Tata 69l. PSA 59 ng/ml BxGl.4+3 cT3a?

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Re: Tata 69l. PSA 59 ng/ml BxGl.4+3 cT3a?

Nieprzeczytany postautor: zosia bluszcz » 16 wrz 2017, 22:52

Czy gorączka może być związana z rakiem, czy raczej chodzi o coś innego?


Gorczka nie jest zwiazana z rakiem. Gorączka jest zwiazana z infekcją.
Moim zdaniem Tata powinien wrocic do szpitala, w ktorym byl leczony. Im szybciej, tym lepiej.
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Re: Tata 69l. PSA 59 ng/ml BxGl.4+3 cT3a?

Nieprzeczytany postautor: ewelinka8 » 17 wrz 2017, 07:58

Dokładnie. Nie ma co czekać na jutro bo temp wysoka. Zapewne na wypisie macie zaznaczone że zgłosić się trzeba do najbliższego SOR w razie wystąpienia np. wysokiej temperatury. Nie można lekceważyć takich stanów przy przebytej sepsie, to znak że znów organizm walczy !
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Re: Tata 69l. PSA 59 ng/ml BxGl.4+3 cT3a?

Nieprzeczytany postautor: ewazosia2006 » 19 wrz 2017, 13:14

tomografia.jpg

Dzień dobry wszystkim.
Odebraliśmy dzisiaj wyniki tomografii. Z wniosków wynika tyle,że jest podejrzenie meta w węźle biodrowym,ale co oznacza obszar naciekowy w okolicy połączenia miedniczkowo-moczowodowego lewego?
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Re: Tata 69l. PSA 59 ng/ml BxGl.4+3 cT3a?

Nieprzeczytany postautor: bela71 » 19 wrz 2017, 21:46

co oznacza obszar naciekowy w okolicy połączenia miedniczkowo-moczowodowego lewego?


Coś się dzieje w miejscu, gdzie moczowód wychodzi z nerki (czyli w jego górnej części). Opis nie precyzuje, czy to naciek zapalny (możliwy przy kamieniach i cewniku), czy nowotworowy. Trzeba to dalej badać/obserwować.
Przerzuty z prostaty do nerki zdarzają się rzadko.

Jak się tata czuje?
Tata ur.1936 Od 2005 leczenie BPH, PSA przy finasterydzie oscylujące między 5 a 11(!).
Po odstawieniu Proscaru VII.2012 PSA 20,81ng/ml, biopsja GL 4+3, zatarta torebka, scyntygrafia czysto. cT3NxM0 Gleason 7 (4+3)
X.2015 Apo-Flutam (1mc), Diphereline co 3m-ce, zmieniona po roku na Eligard 45. 4.XII.12 PSA 1,15.
XII.2012-I.2013 RT 65 Gy IGRT w 25 frakcjach (Wieliszew).
PSA 21.II.13 - 0,089; 25.IV.13 - 0,076; VI.13 - 0,067; IX.13 - 0,065; XII.13 - 0,044,(testosteron 0,035); III.2014 - 0,057, (T<0,025 od tego momentu); V.14 - 0,021; IX.14 - 0,016; XI.14 - 0,009; I.2015 - 0,01; IV.15 - 0,011 KONIEC HT VIII.15 PSA - 0,008; XI.15 PSA 0,010, T 0,14; II 2016 PSA 0,025, T 0,4; V 2016 PSA 0,017, T 0,68; VIII 2016 PSA 0,021, T 0,9; XI 2016 PSA 0,016, T 0,966; III 2017 PSA 0,003[?], T 1,38; IX 2017 PSA 0,035 T 1,63; XI 2017 PSA 0,051, T 1,79

3.12.15 – Kolonoskopia i APC zmian naczyniowych (angiodysplazja odbytnicy po RT); 2016 2 serie czopków łagodzących podkrwawianie; 29.05.2017 - ponowna koagulacja laserowa niewielkich zmian naczyniowych w odbycie
Wątek: http://rak-prostaty.pl/viewtopic.php?f=2&t=2137
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Re: Tata 69l. PSA 59 ng/ml BxGl.4+3 cT3a?

Nieprzeczytany postautor: zosia bluszcz » 19 wrz 2017, 22:17

Mysle, ze moze to byc raczej stan zapalny.

Tak wyglada dJ stent (double J czyli podwojne Jot):


ureteric-stent-img.jpg
ureteric-stent-img.jpg (24.02 KiB) Przeglądany 280 razy

http://www.kidneystoneclinic.com.au/uri ... ble-j.html
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Re: Tata 69l. PSA 59 ng/ml BxGl.4+3 cT3a?

Nieprzeczytany postautor: ewazosia2006 » 20 wrz 2017, 12:28

Jeśli chodzi o samopoczucie taty....To nie jest najlepiej. Jest bardzo osłabiony,boli go kręgosłup,nerka,o od paru dni doszły bóle zębów.W szybkim czasie posypały się tacie trzy zęby,dentysta powiedział,że nie wygląda to dobrze... :( Do tego ciągła temperatura dochodząca do 39st...onkolog twierdzi,że nie jest ona spowodowana stanem zapalnym,tylko rakiem. W poniedziałek tata ma przyjąć pierwszą dawkę Eligadu,co dalej nie wiem.
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Re: Tata 69l. PSA 59 ng/ml BxGl.4+3 cT3a?

Nieprzeczytany postautor: bela71 » 20 wrz 2017, 16:26

Przypadki gorączki powiązanej z rakiem prostaty są bardzo rzadkie. Poniżej link do artykułu z dwoma opisanymi przypadkami, w obu po rozpoczęciu HT nastapiła poprawa. Istotna jest lista tego, co wykluczono najpierw, zanim winę za gorączkę zrzucono na nowotwór - najpierw wykluczono udział znanych patogenów, zarówno bakterii jak i grzybów oraz wirusów. Tata niedawno przeszedł sepsę, ma w nerce potencjalne źródło stanów zapalnych.
http://www.medscape.org/viewarticle/733640_7

Poniżej niezły artykuł o gorączce u pacjentów z nowotworami - kopiuję część o przeprowadzaniu diagnozy:

Fever in Patients with Cancer
Mark A. Marinella
http://www.antimicrobe.org/new/e13.asp

DIFFERENTIAL DIAGNOSIS

Infection
Bacterial Versus Viral Infection


The astute, thoughtful clinician always entertains infection as a possible cause of fever in any patient, especially those with cancer since these patients are especially prone to infection. Bacterial infections of the respiratory and urinary tractspredominate. However, other sites include the sinuses, mouth, abdomen, skin and soft tissue, and bloodstream. The most common microbes isolated from the blood include Gram-positive cocci (e.g., Staphylococci and Streptococci) and Gram-negative bacilli, such as theEnterobacteriaciae and Pseudomonas species. Pneumococcal pneumonia and E. coli urinary infections remain common in cancer patients as well. Table 3 displays some of the common infection types in cancer patients and Table 4 displays some of the more frequently isolated bacterial species.

An in-depth discussion of microbiology is beyond the scope of this text, but viral pathogens may infect patients with solid tumors and hematologic malignancies, especially leukemics who have had total marrow ablation for a bone marrow transplant. Some of the viruses that may cause infection in these groups include Cytomegalovirus, Epstein-Barr virus, Adenovirus, Echovirus, Influenza A virus, respiratory syncytial virus, Parvovirus, and human herpes virus-8. If any of these pathogens are suspected, an infectious diseases consultation should be considered since viral infections are often difficult to diagnose, and often even harder to treat.

Risk Factors for Infection

Venous Catheters
Indwelling central venous catheters for long-term chemotherapy or parenteral nutrition place the cancer patient at significant risk for bloodstream infection, especially with Staphylococcal species. Implanted surgical ports, central venous lines, or peripherally inserted central catheters (PICC) lines may all become infected, especially if strict aseptic technique is breached during insertion or port manipulation. A central catheter can become infected in three primary ways. First, during insertion, bacteria on the skin can infect the insertion tract, thereby contaminating the soft tissue which can lead to a tunnel or soft tissue infection. The bacteria can migrate along the line into the bloodstream resulting in bacteremia. A second way a central line can become infected is thru contamination of the port during drug or fluid administration. Third, the line itself can become colonized after insertion and lead to bacteremia. Some pathogens (e.g., Staphylococcus sp. Pseudomonas sp. and Candida sp.) produce a biofilm on the catheter which prevents immune cells from destroying the bacteria as well as decreasing antibiotic efficacy. As a result, one should consider line removal if catheter-associated bloodstream infection is diagnosed.

Chemotherapy Induced Mucositis
The intent of systemic chemotherapy is to arrest growth and destroy actively dividing neoplastic cells. However, rapidly proliferating cells of the oral and alimentary mucosa are also susceptible to chemotherapy resulting in cell death, inflammation, and regeneration. This denudation of the oral and gut mucosa (“mucositis”) may lead to bacterial translocation with fever and sepsis, especially with Gram-negative bacilli and microaerophilic streptococci.

Surgical Procedures
Surgery results in disruption of normal tissue and organs and invokes a reparative and inflammatory response. Cancer surgery (e.g., breast, colon, other viscera) often results in large incisions and, at times, empty tissue spaces that can fill with fluid or blood and become infected. Cancer patients with immune dysfunction, neutropenia, or recent chemoradiotherapy administration are more prone to developing wound and incision infections or, less commonly, a bacterial infection at the surgical bed site, resulting in fever. Fever in patients who have had cancer surgery may also result from venous thrombosis, drug fever, or catheter-related infection. Also, it is prudent to remember that surgery itself results in liberation of cytokines from migrating leukocytes at the interface of surgery-induced tissue trauma, which can also cause fever.
Foreign Bodies

Cancer patients with implanted foreign bodies may develop fever as an immune reaction to the device or due to subsequent infection. For instance, a cancer patient with a neoplastic fracture of the femoral neck may require a palliative hip hemiarthroplasty. Fever is almost universal following prosthetic joint implantation and is due to mononuclear cells releasing cytokines that cause fever. As noted, foreign body infection can also cause fever. Cancer patients may have pre-existing prosthetic heart valves that could become seeded with bacteria during chemotherapy-induced mucositis. Prosthetic joints, pacemaker wires, surgical drains, ventriculo-peritoneal shunts, and surgical mesh to repair an abdominal wall defect following cancer surgery are other examples of foreign bodies that can become infected leading to fever.
Miscellaneous

Other risk factors for infection in this population include bedrest with subsequent decubiti formation or aspiration pneumonitis; long-term broad spectrum antibiotics for neutropenic fever resulting in candidemia; mucormycosis of the nasal cavity complicating metabolic acidosis or hyperglycemia; and necrotizing fasciitis or Fournier’s gangrene in patients with breeches of the skin.

Non-Infectious Etiologies

Deep Venous Thrombosis

Venous thromboembolism (VTE) is an important diagnosis that may cause fever in the cancer patient and should be considered in any patient without clear evidence of infection-associated fever. Many tumor histologies have been linked to venous thrombosis, but adenocarcinomas of the breast, lung, prostate, alimentary tract, and kidney are most common. These tumors create a biochemical hypercoagulable state by secreting various clotting factors. Classically, migratory thrombophlebitis, known as Trousseau’s syndrome, is a harbinger of cancer, usually visceral (especially pancreatic). Brain tumors, lymphoma, and melanoma may also be associated with venous thromboembolism.

Other reasons that cancer patients are predisposed to venous thromboembolism include immobility, surgery, venous occlusion or stasis from tumor masses or lymphadenopathy, dehydration, and endothelial injury from chemotherapy. As a result, the clinician needs to maintain a high index of suspicion of venous thromboembolism in any febrile cancer patient, and realize that venous thromboembolism may coexist with ongoing infection.

A unique manifestation of hypercoagulability, especially with adenocarcinomas, is non-bacterial thrombotic endocarditis (NBTE), or marantic endocarditis. This phenomenon results in sterile vegetations that typically occur on the mitral or aortic valves. Fever may be a prominent manifestation, as well as peripheral vascular or central nervous system embolic phenomena, which can be devastating.

Tumor Fever

As noted above, various neoplasms can invoke a febrile response by liberating cytokines such as interleukin-2, TNF, interleukin-6, amongst others. Some of the tumors classically associated with tumor-induced fever include renal cell carcinoma, atrial myxoma, non-Hodgkin’s lymphoma see photos , Hodgkin’s lymphoma, and leukemia. Many other solid tumors see photos have been implicated in causing tumor fever as well, but an in-depth discussion of this topic is beyond the scope of this text.

Drug Fever
Various classes of drugs can invoke a febrile response. One of the challenges of evaluating fever in a cancer patient is the protean differential diagnostic possibilities of fever in this population such as infection, neoplastic tissue, thrombosis and various drugs. Chemotherapeutic agents, antibiotics, and other drug classes can cause fever, which often make pinning down the etiology very difficult. Suffice it to say, the clinician should consider drug fever as a possible cause of fever in the cancer patient, especially in the presence of rash, eosinophilia, or temperature-pulse dissociation. Table 5 lists some of the more notable causes of non-infectious fever in the cancer patient.

DIAGNOSIS OF FEVER IN THE PATIENT WITH CANCER OR SUSPECTED CANCER
Clinical Clues
History

As in all areas of medicine, the history is the crux of diagnosis in the febrile patient. Many historical clues may elicit the cause of fever, but only a few will be noted since not all scenarios can be covered in this limited space. Drenching night sweats, significant weight loss, and anorexia often accompany fever complicating neoplastic disease, especially Hodgkin’s or non-Hodgkin’s lymphoma. Fullness or a “dragging” sensation in the left upper quadrant may signify splenic enlargement that may complicate chronic myelogenous leukemia or disseminated lymphoma. Rigors and chills during the daytime should make the physician consider infection, although some tumors can evoke chills as well. Fever and early satiety may indicate gastric cancer or extrinsic impingement upon the stomach wall by intra-abdominal lymphadeonpathy or splenomegaly from lymphoma. Fever and hemoptysis may be due to lung cancer or post-obstructive pneumonia resulting from a thoracic mass lesion such as bronchogenic carcinoma or massive lymphadenopathy from lymphoma. Alternatively, immunosuppressed cancer patients could develop reactivation tuberculosis or a fungal infection which may cause fever, systemic symptoms, and hemoptysis. To summarize, a thorough history in any febrile patient is the cornerstone to a prompt, accurate diagnosis.

Physical Examination
In febrile patients with known cancer or those undergoing chemotherapy, the physical examination should focus on potential sites of infection such as the oral cavity, nasal sinuses, neck, chest, abdomen, perineum, perirectal area, skin, and joints. Febrile patients with undiagnosed but suspected cancer should also have a thorough search for infection. In addition, major lymph node chains should be thoroughly palpated (e.g. neck, supraclavicular, occipital, axillae, epitrocholear, inguinal, popliteal areas) since enlargement of lymph nodes in these areas may occur with lymphomas, leukemias, and metastatic adenocarcinoma. The presence of a supraclavicular node (Virchow node) should prompt a search for intrathoracic or visceral malignancy. A peculiar lymph node lesion known as the Sister Mary Joseph nodule is invariably associated with metastatic intra-abdominal cancer (e.g., ovary, gastric, etc.). Another area to focus attention on in a febrile patient with suspected cancer includes the skin, since metastatic renal cell or bronchogenic cancer may involve the integument as may leukemia (“leukemia cutis”). A palpable renal mass may signify renal cell carcinoma, which can cause fever, systemic symptoms, hematuria, and multiple laboratory derangements earning this neoplasm the title of the “Internist’s tumor.” A unique cause of fever and systemic illness in a leukemic patient receiving chemotherapy is typhlitis, an inflammatory/infectious phlegmanous process involving the appendix and cecum. Physical examination may reveal right lower quadrant tenderness, rebound tenderness, or a doughy, mass-like area to palpation.
Fever Curves
No fever pattern is specific for any type of malignant disease. As noted in a preceding section, the Pel-Ebstein fever pattern is classically associated with Hodgkin’s lymphoma. This pattern manifests as episodic fever at various times of day and in various intervals, typically consisting of a three to ten day period of fever, followed by a three to ten day period of apyrexia. Nonetheless, it is best to remember that any prolonged fever can be associated with a variety of solid and hematologic cancers.
Non-steroidal Anti-inflammatory (NSAID) Challenge
Diagnosing cancer rests on collection and analysis of multiple data sets of which include history, physical examination, laboratory and serologic studies, radiography, and tissue biopsy. However, at times the diagnosis of prolonged fever can remain elusive despite the initial evaluation. Chang and colleagues demonstrated that the NSAID agent naproxen was very effective in suppressing tumor fever and this property may be useful in elucidating the clinician’s suspicion of cancer in patients with prolonged, undiagnosed fever. Naproxen has been the classically touted agent for suppressing tumor fever due to its unique ability to suppress tumoral cytokines in preference over infectious cytokines. While the “naproxen challenge” may be useful in evaluating prolonged fever suspected to be of neoplastic origin, it must be utilized in the context of a thorough, clinically-driven assessment.

LABORATORY ASSESSMENT
Infectious Disease Evaluation


Other chapters in this work cover this aspect in greater detail, but a few salient features of an infectious work-up in the febrile cancer patient will be mentioned.
Cultures
Cultures of the blood, urine, and sputum are fairly standard in any cancer patient suspected of having a bacterial infection. Cultures of other body fluids should be based on the clinical situation but include cerebrospinal fluid, pleural fluid, peritoneal fluid, or abscess fluid. Typically, culture of these sites requires an invasive procedure.
Patients suspected of having a bacterial infection due to a fastidious bacterial organism (e.g., nutritionally deficient streptococci) or a virus require special media and notification of the microbiology laboratory. In this circumstance, Infectious Disease consultation should be arranged.
Serologies/Antigen Studies
Acute and convalescent serologies for viral infections may be useful, as may heterophile tests for cytomegalovirus or Epstein-Barr virus. If Legionella infection is suspected, the urine antigen study is approximately 70% sensitive for detecting infections with Legionella pneumophilia, serogroup 1. For more discussion on serologic and antigenic testing, the reader is referred to specific chapters in the Microbes section. Acute Phase reactants Supplemental testing in the diagnosis of fever in the cancer patient may include many laboratory tests, most of which are non-specific.
Acute Phase Reactants
The ESR is a non-specific test of systemic inflammation which measures the distance a drop of blood falls within a microtube in one hour. The result is reported in mm/hr, and values of greater than 100 mm/hr are suggestive of malignancy, deep seated infection, or autoimmune disease. However, the ESR is only a general screen as to the presence of systemic inflammation and is by no means diagnostic of any disease process. C-reactive protein is an acute phase reactant produced by hepatocytes, and may be elevated in the same clinical scenarios as the ESR. Again, this test is not diagnostic of cancer and shares the limitations of the ESR, but may be more sensitive to diagnose an inflammatory process.
Radiology
When to Order Computed Tomographic (CT) Scanning
CT scanning has revolutionized the diagnostic approach to a variety of diseases, especially cancer. Fever in the cancer patient can be due to neoplasia itself which can manifest on CT imaging as a primary mass lesion, metastases, body cavity effusions, pneumonia, hydronephrosis, biliary dilatation, and lymphadenopathy. Perhaps the greatest utility of CT imaging is the ability to obtain a tissue diagnosis with aspiration cytology or a needle core biopsy. As such, CT imaging should be considered in a febrile patient when cancer is suspected, when a tissue diagnosis is needed, or if an infectious process may be present.
When to Order Magnetic Resonance Imaging (MRI)
Fever in a patient with known or suspected cancer can typically be diagnosed with history, physical examination, basic laboratory studies, and CT scanning. The use of MRI is more limited in this situation but may prove helpful for diagnosing pancreatico-biliary neoplasms (with magnetic resonance cholangiopancreaticography, MRCP), soft tissue or muscle tumors, or even bone sarcomas or osteomyelitis. Occasionally, brain metastatisis or gliomas can induce fever, and cerebral MRI is very sensitive in diagnosing brain lesions.
When to Order Nuclear Medicine Imaging
Nuclear imaging studies are occasionally helpful in evaluating fever in the cancer patient. Technitium bone scanning is useful in assessing for osseous metastases, especially osteoblastic metastases. Indium-111 scanning may assist in the diagnosis of an abscess or infected fluid collection. Gallium-67 scanning has been utilized in the diagnosis of lymphoma. Perhaps the most useful nuclear imaging test is positron emission tomography (PET) scanning which utilizes radio-labeled glucose (typically 18-flourodeoxyglucose, FDG) to identify areas of increased metabolic activity that occur with a variety of neoplasms, such as lung cancer and lymphoma. Not only is PET making an impact in diagnosis of malignancy but also on the assessment of recurrence after surgery or chemotherapy. This modality may also identify areas of focal inflammation or infection, which can make diagnosis challenging in certain patients.

EMPIRIC ANTIBIOTIC THERAPY
Empiric Antibiotics Versus Watchful Waiting

Other chapters in this text address antibiotic therapy in the cancer patient in more detail. However, a few basic principles will be discussed. First and foremost, any cancer patient with febrile neutropenia (absolute neutrophil count <500 cells/mm3) should be rapidly assessed to identify an obvious infectious source. In general, any patient with neutropenia and fever with unstable vital signs, acidosis, clouded sensorium, or co-morbidities should be admitted and administered broad-spectrum anti-microbials (e.g., ceftazidime, piperacillin-tazobactam). Febrile neutropenic patients who are clinically stable and appear well can be managed as an outpatient with oral agents such as a fluoroquinolone combined with amoxicillin-clavulonate. For a more detailed discussion, the reader is referred to other chapters in this text or to textbooks in medical oncology.
ADJUNCTIVE THERAPY
Supportive Care

General medical care should be offered to the cancer patient with fever and typically includes intravenous fluids to replace insensible water loss from pyrexia, pain control, venous thromboembolism prophylaxis, nutrition support, and physical therapy. This should all be done simultaneously with fever evaluation.
Antipyretic Therapy
Fever is a normal host response to inflammation and infection and may confer an immunologic benefit, especially in patients with bacterial infection. Nonetheless, anti-pyretic therapy with acetaminophen, aspirin, or NSAIDS may be considered in certain situations. First, if a patient requests fever suppression for comfort, it should be provided. Another indication for treatment of fever is the potential adverse effects of fever-induced insensible water loss and increased metabolic demands in ill patients with multiple co-morbidities, especially the elderly. In addition, sinus tachycardia from fever can lead to decreased filling of the ventricle and result in congestive heart failure in patients with limited cardiac reserve. In general, acetaminophen is the agent with the most favorable side-effect profile since it lacks gastropathic and nephrotoxic effects at clinical doses, although caution should be exercised in patients with significant liver disease.
Naproxen Challenge Test
In 1982, Chang and Gross published the sentinel paper on the use of naproxen in the diagnosis of cancer-induced fever. They noted that 14 of 15 patients found to have a malignant disease had suppression of fever when naproxen 375 mg was administered orally twice daily for three days. This was in distinction to the group of eight patients with documented infection of whom only one patient experienced lysis of their fever. Other authors have noted similar results with naproxen, and although not pathognomic for cancer fever, the naproxen challenge test may be useful in narrowing down the cause of undiagnosed fever when cancer is suspected.
Tata ur.1936 Od 2005 leczenie BPH, PSA przy finasterydzie oscylujące między 5 a 11(!).
Po odstawieniu Proscaru VII.2012 PSA 20,81ng/ml, biopsja GL 4+3, zatarta torebka, scyntygrafia czysto. cT3NxM0 Gleason 7 (4+3)
X.2015 Apo-Flutam (1mc), Diphereline co 3m-ce, zmieniona po roku na Eligard 45. 4.XII.12 PSA 1,15.
XII.2012-I.2013 RT 65 Gy IGRT w 25 frakcjach (Wieliszew).
PSA 21.II.13 - 0,089; 25.IV.13 - 0,076; VI.13 - 0,067; IX.13 - 0,065; XII.13 - 0,044,(testosteron 0,035); III.2014 - 0,057, (T<0,025 od tego momentu); V.14 - 0,021; IX.14 - 0,016; XI.14 - 0,009; I.2015 - 0,01; IV.15 - 0,011 KONIEC HT VIII.15 PSA - 0,008; XI.15 PSA 0,010, T 0,14; II 2016 PSA 0,025, T 0,4; V 2016 PSA 0,017, T 0,68; VIII 2016 PSA 0,021, T 0,9; XI 2016 PSA 0,016, T 0,966; III 2017 PSA 0,003[?], T 1,38; IX 2017 PSA 0,035 T 1,63; XI 2017 PSA 0,051, T 1,79

3.12.15 – Kolonoskopia i APC zmian naczyniowych (angiodysplazja odbytnicy po RT); 2016 2 serie czopków łagodzących podkrwawianie; 29.05.2017 - ponowna koagulacja laserowa niewielkich zmian naczyniowych w odbycie
Wątek: http://rak-prostaty.pl/viewtopic.php?f=2&t=2137
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Re: Tata 69l. PSA 59 ng/ml BxGl.4+3 cT3a?

Nieprzeczytany postautor: zosia bluszcz » 20 wrz 2017, 22:19

Ja rowniez znalazlam ten artykul CME.
Ponizej cytuje fragment dotyczacy dwoch opisanych przypadkow wystapienia objawow paraneoplastycznych, rowniez dlugotrwalej wysokiej goraczki u pacjentow z niezdiagnozowanym uprzednio CaP.

Jakie Tata ma obecnie CRP i OB?
Mysle, ze nie nalezy zwlekac z podaniem hormonow, w obydwu opisanych w artykule przypadkach zastosowana HT zadzialala blyskawicznie, oby tak bylo rowniez w przypadku Taty.


CME
Paraneoplastic Syndromes in Prostate Cancer: Clinical Management


Clinical Management

We present two cases that typify the presentation and management of prostate cancer-associated para-neoplastic syndromes; they involve high levels of PSA, late tumor stages, moderate to poorly differentiated adenocarcinoma, and resolution of the syndrome with treatment of the underlying malignancy. In both cases, immunohistochemical studies demonstrated production of putative markers responsible for the paraneoplastic syndrome within the primary tumor.


Case 1
A 69-year-old man presented with 10 days of fevers measuring up to 39.1°C, rigors and night sweats.
His medical history included heavy smoking, chronic airways disease and osteoarthritis. Some weeks earlier, he was seen in the primary care setting for lower urinary tract symptoms and had a screening serum PSA level of 36 ng/ml. He was awaiting specialist urological consultation at the time of presentation.

Detailed history and physical examination was not suggestive of any septic focus. Blood tests revealed raised inflammatory markers (C-reactive protein 206 mg/l [normal range 0.08-3.1 mg/l] and erythrocyte sedimentation rate 118 mm/h [normal range 0-20 mm/h]), mild neutrophilia with no leukocytosis, and a mildly raised serum alkaline phosphatase level of 333 IU/l (normal range <120 IU/l). The patient was admitted for further management under the care of a specialist infectious diseases unit at a tertiary referral center.

Detailed septic workup did not yield a diagnosis. Blood and urine microscopy and cultures were repeatedly negative. Fungal screens were negative. PCR results for other bacteria including Q fever, Mycoplasma, leptospirosis, brucellosis, and tuberculosis were negative. Tests for cytomegalovirus, Epstein-Barr virus, and HIV and an autoimmune screen were also negative.

Despite the commencement of empiric antibiotics, including flucloxacillin, ceftriaxone, doxycycline, piperacillin, antivirals and even antifungal agents, the patient remained unwell with persistent fevers. Given the raised PSA and with a possibility of bacterial pros-tatitis, the patient was referred to our Urology service for an opinion. Digital rectal examination of the prostate revealed a mildly enlarged, nontender but craggy prostate consistent with clinical stage T3 prostate cancer. Repeat PSA measured 40.1 ng/ml. CT of the chest, abdomen and pelvis revealed sclerotic bone lesions scattered throughout the axial skeleton, and a follow-up bone scan confirmed these to be metastases. Transrectal ultrasonography (TRUS)-guided prostate biopsy performed at the bedside revealed infiltrating, poorly differentiated, Gleason score 9 (4 + 5) prostate adenocarcinoma in one of three cores. The tumor stained strongly for cytokeratin and PSA confirming its prostatic epithelial origin.

5 days after admission the patient was diagnosed with metastatic prostate cancer and commenced on ADT (bicalutamide 50 mg three times daily). All antibiotics except doxycycline had been ceased by this time. Within 24 h he had clinically improved and his fevers had abated (Figure 1). Goserelin injections were commenced a week later and, after a total of 3 weeks in hospital, the patient was discharged afebrile and feeling well. At 3 months follow-up, the patient reported no further fevers and PSA was 1.4 ng/ml.

Figure 1.
Temperature chart. A 69-year-old man presented with 10 days of fevers measuring up to 39.1°C, rigors and night sweats. Blood tests revealed raised inflammatory markers and erythrocyte sedimentation rate, mild neutrophilia with no leukocytosis, and a mildly raised serum alkaline phosphatase level. The patient was admitted for further management and his temperature was measured four times a day. 5 days after admission the patient was diagnosed with metastatic prostate cancer and commenced on androgen deprivation therapy (arrow), after which the swinging fevers abated.

Further analysis of the prostate biopsy specimens was undertaken to confirm histologically that the fevers were a paraneoplastic phenomenon caused by the prostate cancer. Immunohistochemical staining for IL-6 was performed using normal lung tissue as a positive control. Staining of lung tissue without the primary antibody was performed for the negative control. Benign prostate tissue in biopsy cores served as a local control. Strong staining for IL-6 was shown by the tumor (Figure 2), strongly suggesting that prostate cancer was the underlying cause of a systemic inflammatory response.

Figure 2.
Immunohistochemical staining for Interleukin 6 (IL-6). a | Lung tissue as a positive control (magnification: 100x). b | Negative staining in lung tissue (magnification: 100x). c | Positive staining in prostate tumor tissue (magnificiation: 250x). d | Negative staining in benign prostate tissue (magnification: 250x). Strong staining for IL-6 was seen in the prostate cancer tissue, indicating that prostate cancer was the underlying cause of a systemic inflammatory response.

Case 2
A 66-year-old man presented to the emergency department with collapse, confusion and gross hematuria of 1 week's duration. On physical examination there was evidence of neuromuscular excitation and the patient required a three-way catheter with bladder irrigation for clot retention. The patient was normotensive and clinically euvolemic.

Initial laboratory tests detected a serum sodium concentration of 111 mmol/l (normal range 135-143 mmol/l), serum chloride of 80 mmol/l (normal range 99-107 mmol/l), whole blood hemoglobin 83 g/l (normal range 122-170 g/l), serum osmolality 232 mmol/kg (normal range 275-300 mmol/kg), urinary osmolality 241 mmol/kg (normal range 300-900 mmol/kg) and urinary sodium 90 mmol/l (normal <20 mmol/l). Renal function tests, chest radiography, serum cortisol, serum glucose, thyroid function tests, drug screen, and CT of the brain and abdomen showed no abnormalities. Serum PSA was 456 ng/ml and digital rectal examination revealed a hard nodular prostate. Subsequent staging with whole body bone scan identified widespread osseous metastasis.

TRUS-guided prostate biopsy was performed and histology revealed Gleason score 9 (5 + 4) adenocarcinoma in five of six cores. Tumor cells were arranged in a predominantly solid, single file and single cell pattern. The tumor stained positive for PSA but negative for neuroendocrine markers CD56 and synaptophysin, the presence of which is associated with neuroendocrine differentiation, namely SCC.

The patient was admitted to hospital and initially managed with 3% hypertonic saline and fluid restriction. On the second day of admission, ADT with bicalutamide 50 mg three times daily and goserelin acetate injections was commenced. Serum sodium levels normalized after 3 days (Figure 3) and the hematuria resolved spontaneously. At 3 months follow-up, serum PSA measured 256 ng/ml, testosterone was undetectable, and serum sodium concentration was 141 mmol/l. The patient remained free of bone pain and lower urinary tract symptoms.

Figure 3.
Serum sodium. A 66-year-old man presented to the emergency department with collapse, confusion and gross hematuria of 1 week's duration. On physical examination there was evidence of neuromuscular excitation and the patient required a three-way catheter with bladder irrigation for clot retention. The patient was normotensive and clinically euvolemic. Initial laboratory tests detected a low serum sodium concentration of 111 mmol/l. The patient was admitted to hospital and initially managed with 3% hypertonic saline and fluid restriction. On the second day of admission, androgen deprivation therapy with bicalutamide and goserelin acetate injections was commenced (arrow), after which serum sodium levels normalized.

Immunohistochemical staining for ADH was performed on prostate tissue obtained from the biopsy and showed moderate staining in all cores, thus suggesting that the prostate cancer was the source of circulating ADH responsible for the paraneoplastic SIADH. Normal pituitary tissues were used as negative (anterior pituitary) and positive (posterior pituitary) controls. Benign prostate tissue in biopsy cores served as a local control (Figure 4).

Figure 4.
Immunohistochemical staining for antidiuretic hormone (ADH). a | Positive staining for ADH in posterior pituitary gland (magnification: 100x). b | Negative staining for ADH in anterior pituitary gland (magnification: 100x). c | Positive staining in prostate tumor tissue (magnification: 250x). d | Negative staining in benign prostate tissue (magnification: 250x). Strong staining for ADH was seen in the prostate cancer tissue, suggestive that prostate cancer was the source of circulating ADH responsible for the paraneoplastic syndrome of inappropriate antidiuretic hormone secretion.


https://www.ncbi.nlm.nih.gov/pubmed/16144664
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