This document discusses prostate cancer. It is the most common non-skin cancer and second leading cause of cancer death in men in North America. Risk factors include advancing age, family history, and African ancestry. Prostate cancer is typically asymptomatic in early stages and detected by elevated PSA levels and digital rectal exam. Biopsy is used for diagnosis and Gleason score determines grade. Treatment options depend on stage and grade and include surgery, radiation therapy, active surveillance, or observation.

1. CES2018-02: Cáncer de próstata
Mauricio Lema Medina MD

2. Most common non-cutaneous
malignancy in men in North
America
2nd most common cause of
cancer-related deaths in men
1 in 7 men will be diagnosed
Lifetime risk of being diagnosed
with prostate cancer is 18/100 but
risk of dying of prostate cancer is
only 3/100

3. Risk factors
Established
Advancing age
Presence of androgens
Family history 1st degree
relative
African ancestry

4. RISK FACTORS
Potential
High dietary fat
Obesity
Inherited mutations (BRCA1 or
BRCA2 genes)
Vitamin D or E deficiency
Selenium deficiency?

5. Early stages usually asymptomatic
Most cases detected by serum PSA
screening
Palpable nodule or firmness on DRE
Advanced stages
Urinary retention/renal failure
Bone pain
Anemia
Weight loss, fatigue
Spinal cord compression

6. Cáncer de próstata
• En las fases iniciales no hay síntomas en la mayoría de
los pacientes
• Con el tamizaje con PSA y tacto rectal se puede
detectar cáncer de próstata temprano
• Los síntomas más comunes incluyen:
– Dificultad para orinar
– Disminución de la fuerza del chorro urinario
– Hematuria
– Hemospermia
– Edema de miembros inferiores
– Dolor en región pélvica
– Dolores óseos
Adicionada por MLM en 2013. Tomado de la Mayo Clinic
Test de elección:
PSA / Ecografía transrectal de próstata

7. SCREENING
Goal
To identify the presence of
disease at a stage when
treatment can be given that
will cure it
Use a combination of DIGITAL
RECTAL EXAMINATION (dre) and PSA

8. DRE (digital rectal exam)
has a 50/100 positive
predictive value
DRE alone is not a good
screening tool
BUT it is an
important part
of screening

9. A Serine protease
(enzyme) found in
the prostate
Secreted by
prostate
epithelial cells
Found in ejaculate
As diagnostic tool
for:
Screening
Staging
Prognostic
indicator
Surveillance
PROSTATE SPECIFIC ANTIGEN (PSA)

10. SCREENING WITH PSA
No clear cut-point between normal and abnormal PSA levels. Even
PSA cut-off of 1.1 ng/ml misses up to 15% of prostate cancer (The
Cancer Prevention Trial – 2003)
Positive predictive value for PSA > 4ng/ml = 30% (i.e. About 1 in 3
men with elevated PSA have prostate cancer detected at time of
biopsy
PPV increases to 45-60% for PSA > 10ng/ml
Nearly 75% of cancers detected in the grey zone (PSA 4-10) are
organ confined; potentially curable.
<50% of prostate cancers organ confined if PSA >10

11. SCREENING WITH PSA
Pros
 Early detection of disease leads to higher cure rates
 By the time symptoms of prostate cancer present usually not curable
 Screening offers a modest effect on mortality
 The “number needed to screen” is similar to studies on
mammography for Breast Ca and fecal occult blood testing for Colon
Cancer
Cons
 If tests abnormal, need for prostate biopsy
 If cancer found & treatment chosen, morbidity from therapy
 If insignificant cancer found, treatment was unnecessary
 Risk of overdiagnosis, overtreatment

12. SCREENING WITH PSA:
RECOMMENDATIONS
Discuss with the patient and if he decides to be
screened
Annual PSA and DRE
Age 50-70 yrs (with at least 10 yr life expectancy)
Begin screening at age 40 if risk factors
African ancestry
First degree relative(s) with prostate cancer
A shared decision-making approach to PSA screening
seems most appropriate

13. CAUSES OF AN ELEVATED PSA
1. Prostate cancer
2. Age
3. Prostate size (BPH)
4. Infection/inflammation
5. Recent instrumentation (biopsy,
catheterization, etc)
6. Physiological variation
Recent ejaculation

14. Andriole GL, Crawford ED, Grubb RL, et al .,
the PLCO Project Team, Mortality Results
from a Randomized Prostate-Cancer
Screening Trial. N Engl J Med 2009 360:
1310-1319
n=76.693

15. Schroder FH, Hugosson J, Roobol MJ, et al. the ERSPC Investigators, Screening
and Prostate-Cancer Mortality in a Randomized European Study N Engl J
Med 2009 360: 1320-1328
n=162.203
Riesgo acumulado de muerte por cáncer de próstata
Casos: 216 vs 326 – RR: 0.8 CI 0.65-0.9 p=0,04

16. 55-74 yo
Males
Andriole GL, et al. J Natl. Cancer Inst, 104: 125-132, 2012
R
PSA screening
No PSA screening
PSA every year x6, DRE every year x4
n=76.685
n=38.340
n=38.345
Variable PSA No PSA RR
PrCa detection* 4250 (9.6%) 3815 (6.0%) 1.12
PrCa Mortality* 3.7/10.000 py 3.4/10.000 py 1.09 (NS)
PrCa: Prostate cancer
PLCO – 13 years follow-up
After 13 years of follow-up, there was no evidence of a
mortality benefit for organized annual screening in the
PLCO trial compared with opportunistic screening, which
forms part of usual care, and there was no apparent
interaction with age, baseline comorbidity, or pretrial PSA
testing.
Opportunistic screening in about 40%

17. 50-74 yo
Males
Schroeder FH, et al. N Engl J Med, 366: 981-990, 2012
R
PSA screening
No PSA screening
On average 1 every 4 years
n=182.000
n=71.891
n=89.162
Variable PSA No PSA Rate ratio
No PrCa Biopsy 76%
False positive 13%
PrCa detection* 6.963 (9.6%) 5396 (6.0%)
PrCa Mortality* 29% reduction
PrCa: Prostate cancer
NNS: 673 and 33 PrCa detected to save
one life
ERSPC – 11 years follow-up

18. Page  18

19. FREE/TOTAL PSA RATIO: IMPROVES
SPECIFICITY
Prostate cancer maybe
associated with more
protein-bound PSA (less
free PSA) than in BPH
F/T ratio is lower in
patients with prostate
cancer
Can improve test
specificity
Useful when total PSA in
4-10 ng/ml range
BPH
Prostate Ca

20. Biología del cáncer de próstata

21. Fusión TMPRSS2-ERG
• En hasta 80% de los cánceres de próstata
• ERG es un factor de transcripción
– Proliferación
– Fenotipo resistente a la castración
• TMPRSS2 es un gen que responde al AR
– Es una serina proteasa
• Es una diana molecular potencial
– El silenciamiento ERG con RNAi disminuye
proliferación

22. Prostate cáncer diagnosis
Indications for transrectal ultrasound (TRUS)
guided biopsy
Palpable nodule on DRE
Elevated serum PSA
Biopsy involves 10-18 needle cores taken mostly
from the peripheral zone of the prostate
Transrectal ultrasound alone/CT scan/MRI not
sensitive enough to make the Diagnosis

23. Enfoque diagnóstico – Cáncer de
Próstata
Enfoque
diagnóstico –
cáncer de
próstata
Síntomas
urinarios o
PSA anormal
Evaluación
rectal digital
(DRE) / PSA
(si falta)
DRE: Normal
PSA: Normal
PSA de 2, o
menos
PSA de 2+
Velocidad PSA
0.75+/año
TRUB
Repetir 1-3
años
DRE: Anormal
o
PSA: Anormal
TRUB
PSA 10, o menos
+ PSA libre 15%
o menos
Repetir en 6
meses
TRUB: Biopsia transrectal eco-dirigida
PSA: Antígeno específico de próstata
No
Si
No
PSA 10+

24. - histology:
- Gleason scores

25. Prostate cáncer pathology
Adenocarcinoma
Gleason “grade” is from 1-5
based on glandular
architecture
Gleason score is the total
primary grade (1-5) +
secondary grade (1-5) = 2-10
 4-6/10=well-differentiated
 7/10=moderately differentiated
 >8/10=poorly differentiated

26. Gleason 6
www.cancernetwork.com - Cesar A Moran, 07.02.2014

27. Gleason 7
www.cancernetwork.com - Cesar A Moran, 07.02.2014

28. Gleason 8
www.cancernetwork.com - Cesar A Moran, 07.02.2014

29. Gleason 9
www.cancernetwork.com - Cesar A Moran, 07.02.2014

30. PATHOLOGY GROUPINGS IN PROSTATE
CANCER
• GROUP 1
– Gleason score 3+3, or less.
• GROUP 2
– Gleason score 3+4
• GROUP 3
– Gleason score 4+3
• GROUP 4
– Gleason total score 8
• GROUP 5
– Gleason total score 9 or 10

31. Prostate cáncer staging
Can spread to adjacent organs (seminal
vesicles, bladder), lymph nodes, bone
Most bone mets are osteoblastic
Prior to initiating treatment consider
Bone scan (PSA>10, Gleason Score >7)
CT scan pelvis/abdomen (PSA >10, Gleason
Score >7))
These tests are typically not required in
asymptomatic men with low risk prostate
cancer

32. Maniobras de estadificación
• Consideraciones
– Tumores MUY tempranos pueden no necesitar estudios
adicionales para metástasis a distancia
• T1c/T2a; PSA de 10, o menos; Gleason 6, o menos.
• RM de próstata con antena rectal – para planeación terapia
– Tumores MUY avanzados pueden ser investigados con:
• Gammagrafía ósea / TAC de tórax, abdomen y pelvis
– Tumores POTENCIALMENTE avanzados pueden beneficiarse de:
• RM corporal total
• El PET-CT es ineficaz en cáncer de próstata
– Tumores candidatos a terapia local (Prostatectomía /
Braquiterapia) o candidatos a Radioterapia
• RM Multiparamétrica de próstata con antena rectal

33. Práctica usual
• Gammagrafía ósea
• TAC de tórax contrastado
• RM de pelvis / Próstata con antena rectal
• PSA

34. Carcinoma de Próstata
TNM
• T1 - Tumor primario no aparente clínicamente ni visible por imágenes.
T1a - Hallazgo incidental que compromete <= 5% del tejido resecado.
T1b - Hallazgo incidental que compromete > 5% del tejido resecado.
T1c - Diagnóstico obtenido por biopsia ciega inducida por un PSA elevado.
• T2 - Tumor confinado a la próstata.
T2a - Compromete sólo un lóbulo de la próstata.
T2b - Compremete ambos lóbulos de la próstata.
• T3 - Tumor que se extiende más allá de la cápsula prostática.
T3a - Extensión extracapsular.
T3b - Invade la vesícula seminal.
• T4 - Fijado a otras estructuras distinto a las vesículas seminales.
• N1 - Ganglios linfáticos comprometidos.
• M1 - Metástasis a distancia.
M1a - Ganglios linfáticos no regionales.
M1b – Huesos.
M1c - Otros sitios.

35. Carcinoma de Próstata
Clasificación por etapas
• Estadío I: T1a de bajo grado N0 M0;
• Estadío II: T1a de alto grado-T2 N0 M0;
• Estadío III: T3 N0 M0;
• Estadío IV: T4 N0 M0, Cualquier T N1 M0, Cualquier T Cualquier N M1.

36. Very low risk (must fulfill all)
T1c
Grade Group 1
PSA less than 10
Less than 3 core+, with less
than 50 per-cent cancer in
each
Psa density less than 0.15

37. low risk (must fulfill all)
T1-T2a
Grade Group 1
PSA less than 10

38. Favorable intermediate
T2b-T2c or
Grade Group 2 or
PSA 10-20 and
positive biopsy cores less 50
per-cent

39. unfavorable intermediate
T2b-T2c or
Grade Group 2 or group 3 or
PSA 10-20

40. high
T3a or
Grade Group 4 or group 5 or
PSA greater than 20

41. VERY high
T3b-t4 or
Grade group 5 or
More than 4 cores with grade
group 4 or 5

43. Prostate cáncer treatment
Considerations
Patient’s age
Co-morbid health conditions
Tumor stage
Tumor grade (Gleason score)
Often a patient choice
Surgery and

44. Early stage Prostate cáncer
treatment
Early stage Cancer
1. Radical Prostatectomy
2. External Beam Radiotherapy
3. Radioactive Seeds (Brachytherapy)
4. Active Surveillance
5. Observation – Watchful Waiting

45. Early stage Prostate cáncer
treatment: radical prostatectomy
Radical Prostatectomy
Complete surgical removal of entire prostate,
seminal vesicles
Considered a good treatment for men <70
years of age with clinically organ confined
cancer who are healthy
Open or laparoscopic/robotic approaches

46. Early stage Prostate cáncer
treatment: radical prostatectomy

47. radical prostatectomy:
complications
<10% risk of blood transfusion
Wound infection
Rectal injury (<1%)
Urinary incontinence (~10%)
Erectile dysfunction (variable but common)
Anesthetic related

48. Prosate cancer treatment:
radiotherapy
Radiotherapy Options
External Beam
Brachytherapy (seed implant)
Concept of maximizing dose to the tumor and
minimizing collateral damage
Curative options for patients at high risk for
morbidity from radical prostatectomy
Age, medical co-morbidities
Patient preference

49. Prosate cancer treatment:
radiotherapy

50. Radiotherapy: complications
External Beam Radiation Therapy
Hematuria
Radiation proctitis
Loose, bloody stools
Urinary retention
Strictures (urethra and ureter)
Erectile dysfunction
Secondary malignancies
Bladder, rectal, hematological

51. Proctitis Actínica

52. Prostate cancer therapy:
brachytherapy

53. Brachytherapy: complications
Urethral strictures
Seed migration
Urinary retention
Erectile dysfunction
Irritative voiding symptoms

54. Active surveillance
Observing low grade tumors in men <70 yrs and >10 yr
life expectancy
Delay definitive treatment until it is necessary and
cancer is still curable
Goal is to delay potential treatment-related morbidity
Monitor DRE, PSA, and periodic repeat biopsy
Ideal candidate:
 PSA < 10
 Normal DRE
 Gleason <7 (low grade)
 Only 1-3 / 12 biopsy cores positive

55. Watchful waiting
Observing low grade tumors in men
>70 yrs or <10 yrs life expectancy
Institute hormonal therapy when
patient becomes symptomatic
No curative intent

56. Treatment options by risk
1/2
Risk Group
Very-low risk
Active surveillance
External-Beam Radiotherapy
Radical prostatectomy +/- RPLND
Observation
Low risk
Active surveillance
External-Beam Radiotherapy
Radical prostatectomy +/- RPLND
Observation
Favorable intermediate
Active surveillance
External-Beam Radiotherapy
Radical prostatectomy +/- RPLND
Observation
RPLND: Retroperitoneal Lymph-Node Dissection

57. Treatment options by risk
2/2
Risk Group
Unfavorable intermediate risk
External-Beam Radiotherapy + ADT (4 mo)
Radical prostatectomy +/- RPLND
Observation
High risk
External-Beam Radiotherapy + ADT (18 mo)
Radical prostatectomy + RPLND
Very High risk
External-Beam Radiotherapy + ADT (18 mo)
Radical prostatectomy +/- RPLND
RPLND: Retroperitoneal Lymph-Node Dissection

58. Position statement: Non metastastic prostate cancer
Mauricio Lema - 2014
Watchful waiting and Active
Surveillance are NOT without
side-effects. Recommendations
need to be INDIVIDUALIZED
RP or RT or Active Surveillance (AS) or Watchful Waiting
(WW), or Brachytherapy (BT)*
Localized Low-Risk
T1c-T2a
PSA 10, or less
Gleason 6, o less
AS: Prostate US/PSA q3 Mo; Biopsy if
indicated. Treatment if progression.
WW: PSA q6 Mo, treatment if indicated
65 yo, or less: RT, RP or AS
Adverse features
PSA velocity 2+/year
50%+ positive findings in biopsy
Perineural invasion
Adverse features: active
treatment (RT, RP or BT)
*BT if feasible
Low risk
Small tumors
Adequate anatomy

59. Position statement: Non metastastic prostate cancer
Mauricio Lema - 2014
Radiation (RT) + LH-RH/Antiandrogen x6-24 Mo+ Mo
Locally-Advanced
(T3/T4)
Localized High-
Risk
T2c
PSA 20+
Gleason 8+
RT + LH-RH/Antiandrogen x4 Mo or RP
Localized
Intermediate-Risk
T2b
PSA 10-20
Gleason 7
Antiandrogen for at least 1 Mo
Antiandrogen for at least 1 Mo
“Would NOT use hormonal therapy in patients with known
coronary artery disease, unless benefit clearly outweigh risk”
RT + LH-RH/Antiandrogen x6-24 Mo or Radical
prostatectomy (RP)
Antiandrogen for at least 1 Mo
RP or RT or Active Surveillance (AS) or
Watchful Waiting (WW), or Brachytherapy
Localized Low-Risk
T1c-T2a
PSA 10, or less
Gleason 6, o less
AS: Prostate US/PSA q3 Mo; Biopsy if
indicated. Treatment if progression.
WW: PSA q6 Mo, treatment if indicated

60. Advanced or metastatic prostate
cancer
Not curable disease
Goals shift to disease control
Development of cancer cells unresponsive
to androgen deprivation
Typically occurs slowly over time, although
it can occur rapidly

61. Treatment strategies for
metastatic prostate cancer
Androgen Deprivation (Hormonal Rx)
Orchidectomy
LHRH analogues
Antiandrogens
Supportive therapies
Analgesics
Steroids
Bisphosphonates/Vitamin
D/Calcium for bone health
Chemotherapy
 Taxotere, Docetaxel
Last line of treatment

63. Only Canadian-born doctor ever to
receive the Nobel Prize in Physiology or
Medicine.
Nobel Prize received in 1966.
For his discoveries concerning
hormonal treatment of prostatic cancer.
Born in Halifax, Nova Scotia.
B.A (Acadia)
©The Nobel Foundation
Charles brenton huggins (1901-1998)

64. Carcinoma de Próstata
Tratamiento de enfermedad metastásica (Estadío IV)
La intención del tratamiento es paliativo. Se recomienda iniciar
terapia hormonal.
EL bloqueo androgénico (ie, análogos de LHRH) / orquidectomía son
estándar.
En metástasis de alto riesgo (5 sitios metastásicos óseos, o más;
enfermedad metastásica visceral) se recomienda iniciar con terapia
quimiohormonal (ie, bloqueo androgénico + docetaxel).
El tratamiento de la enfermedad ósea es esencial (en presencia de
enfermedades metastásica) con bisfosfonatos o denosumab
La secuencia de tratamiento debe ser individualizada

65. Prostate ca prognosis
Depends upon grade, stage and treatment
Early stage/well-differentiated Ca treated
by radical prostatectomy:
 85% + 10 year survival
Metastatic disease
<10% 5 year survival

66. Prostate ca chemoprevention
Two major studies using 5 a reductase inhibitors vs
placebo
Similar reduction in prostate cancer diagnosis in the
treatment arms (23-24%)
Not currently approved for prostate cancer prevention
PCPT (Thompson et al NEJM 2003)
Finasteride
Reduce (Andriole et al NEJM 2010)
Dutasteride

67. Prostate ca chemoprevention
Problems
Potential for the development of high risk
prostate cancer
Expensive
Sexual/ejaculatory dysfunctions side
effects may be occur and aren’t always
reversible
Long time to see the results of prevention
10-20 years

68. BACK-UP SLIDES
Treatment considerations

71. Hipotála
mo
Hipófisis
Testículo Adrenal
LHRH CRH
FSH/LH ACTH
Próstata
Testosterona
DHT
Androstenediona
DHE
DHE-S
AR

72. Hipotála
mo
Hipófisis
Testículo Adrenal
LHRH agonista (Leuprolide/Goserelina)
LHRH antagonista (Degarelix)
Estrógenos (DES)
Antiandrógeno esteroideo (Ciproterona)
CRH
FSH/LH ACTH
Próstata
Testosterona
DHT
Androstenediona
DHE
DHE-S
Dutasterida (Inhibidores
5α Reductasa)
Abiraterona (ABI)
Ketoconazol
Glucocorticoides
Abiraterona (ABI)
Ketoconazol
Enzalutamida (ARI)
AR
Bicalutamida/Ciprotero
na (antiandrógenos)
Orquiectomía

73. Hipotála
mo
Hipófisis
Testículo Adrenal
LHRH agonista (Leuprolide/Goserelina)
LHRH antagonista (Degarelix)
Estrógenos (DES)
Antiandrógeno esteroideo (Ciproterona)
CRH
FSH/LH ACTH
Próstata
Testosterona
DHT
Androstenediona
DHE
DHE-S
Dutasterida (Inhibidores
5α Reductasa)
Abiraterona (ABI)
Ketoconazol
Glucocorticoides
Abiraterona (ABI)
Ketoconazol
Enzalutamida (ARI)
AR
Bicalutamida/Ciprotero
na (antiandrógenos)
Orquiectomía

74. 

22%
(n=32)
78%
(n=115)
0
20
40
60
80
100
Goserelin Orchidectomy
Patients’preference
Cassileth BR, et al. Qual Life Res 1992; 1: 323–
330
GnRH agonist efficacy
is similar to
orchidectomy

75. LHRH análogo
Hipófi
sis
Testíc
ulo
FSH/LH  Próst
ata
Testosterona
Pulsado
LHRH análogo
Hipófi
sis
Testíc
ulo
FSH/LH  Próst
ata
Testosterona
Continuo
LHRH antagonista
Hipófi
sis
Testíc
ulo
FSH/LH  Próst
ata
Testosterona
LHRH-R Downregulation

76. Boccon-Gibod L et al. Presentazione poster. 23esimo Congresso EAU, Milano, Italia,

77. LHRH agonistas
• Pueden causar aumento (transitorio) de la
Testosterona
– Exacerbación del tumor (tumor flare)
• Considerar el uso de antiandrógenos (1
semana) ANTES de LHRH agonistas

78. Attard G, et al. J Clin Oncol. 2008;26:4563-4571.
Pregnenolone Deoxycorticosterone Corticosterone Aldosterone
Cortisol11-deoxycortisol17OH-Pregnenolone
CYP17:
17α-hydroxylase
CYP17:
C17,20-lyase
DHEA Androstenedione
Testosterone
Estradiol
x 3
x 2
< 2 ng/dL
< 1 ng/dL
< 80 ng/dL

79. Efectos secundarios de la
hormonoterapia
• PÉRDIDA DE LA LIBIDO Y DEL
INTERÉS SEXUAL, DISFUNCIÓN
ERÉCTIL, IMPOTENCIA
• FATIGA
• CALORES (VASOMOTORES)
• DECLINAR EN LA CAPACIDAD
INTELECTUAL, DEPRESIÓN
• DISMINUCIÓN DE LA FUERZA
MUSCULAR
• INCREMENTO EN LA APOSICIÓN
ABDOMINAL GRASA
• MENOR ACTIVIDAD FÍSICA Y
VITALIDAD
• OSTEOPOROSIS
• ENFERMEDAD CARDIOVASCULAR

80. Ginecomastia inducida por
antiandrógenos
Michalopoulus VN, Keshtgar MR, NEJM, 2012

81. Medicamentos Efectos secundarios
LHRH agonistas Tumor flare
Síntomas vasomotores
Síntomas sexuales
Incremento de peso & adiposidad
Ginecomastia
Ostoporosis
Cardiovascular
LHRH antagonistas Igual a los LHRH agonistas menos el Tumor flare
Antiandrógenos
esteroideos
Igual a LHRH agonistas, aumenta la mortalidad
Antiandrógenos no
esteroideos
Igual a LHRH sin el tumor flare (requieren de
castración
Abiraterona Hipertensión / hipokalemia & retención de
líquido (requiere de castración para
complementar su eficacia, requiere de
suplemento de glucocorticoide para evitar
Addison)
Orquiectomía Definitiva / menos aceptable para los pacientes
Enzalutamida Astenia / diarrea / dolor de espalda & articular /

85. Denosumab and Zoledronic Acid:
Indications in Advanced Prostate
Cancer
Indication Denosumab
120 mg SC Monthly
Zoledronic Acid
4 mg IV Monthly
Bone metastases from
hormone-sensitive
disease
Yes No
Bone metastases from
CRPC
Yes Yes

86. Α AND Β PARTICLES
Presented By Chris Parker at 2014 ASCO Annual Meeting

87. RADIUM ACTS AS A CALCIUM MIMETIC
Presented By Chris Parker at 2014 ASCO Annual Meeting

89. Docetaxel
• Droga contra el cáncer
– Veneno de los microtúbulos (inhibe la
despolimerización)
• Se administra por la vena
– Lentamente
• Requiere de premedicación para evitar
reacciones durante la administración
– Esteroides (ie, Dexametasona)
– Antihistamínicos H1 (ie, Hidroxicina)
– Antihistamínicos H2 (ie, Ranitidina)

90. Docetaxel
• Efectos secundarios más comunes
(Generalidades)
• 1. Disminución de las defensas (neutropenia)
• 2. Caída del cabello (alopecia)
• 3. Reacciones de hipersensibilidad
• 4. Retención de líquidos
• 5. Toxicidad en la piel
• 6. Neurotoxicidad
• 7. Misceláneos

91. Día 1 8 15 *
1 8 15…
Docetaxel
Tiempo
Ciclo 1
Ciclo 2
Prednisolona 5 mg vía oral cada 12 horas + Bloqueo and

92. Cabazitaxel
• Droga contra el cáncer
– Veneno de los microtúbulos
• Se administra por la vena
– Lentamente (durante 1 hora)
• Requiere de premedicación para evitar
reacciones durante la administración
– Esteroides (ie, Dexametasona)
– Antihistamínicos H1 (ie, Hidroxicina)
– Antihistamínicos H2 (ie, Ranitidina)

93. Cabazitaxel
• Efectos secundarios más comunes
(Generalidades)
• 1. Disminución de las defensas (neutropenia)
• 2. Caída del cabello (alopecia)
• 3. Diarrea
• 4. Retención de líquidos
• 5. Astenia o fatiga
• 6. Neurotoxicidad
• 7. Misceláneos

94. Cabazitaxel (indicaciones)
• Carcinoma de próstata refractario a la
castración y que ha recibido docetaxel