You will be presented with the full text of a biomedical research paper. Please write an abstract for this paper. Your response should include the abstract and no additional text.

Paper text:
a 54-year - old man presented with acute right - sided abdominal pain and nausea .
1a ) with multiple lesions of poor contrast enhancement ( fig . 1b ) and a mass in his pancreas .
a fine needle aspirate of one of the liver lesions showed cellular smears with moderate variation in nuclear size and shape with delicate cytoplasm ( fig .
2b ) but synaptophysin , ck7 , ck20 , ttf-1 , hepar-1 , cd10 , carcinoembryonic antigen and alpha - fetoprotein were all negative .
in addition , a lutetium octreatate - positive emission tomography scan showed no accumulation of tracer activity in the multiple hepatic metastases .
he was found to have multi - organ failure with abnormal renal function ( creatinine 190 mol / l ) , deranged liver enzymes ( bilirubin 36
mol / l ; alkaline aminotransferase ( alt ) 184 u / l ; gammaglutamyl transferase ( ggt ) 468 u / l ; alkaline phosphatase ( alp ) 322 u / l ) , and no radiological evidence of biliary duct obstruction .
he developed disseminated intravascular coagulation ( dic ) with a platelet count of 10  109/l , an international normalised ratio ( inr ) of 2.8 , a fibrinogen level of 0.5
he showed no signs of bleeding . over the next 3 days , the patient became anuric and dyspnoeic .
he was treated with fluid resuscitation , blood products and vitamin k. he gradually improved over a period of 10 days .
his renal impairment resolved ( creatinine 94 mol / l ) , liver function tests improved ( bilirubin 24 mol / l ; alt 59 u / l ; ggt 220 u / l ; alp 247 u / l ) and the coagulation profile normalised ( platelet count 447  109/l ; inr 1.1 ; fibrinogen 5.6
one week later , he received his first cycle of chemotherapy  carboplatin ( auc 5 ) and etoposide ( 100 mg / m ) with a 20% dose reduction .
three weeks later , he presented with a 5-day history of fatigue , dyspnoea , haematuria and extensive bruising ( fig .
he had recurrent dic with active bleeding as evidenced by a drop of haemoglobin to 43
g / l , a platelet count of 11  109/l , an inr of 4.3 , a fibrinogen level of < 0.2
his renal and liver functions remained relatively stable initially ( creatinine 128 mol / l ; bilirubin
24 mol / l ; alt 48 u / l ; ggt 286 u / l ; alp 254 u / l ) .
he rapidly deteriorated with worsening dyspnoea , ischaemic chest pain and increasing blood product requirement with no improvement in his blood counts .
further chemotherapy was contemplated as it was thought that malignancy was the underlying cause of the dic . however , due to his rapid decline , this was deemed futile , hence palliative measures were implemented .
he died 3 days after his second admission  2 months after his initial presentation .
neuroendocrine tumours have a wide range of clinical presentations , from the more indolent low - grade carcinoid tumours to aggressive high - grade disease similar to small cell carcinomas .
they are often associated with the secretion of hormones and peptides leading to classical syndromes [ 2 , 3 , 4 , 5 ] .
the fulminant nature of the dic in this case is reminiscent of tumour lysis syndrome which is similarly associated with malignancy with a high proliferative rate , large tumour burden and high sensitivity to cytotoxic agents . in tumour lysis syndrome ,
massive quantities of intracellular contents , including potassium , phosphate and nucleic acid that metabolized to uric acid , are released to the systemic circulation , causing acute metabolic imbalance and renal failure . in our case
, it appears that manipulation by core biopsy caused self - limiting and , later , cytotoxic agents caused fulminant dic by the release of procoagulants and cytokines from lysed tumour cells .
dic is characterised by a widespread , intravascular activation of coagulation leading to intravascular fibrin deposition and simultaneous consumption of coagulation factors and platelets .
the consequence of dic depends on its cause and the rapidity with which the activating event is propagated .
if the activation occurs slowly , an excess of procoagulants is produced , leading to thrombosis .
the hallmark of chronic , compensated dic is that the liver can offset the consumption of clotting factors and the bone marrow maintains an adequate platelet count .
if the activation is brisk , the clinical picture is dominated by intravascular coagulation leading to profound systemic bleeding diathesis .
our case was an unusual presentation as dic in cancer usually is a less fulminant presentation compared to dic associated with sepsis and trauma .
tissue factor ( tf ) and cancer procoagulant - mediated activation of coagulation , platelet aggregation and activation , suppression of the fibrinolytic pathway and cytokine - regulated defective anticoagulant mechanisms form pivotal roles in activating coagulation and the ensuing procoagulant state in cancer .
complications are typically related to excess procoagulants causing venous thrombosis ( deep venous thrombosis , superficial migratory thrombophlebitis and , less commonly , arterial thrombosis ) , digital ischaemia , renal infarction and stroke .
the physiological response to the exposure of tumour - specific antigens results in the release of potent inflammatory mediators such as tumour necrosis factor and interleukin-1 from activated macrophages and stimulated t cells .
this further propagates the prothrombotic process as besides from being potent mediators of inflammation these cytokines can also induce tf expression , activate platelets and downregulate the protein c pathway .
in addition , these cytokines induce endothelial expression of plasminogen activator inhibitor-1 and impair the protein c anticoagulant pathway by downregulating thrombomodulin and endothelial protein c receptor . as a consequence , fibrinolytic and anticoagulant activities are decreased .
laboratory evidence of coagulation activation has been documented with exposure to chemotherapy ( e.g. cyclophosphamide , methotrexate and 5-fluorouracil ) and hormonal therapy ( e.g. tamoxifen ) , but usually the abnormalities in coagulation markers are modest and do not correlate with the development of dic .
it is postulated that the release of procoagulants and cytokines from lysed tumour cells as well as endothelial cell damage are caused by cytotoxic agents rather than being a direct effect of chemotherapy itself .
in addition , by direct surgical trauma of tumour blood vessels , exposure to subendothelial tf causes the release of cytokines with their procoagulant activity .
management is limited to supportive care by replacing blood products and treating the underlying malignancy .
this poses a dilemma as cytotoxic agents may worsen dic and may also directly suppress bone marrow production .
malignancy is a common cause of disseminated intravascular coagulation and usually presents as a chronic disorder in solid organ tumours . 
 we present a rare case of recurrent acute disseminated intravascular coagulation in neuroendocrine carcinoma after manipulation , firstly , by core biopsy and , later , by cytotoxic therapy causing a release of procoagulants and cytokines from lysed tumour cells . 
 this is reminiscent of tumour lysis syndrome where massive quantities of intracellular electrolytes and nucleic acid are released , causing acute metabolic imbalance and renal failure . 
 this case highlights the potential complication of acute disseminated intravascular coagulation after trauma to malignant cells .