A 59 year old man is admitted to hospital with severe backache and urinary retention which is accompanied by discomfort in the suprapubic region. There is also some evidence of blood loss in the urine and on examination; he has some bruising and a rash. The patient has felt well until recently and has been attending work on a regular basis.
Table 1: Shows Haematology report
Full Blood Count
10.1 x 109/ ul
4.0 - 11.0 x 109/ ul
3.0 X 109
13.5 -17.5 g/dl
MCV ( Mean Cell Volume)
80 - 95 fl
10 x 109/ ul
150 - 450 x 109/ ul
Deferential WBC count
55 - 65%
20 - 40%
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4 - 10%
1 - 3%
Blood Film examination:
Blood film examination shows presence of crenated Red Blood Cells, schistocytes, polychromasia and spherocytes cells.
Table 2: Shows Coagulation profile results
Prothrombin time (PT)
10 -14 sec
Activated Partial Thromboplastin
30 - 40 sec
Table 3 : Shows Biochemistry report
15 mmol /L
2.5 - 6.4 mmol/L
0 - 17 Î¼mol/l
3.5 - 5.0 mmol/L
30 - 90 IU/ml
Prostatic Acid Phosphatase
Table 5 : shows Microbiology urine Culture report
Heavy growth (>105)of E.coli infection colonies
Pure growth of round, pink, mucoid like colonies, lactose
fermenting, moist and slightly large colonies
Pure medium growth of round yellow colonies, moist lactose
Table 6: shows Histology Smears Report
an example of normal prostate tissue stained with H&E.
showed what the majority of the prostatic tissue looked like .There was a lot less stromal tissue between the glands and the glands were rather crowded together. They were smaller that seen usually and they were round, rather than oval. No basal cells could be identified in them and the epithelial cells were crowded and showed darker staining, particularly of the nucliei. The nuclei also varied in size and shape.
showed what a smaller amount of the prostatic tissue looked like. On one side of the slide, glandular structures were evident, although they were not clearly defined. On the right hand side, small amounts of stromal tissue were seen scattered within large sheets and groups of small, darkly staining, abnormal cells. These cells did not contain particularly large amounts of cytoplasm.
According to the presented patient's clinical information and laboratory investigations , it seems that this patient has primary prostate cancer (Adenocarcinoma), which has metastasized to the liver, causing secondary liver cancer and blocked the urinary tract causing acute renal failure. This resulted in urinary tract infection with Escherichia. coli. The kidney failure and along with UTI are causing the symptomatic backache experienced by the patient. The mucin-secreting adenocarcinoma of the prostate is causing the haematological effect, disseminated intravascular coagulation (DIC), which together with the liver problems is reducing the level of clotting factors and platelets.
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Prostate cancer is a malignant growth of prostate glandular cells in the prostate gland which is located at the bottom of the urinary bladder and helps in controlling urination and forming part of the semen. These cells have the potential to spread to other organs, bones, and tissues(1) . Frequently, prostate cancer develops in men over 50 years old.
Considering this patient we can see that, he has grossly raised Prostatic Specific Antigen (APS) of 80ng/ml, which strongly suggests prostate cancer. This test is measuring the level of prostate specific antigen, which is a protein produced by the cells of the prostate
gland including cancer cells. Additionally, high APS level in the blood indicates an abnormal condition of the prostate gland, either benign or malignant. It can be used as a screening test for prostate gland to detect potential problem and as a monitoring test of prostate cancer therapy . PSA is a glycoprotein produced in the prostate gland that keeps semen in liquid form, thus elevated quantities produced by the prostate cancer cells. However, up to one third of patients with localized prostate cancers have normal PSA values(1) .Therefore, PSA measurement cannot be a definitive test for prostate cancer, as PSA level can be elevated with advancing age and benign condition such as enlarged prostate(2) .
The Prostatic Acid Phosphatase (PAP) of this patient is elevated too, which also suggests a prostate cancer but not as specific as PSA. This test measures prostatic acid phosphatase (an enzyme found in men, mainly in prostate gland and semen) to determine the prostate gland health . Prostate dysfunction consequences in the PAP release into the blood. The maximum levels of PAP are detected in metastasized prostate cancer. As the patient has elevated PAP level, it provide more evidence of prostate carcinoma presence(3) .
The definitive diagnosis of prostatic cancer is confirmed by histopathology as the this patient's prostate tissue section examination confirm the diagnosis of prostate cancer. The prostate is consist of glands that normally lined by pale cytoplasm and two cell layers. The two cell layers contain secretory cells (have cytoplasm, produce prostatic secretions) and basal cells, which are the stem cells of prostate. Prostate cancer lacks basal cells which is important for prostate diagnosis and the epithelial cells were crowded and showed darker staining, specifically of the nuclei. In addition, cancerous glands tend to be smaller and there was less stromal tissue between the glands as we saw in this case the picture lost glandular differentiations which indicates a high grade tumor (4).
Haematuria is sometimes linked with localized prostate cancer and this explains the blood loss in the patient's urine. Typically, haematuria is caused by internal growth of the prostate into the urethra or growth of metastatic deposits within the wall of the bladder (5).
The elevated urea level indicates that the patient may has developed renal failure. Moreover, plasma sodium and potassium values shows a predictive sign of kidney impairment . This is one of the prostate cancer common complications, due to the prostate overgrowing which can obstruct urethra impeding urine flow. Consequently leads to increase the hydrostatic pressure, which contests the glomerular filtration rate and ultimately leads to renal failure. This explained the urinary retention and the backache which experienced by the patient (6).
The urinary tract blockage will result in stagnant urine, thus allowing bacteria to grow and cause urinary tract infection(UTI). The urinary tract infection is an infection that can affect any part of the urinary tract (kidney, bladder, ureter or closest structures). The main contributory agent is : Escherichia coli (Gram-negative bacteria) as it was clearly identified in the patient urine culture. Furthermore, this explain the discomfort in the suprapubic region and backache which were experienced by the patient (7).
Additionally, it seems that the tumor has metastasized to the liver, which can be concluded from the high bilirubin and alkaline phosphatase (ALP) levels. ALP is found in the liver, among other tissues. In liver disease the synthesis of ALP increased due to elevated tissue bile salt concentrations in cholestasis. ALP has been considered to be a relatively sensitive screening test for metastatic tumors of the liver(8). However, ALP activity may increased in bone disorders e.g. (Pagent's disease, metastases to the bone). Therefore, a bone disease should be ruled out, although due to the laboratory finding (i.e. raised bilirubin and coagulation times) it is seem likely to be produced by the liver.
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High bilirubin level indicates that the patient has jaundce, which means too much bilirubin is produced (usually because of hemolysis) or that the liver is unable of sufficiently removing bilirubin in a appropriate way due to blockage of bile ducts or liver disease(8).
Another lab finding which support our conclusion is the prolonged results of the coagulation tests, which can be due to the liver dysfunction.The prothrombin time measures factors VII, X, V, prothrombin and fibrinogen. The activated partial thromboplastin time measures factors VIII, IX, XI and XII in addition to factors X, V, prothrombin and fibrinogen. All the coagulation factors are synthesized by the liver except factor VIII. Hence any defect in the liver function can directly reflect on the performance of clotting factors, which explains the patient's bruising, rash and low platelets count (9).
The patient is anaemic as his full blood count results show low RBC count, haemoglobin and haematocrit, which indicates anaemia. The red blood cells morphology shows the presence of:
Polychromasia and spherocytes cells which indicate liver dysfunction.
Crenated red blood cells, which indicate kidney dysfunction, dehydration and electrolytes dysfunction.
Schistocytes , which indicate fibrin clot and clotting disorder such as DIC .
Anemia can be caused by renal failure by a number of factors e.g. iron, folate or vitamin B12 deficiency, decreased erythropoietin production/increased levels of PTH. Thus, the low hemoglobin level can be due to decreased erythropoietin synthesis by the kidneys as a result of kidney failure (10).
Coagulation screening results were all prolonged as well as the patient symptom of haematuria may indicate Disseminated intravascular coagulation (DIC), also called consumptive coagulopathy. Liver dysfunction could interrupt the normal balance of coagulation, thus leading to DIC. Moreover, the adenocarcinomas such as prostate is a common solid tumor associated with DIC. The mechanism of action of DIC associated with this tumor is believed to be an unknown procoagulant substance that stimulates coagulation. Prostate tumor could also release necrotic tissue or tissue enzymes into the general circulation, thus activating the coagulation flow. DIC is a pathological process in the body where the blood starts to coagulate throughout the whole body. This depletes the body of its platelets and coagulation factors, and there is a paradoxically increased risk of haemorrhage(10).
Further laboratory diagnosis:
In spite of the patient history and the laboratory findings ,give a clear support of the diagnosis. Further test should be processed to role out other complications and to confirm the diagnosis.
Imaging tests ,computerized tomography (CT) or magnetic resonance imaging (MRI) scans may identify the location of cancer that has spread beyond the prostate.
Bone scans and x-rays, these tests look for spread of cancer to the bones.
Lymph node biopsy ,a surgical procedure to determine if the cancer has spread to the lymphatic system.
The measurement of other liver enzymes such as 5'-Nucleotidase, leucine aminopeptidase, aspartate aminotransferase (AST) and alanine aminotransferase (ALT) would be of great clinical value in determining liver disease, with the activity of these enzymes being raised.
To distinguish between the sources of elevated ALP, further tests need to be carried out. The serum level of Î³-glutamyl transpeptidase (GGT) should be measured, which corresponds levels of bone and ALP in liver disease but are both usually increased in bone disease (8). As the ALP produced in the liver are different isoenzymes, they can be distinguished by electrophoretic separation.
To confirm the situation and the prognosis of the liver cells damage or dysfunction, ultrasound scanning on liver and liver biopsy can help and provide a lot of information
Further confirmatory tests for renal failure could be measurement of plasma Creatinine, plasma HCO3 Ultrasound(may show obstruction) , and ECG(may show changes due to hyperkalaemia) (11).
With regard the urinary tract infection we need to know what strain of E.coli (API 20E can help us to confirm the type and strain) the patient has as well as antibiotic susceptibility.
To confirm if the patient having DIC, fibrin degradation products (FDPs) or D-dimer tests (markers of fibrinolysis), bleeding time and fibrinogen levels have to be processed. Decreased platelets, elevated FDPs or D-dimers, prolonged bleeding time and decreased fibrinogen are markers of DIC (6).
Treatment for prostate cancer may involve watchful waiting, surgery, radiation therapy, High Intensity Focused Ultrasound (HIFU), chemotherapy, cryosurgery, hormonal therapy, or some combination depending on how the tumour is growing , stage of the cancer, whether it has metastases to other organs and the age of the patient.
Renal failure can be treated by with deferent method, this includes Hemodialysis, Peritoneal dialysis and Kidney transplants (6).
Treatment for DIC varies the primary cause has to be removed, antibiotics, supportive therapy e.g. Fresh Frozen Plasma, platelets and Red cells concentrate and Anticoagulants therapy e.g. Heparin.
This patient seems to has advanced stage of prostate cancer that may metastasized to the other body organs leading to many diseases complications such as DIC, renal failure and UTI. Nevertheless, the patient has an enormously complicated multifactorial pathogenesis as explained. Hence, it is impossible to set up a correct explanation of the pathological occasions occurring in the patient from the clinical informations and laboratory results. Subsequently, to confirm the patient's suspected disorder, further tests, as described above, should be performed.
Miller DC, Hafez KS, Stewart A. Prostate carcinoma presentation, diagnosis, and staging: an update form the National Cancer Data Base. Cancer 2003; 98:1169.
Barry MJ. Clinical practice. Prostate-specific-antigen testing for early diagnosis of prostate cancer. New England Journal of Medicine 2001; 344(18):1373-1377.
Sharma S, Pirila P, Kaija H, Porvari K, Vihko P, Juffer AH. Theoretical investigations of prostatic acid phosphatase. Proteins 2005; 58: 295-308.
Kai HH, Gustavo EA, Thomas MW. Prostate Cancer. Cambridge: Cambridge University Press; 2009.
Foley SJ, Soloman LZ, Wedderburn AW. A prospective study of the natural history of hematuria associated with benign prostatic hyperplasia and the effect of finasteride. J Urol 2000; 163: 496-498.
Wallach J. Interpretation of Diagnostic Tests. 7th ed. Philadelphia: Lippincott Williams & Wilkins; 2000.
Bos TJ, Somers KD. Microbiology and Infectious Diseases. US: McGraw-Hill Professional;2005.
Goldman L., Bennet C J. Cecil Textbook of medicine. 21th edition. W.B Saunders company publisher's; 2002.
Hoffbrand AV, Pettit JE. Essential haematology. 3rd edition. Blackwell science publisher's; 2000.
Jhon PG, Jhon F, George MR, Frixos P, Bertil G, Daniel AA, Robert M.Wintrobes Clinical Haematology. 21th edition. Lippincott Wiiliams and Wilins; 2008: (2).
Bos TJ, Somers KD. Microbiology and Infectious Diseases. US: McGraw-Hill Professional; 2005.