HU. Did Jesus Christ die of pulmonary embolism? A rebuttal. J Thromb Haemost 2005; 3: 2131–3. 10 Bucklin R. The shroud of Turin: a pathologist’s viewpoint. J Miss State Med Assoc 1983; 24: 95–8. 11 Bucklin R. The shroud of Turin: a pathologist’s viewpoint. Leg Med 1982; 24: 33–9.

2B or not 2B? What is the role of VWF in platelet–matrix interactions? And what is the role of the VWF:CB in VWD diagnostics? These are the questions E. J. FAVALORO Department of Haematology, Institute of Clinical Pathology and Medical Research (ICPMR), Westmead Hospital, Westmead, NSW, Australia

To cite this article: Favaloro EJ. 2B or not 2B? What is the role of VWF in platelet–matrix interactions? And what is the role of the VWF:CB in VWD diagnostics? These are the questions. J Thromb Haemost 2006; 4: 892–3. See also Baronciani L, Federici AB, Beretta M, Cozzi G, Canciani MT, Mannucci PM. Expression studies on a novel type 2B variant of the von Willebrand factor gene (R1308L) characterized by defective collagen binding. J Thromb Haemost 2005; 3: 2689–94.

It was with considerable interest that I read the recent article by Baronciani et al. [1]. They described a novel type 2B von Willebrand disease (VWD) variant characterized by defective collagen binding. Typically, 2B VWD is characterized by an increased affinity of plasma von Willebrand factor (VWF) for platelet GPIb (evidenced in laboratory testing by enhanced responsiveness to low dose ristocetin in a ristocetin-induced platelet aggregation (RIPA) assay [2–4]). Consequent to enhanced plasma VWF binding of platelets, mild thrombocytopenia, and loss of high molecular weight (HMW), VWF is also usually evident in these patients. In the study of Baronciani et al. [1], the propositus and four related family members had the same mutation (R1308L) and displayed the following phenotypic data for plasma Correspondence: E. J. Favaloro, Department of Haematology, Institute of Clinical Pathology and Medical Research (ICPMR), WSAHS, Westmead, NSW, 2145, Australia. Tel.: +61 2 9845 6618; fax: +61 2 9689 2331; e-mail: emmanuel@ icpmr.wsahs.nsw.gov.au Received 19 December 2005, accepted 3 January 2006

VWF:VWF:Ag 34%–38% (NR 40–169), VWF:RCo 23%– 27% (NR 41–160), VWF:CB 18–20 (NR 45–170), and VWF:CB/VWF:Ag 0.47–0.58 (NR ‡0.7). Such a pattern of results is consistent with type 2B VWD, although somewhat lower relative VWF:RCo and VWF:CB (compared with VWF:Ag) might usually be expected, especially if there is a significant loss of HMW VWF. Those individuals tested (n ¼ 3) all showed responsiveness to low-dose ristocetin (£0.4 mg mL)1) by RIPA [1], and this is characteristic of 2B VWD [2–4]. In contrast to ÔtypicalÕ 2B VWD, however, all patients also showed an uncharacteristic presence of HMW VWF in plasma, and normal platelet counts [1]. Furthermore, in two individuals where DDAVP was trialed, postDDAVP thrombocytopenia did not occur. Thus, Baronciani et al. [1] reported the case as an atypical type 2B VWD. Of further interest, these workers generated recombinant forms of the mutated VWF (rVWF), and tested these against wildtype VWF to show specific reduction in collagen binding as assessed in a VWF:CB assay. These findings raise several interesting questions. As mentioned, it is not unusual, in patients with 2B VWD, that the collagen-binding activity of plasma VWF (i.e. the VWF:CB result) is low relative to the level of VWF present (i.e.  2006 International Society on Thrombosis and Haemostasis