KELAINAN TUMOR PADA SISTEM REPRODUKSI PRIA

kuliah untuk mahasiswa kedokteran

1. TUMOR PADA SISTEM REPRODUKSI PRIA BPH CA PROSTAT CA PENIS CA TESTIS DR EKA YUDHA RAHMAN,M.KES,SPU(K) DIVISI UROLOGI DEPARTEMEN BEDAH FK ULM/ KSM UROLOGI RSUD ULIN

2. BPH (BENIGN PROSTATIC HYPERPLASIA)

3. PENDAHULUAN Benign prostatic hyperplasia (BPH) is a histological diagnosis associated with unregulated proliferation of connective tissue, smooth muscle and glandular epithelium within the prostatic transition zone. BPH may cause physical compression of the urethra and result in anatomic Bladder Outlet Obstruction (BOO). The prevalence of BPH rises markedly with increased age. Autopsy studies have observed a histological prevalence of 8%, 50%, and 80% in the decades of life, respectively. INTRODUCTION: Nishant D. Patel, J. Kellogg Parsons . Epidemiology and etiology of benign prostatic hyperplasia and bladder outlet obstruction . Indian Journal of Urology, Apr-Jun 2014, Vol 30, Issue 2 Alan J Wein, Louis R. Kavoussi, Alan W. Partin, et al. CAMPBELL-WALSH UROLOGY 11 ed. Page: 2433-2434 . Elsevier.

4. ANATOMY Mc Neal ( 1988 ) : Zona transisional, Zona central,Zona peripher ,Zona anterior fibromuskuler stroma.

5. PATHOPHYSIOLOGY Alan J Wein, Louis R. Kavoussi, Alan W. Partin, et al. CAMPBELL-WALSH UROLOGY 11 ed. Page: 2433-2434 . Elsevier.

6. PREVALENCE OF BPH THE MOST FREQUENT BENIGN TUMOR IN MEN 20 % OF MEN 41 - 50 YEARS. 50 % OF MEN 51 - 60 YEARS. 65 % OF MEN 61 - 70 YEARS 80 % OF MEN 71 - 80 YEARS. 90 % OF MEN 81 - 90 YEARS (AUTOPSY STUDY) INDONESIA : THE SECOND AFTER STONE

7. PREVALENSI BPH BPH occurs in about 70% of men over the age of 60. Will increase to 90% in men over 80 years old. The exact incidence of BPH in Indonesia has never been studied, but as an illustration at RSCM since 1994-2013, 3,804 cases were found with an average age of 66.61 years old.

8. ETIOLOGY

9. Theory Dihydrotestosteron hypothesis Oestrogen-testosteron imbalance Stromal-epithelial interactions Reduced cell death Stem cell theory I nflammation Theories for the cause of BPH Cause ↑ 5-α reductase and androgen receptors ↑ Oestrogens ↓ Testosteron ↑ Epidermal growth factor/fibroblast growth factor ↓ Transforming growth factor β ↑ Oestrogens Stem cells infection Effect Epithelial and stromal hyperplasia Stromal hyperplasia Epithelial and stromal hyperplasia ↑ Longevity of stroma and epithelium Proliferation of transit Cells Epithelial and stromal Hyperplasia ?

10. DHT THEORY Testosteron DHT Inskripsi RNA Sintesis Protein Hiperplasia epitel & stroma prostat Reseptor androgen 5 alpha reductase

11. DIAGNOSTIC WORK-UP FOR BPH Questionnaire with quality of life (e.g. IPSS) History Physical examination Urinalysis (sticks, sediment) Blood analysis ( ureum , creatinine, PSA) Ultrasound (bladder, prostate, kidneys) Neurogenic bladder, drug-induced LUTS, genital diseases, palpable prostate carcinoma... Urinary tract infection, haematuria, diabetes... Deterioration kidney function, prostatitis, prostate carcinoma... Bladder tumour, foreign body, bladder stone, bladder diverticulum, post-void residual, urinary retention, stone disease, pelvic tumour... Benign Prostatic Obstruction (BPO)

12. DIAGNOSIS I Anamnesis Cardinal symptoms: Weak Stream Frequency Nocturia S torage symptoms, Voiding Symptoms Scoring System : M.I, IPSS, VPSS

13. ANAMNESES: BPH SYMPTOMS

14. SYMPTOMS Storage F requency U rgency N octuria D isuria Post Voiding I ncomplete emptying T erminal dribbling Voiding W eak Stream H esitancy I ntermittency S training

15. Symptom Score (symptom profile)

16. VPSS A B C D A+B+C = D =

17. I-PSS Score: - Mild : 0 – 7 - Moderate : 8 – 19 - Severe : 20 - 35

18. DIAGNOSIS II Physical examination: flanks : kidneys🡪 bimanual palpation🡪 ballotement Supra sympisis: bladder🡪palpation 🡪bladder distention 🡪 urine `retention Genitalia : urethra, testis, epidydimis

19. DIAGNOSIS II Physical examination : DRE TMSA BCR Prostate: Size Nodule Consistency Tenderness Symetrical/asymetrical enlargement

20. DIAGNOSIS II Uroflowmetry Qmax Voided volume Residual urine TAUS Catheter

21. UROFLOWMETRY CHART Male 70 years old with LUTS

22. LAB TEST Blood Count Serum Electrolyte Serum Creatinine Serum PSA (TPSA) Urine : Proteinuria Sediment Culture

23. IMAGING TRUS TAUS With Indication : IVP Cystography

24. TRUS Hypoechoic lession

25. TAUS

26. IVU

27. CYSTOGRAM

28. INDICATION FOR BIOPSY Rahardjo D, ST Kamil Gardian, Med J Indones 9(1);35-42 Accepted Standard <4 ng No. biopsy 4- 10 ng/ml PSA D > 0.15 Biopsy >10 ng/ml Biopsy Hard Nodule Hypo/hiperchoic lession Biopsy

29. DIFFERENSIAL DIAGNOSIS Urethral stricture Bladder neck contracture Bladder stone Prostate cancer Prostatitis CIS bladder

30. Watchful Waiting (IPSS 0-7) Medical Treatment (IPSS 8 – 19) - 5 α reduktase inhibitor - alpha adrenergic Blockers α1 blocker : Doxazosin Terazosin α1a blocker: Tamsulosin - Phytotherapy FMUI Treatment I : Non Surgical

31. THE CHOICE OF ALPHA BLOCKER AGENTS: TAMSULOSIN MEMILIKI RESIKO PALING MINIMAL MENIMBULKAN EFEK TERHADAP KARDIOVASKULAR Nickel JC et al. Int J Clin Pract 2008;62:1547-59 Odds Ratio > 1: odds of developing vascular-related adverse event higher vs. placebo Odds Ratio (95%CI) 3.71 (2.48-5.53) 3.32 (2.10-5.23) 3.86 (1.86-8.02) 1.66 (1.17-2.36) 1.42 (1.00-2.05)

32. T REATMENT OF MALE LUTS TAILORED TO THE INDIVIDUAL PATIENT Co-morbidities Risk of disease progression Bother Quality of life Patient’s preferences Severity of LUTS Type of LUTS Speakman MJ Eur Urol Suppl. 2008;7:680-9; Oelke M et al. Eur Urol 2013;64:118-40.

33. INDICATION FOR NON SURGICAL TREATMENT IPSS score < 20 Residual Urine < 100 ml PSA < 4 ng/ml No Hard Nodule No complication

34. ABSOLUTE INDICATION FOR SURGERY (COMPLICATION OF BPH) Chronic retention recurrent UTI Decreased Renal Function/Hydronefrosis Haematuria With bladder stone with bladder divertikel

35. RELATIVE INDICATION FOR SURGERY (COMPLICATION OF BPH) Fail After Pharmalogical treatments Patient’s preferences

36. SURGICAL TREATMENT TUR-P TUI-P Open Prostatectomy Laser Ablation Laser Resection Laser Enucleation Thermo Therapy Hyperthermia TUNA

37. Foto : Universitatsklinikum Tubingen, prof. Bichler, Abt.urologie TUR-P

38. ‹#›

39. LASER ND-YAG SIDE FIRING www.endoscopy.com

40. Bleeding Incontinence Bladder neck contracture Stricture Retrograde ejac. Impotence 4 (11%) 1 (3%) 0 (0%) 1 (3%) 21 (70%) ? (0%) 0 (0%) 0 (0%) 1 (4%) 0 (0%) ? 8 (8%) 1 (1%) 2 (2%) 3 (3%) 62 (62%) 4 (4%) 2 (2%) 0 (0%) 0 (0%) 0 (0%) 2 (2%) 1 (1%) Open surg. (n=30) TUIP (n=24) TURP (n=100) VILAP (n=100) Personal Jakarta Experience Morbidity Associated with Surgery Complication of Surgery

41. ALTERNATIVE TREATMENT Balloon Dilatation Stenting Prostatic Urethral Lift

42. FMUI

43. FMUI

44. PROSTATE CANCER KULIAH PSPD

45. INTRODUCTION The most common form of prostate malignancy is adenocarcinoma of the prostate. Prostate cancer is the most common malignancy and cause of death in men in the West. In Indonesia, the number of prostate cancer patients in three hospitals education center (Jakarta, Surabaya and Bandung) for 8 years The last one was 1,102 patients with a mean age of 67.18 years. Pedoman nasional pelayanan kedokteran kanker prostat, 2017

46. Prostate cancer in Asia Growing population Diversity in Culture Diet Health status Environment Man power Economical situation KULIAH PSPD

47. EPIDEMIOLOGY Worldwide Source: Globocan, 2020

48. EPIDEMIOLOGY Indonesia Source: Globocan 2020

49. EPIDEMIOLOGY KEMENKES. Beban kanker di Indonesia. Jakarta: Pusat Data dan Informasi Kementerian Kesehatan RI; 2019.

50. More men > 70 yrs. ↓ More risk of PCa New diagnostic tools (Markers & Imaging) More acurate in early diagnosis ↑ ↓ Increasing localized PCa > 70yrs ↑ KULIAH PSPD

51. PROSTATE CANCER Risk factors High fat diet (obesity) Lack of sunlight Heavy metal Aging Family history Race (afro-amerika) Inflammation of Prostate KULIAH PSPD Prevention factors Soybean & products Green tea Lycopene Anti-oxidant Supplementation (Vit E, Vit D, Selenium) Exercise

52. PROSTATE CANCER IN ASIA KULIAH PSPD Prevention factors:

53. CLINICAL MANIFESTATION (1) No symptoms (was detected during annual check up or screening due to familial history of prostate cancer) LUTS / urinary retention Hemospermia Hematuria Bone pain / pathologic fracture Neurological symptoms KULIAH PSPD

54. CLINICAL MANIFESTATION (2) Abnormality on DRE: - hard consistency - uneven surface - nodule - asymetrical enlargment KULIAH PSPD

55. IMAGING Transrectal ultrasound and ultrasound-based techniques🡪 Abnormality on TRUS: - hypo- or hyper-echoic lesion - Hypervascularisation (Doppler) Multiparametric magnetic resonance imaging Mottet N, van den Bergh RCN, Briers E, et al. EAU-EANM-ESTRO-ESUR-SIOG guidelines on prostate cancer. Netherlands: European Associated Urology; 2019

56. PROSTATE CANCER IN ASIA: DIAGNOSTIC METHODS (%) Author Country Biopsy TUR-P Open Others Ahmad Z et al, 2009 Pakistan 26 74 n.a n.a Peyromaure M et al 2005 China 68 5 1 26 Umbas R, 2008 Indonesia 74 22 2 2 Akaza H et al, 2003 Singapore 75 20 5 Akaza H et al, 2003 Taiwan 77 17 6 Nayyar R & Gupta N, 2009 India 82 18 Cancer Reg JUA, 2005 Japan 89 n.a n.a n.a KULIAH PSPD

57. TRANS RECTAL ULTRA-SONOGRAPHY (TRUS) & BIOPSY: Indication for prostate biopsy: Abnormality on DRE PSA > 4 ng/ml KULIAH PSPD Local anesthesia or regional/general Histopathological report: Tumor type & grade (Gleason score) Percentage of cancer on each “core”

58. GLEASON PATHOLOGIC GRADING SYSTEM KULIAH PSPD Gleason DF. In: Tannenbaum M, ed. Urologic Pathology: The Prostate. Philadelphia, Pa: Lea & Febiger; 1977: 171–197

59. PROSTATE CANCER : TREATMENT MODALITIES As stated in guidelines from many institutions/organizations worldwide , treatment options for prostate cancer were depend on several factors KULIAH PSPD Treatment option Consideration Factors Active surveilance Life expectancy at diagnosis Radical Prostatectomy Tumor grade, PSA Radiotherapy Tumor stage Androgen deprivation therapy Novel Hormonal Agent Co-morbidity Chemotherapy Imunotherapy Target-therapy Patient’s preverence

60. HORMONAL TREATMENT: Bilateral orchiectomy Oestrogens ( DES) LHRH agonists LHRH antagonists Anti-androgens KULIAH PSPD

61. HORMONAL THERAPY

62. Systemic non-hormonal therapy in HRPC Cytotoxic chemotherapy Bone-targeted treatments Immunotherapy “Targeted” therapy KULIAH PSPD Maintain androgen deprivation !! (LHRH analogue or Orchydectomy bilateral) EAU Guidelines 2008 & Nelson WG et al. Prostate Cancer 6th Int’l Consultation 2005

63. CONCLUSION Incidence of prostate cancer in Asia is increasing, moreover with increasing of elderly population Diagnostic procedure was not yet uniform, resulting in huge variation of tumor stage Treatment options for prostate cancer were depend on several factors Surgery, as the best treatment for localized cancer become more popular, not only the standard open procedure, laparoscopic and robotic-assisted RP also being one of the choice ADT could be an option in stage I-III beside as treatment of choice in stage IV prostate cancer KULIAH PSPD

64. PENILE CANCER

65. CA PENIS: EPIDEMIOLOGY Incidence: USA : 0.3-1.8 / 100.000 Highest : 19 / 100.000 (Asia, Africa, South America) Lowest : 0.1 / 100.000 (Israeli Jews, Muslims, Nigeria) RSCM/ RSKD : 7 Pts / year (108 pts/15 years) (EAU Guidelines, 2008; Pow-Sang M et al, Penile Cancer, 2009)

66. (EAU Guidelines, 2010)

67. NATURAL HISTORY OF PENILE CANCER

68. CA PENIS: RISK FACTORS Phimosis Injury to the penis Chronic balanitis Ultraviolet radiation Cigarette smoking Genital warts HPV infection (type 16 & type 18) (Penile Cancer, 2009)

69. CA PENIS: RISK FACTORS & PREVENTIVE FACTORS

70. CA PENIS: SYMPTOMS & SIGNS Induration: papule – exophytic – flat Ulcerative lesion Itching or burning under the foreskin Ulceration of the glans or prepuce Foul preputial odor & discharge with or without bleeding Pain is usually not present

71. CA PENIS: DIAGNOSTIC Primary lesion Size/diameter of the lesion Location on the penis Number of lesions Morphology: papillary, nodular, ulcerous or flat Relationship with other structure Color & boundaries of lesion

72. CA PENIS: DIAGNOSTIC Histopathological examination Incisional biopsy Tissue core biopsy Fine-needle aspiration Brush biopsy Excisional biopsy (therapeutic in some cases)

73. Perubahan pada TNM 2009 T1: tumor menginvasi jaringan ikat subepithelial T1a: Tanpa invasi lymphovascular dan berdiferensiasi baik atau sedang (T1 G1-2) T1b: dengan invasi lymphovascular atau berdiferensiasi buruk/tanpa diferensiasi (T1 G3-4)

74. T2 menginvasi corpora cavernosa T2 menginvasi corpus spongiosum

75. CA PENIS: DIAGNOSTIC Regional nodes Non-palpable - Abdominopelvic CT and MRI are not useful - The probability of inguinal micro metastases can be estimated by using risk group stratification

76. CA PENIS: DIAGNOSTIC Regional nodes Palpable - diameter of node(s) or mass(es) - uni- or bilateral localization - number of nodes in each inguial area - mobile or fixed - relationship to other structure - presence of oedema on leg and/or scrotum Abdominopelvic CT and MRI to determine the presence of pelvic or distant metastases

77. INGUINAL LYMPHNODE

78. CA PENIS: DIAGNOSTIC Distant metastases: Lung/Liver/Brain/Bone An assessment of distant metastases should only be performed in patients with proven positive nodes Chest x-ray Abdominal & pelvic CT Scan: - Pelvic CT if inguinal nodes +ve - Abdominal CT if pelvic nodes +ve - Brain CT / Bone scan if indicated

79. JACKSON STAGING SYSTEM VS TNM

80. CA PENIS: TREATMENT Primary lesion Ta-1, G1-2 - Penis preservation (laser, radiotherapy or brachytherapy, glansectomy) - Partial penectomy in patient who cannot comply with regular follow up T1, G3 or T ≥ 2 - Partial or total penectomy

81. PARTIAL PENECTOMY

82. TOTAL PENECTOMY

83. ROLE OF RADIOTHERAPY IN PENILE CANCER Dose : 40-78 Gy Local control rates: 60%-70% Indications: - Small (<4cm), superficial & exophytic lesions on glans or coronal sulcus - Medically unfit patients & those who refused surgery - As palliative treatment in metastatic disease

84. CA PENIS: LYMPHNODE DISSECTION International Consultation on Penile Cancer, 2009

85. DISTANT METASTASES

86. CHEMOTHERAPY

87. POST-CHEMOTHERAPY LYMPHADENECTOMY

88. (Penile Cancer, 2009)

89. CA PENIS Conclusion: Relatively low incidence, mostly SCC Related to HPV type 16 & 18 Local treatment: Partial or Total Penectomy Lymphnode dissection is important Radiotherapy has limited role Chemotherapy in advanced disease Follow-up depend on primary tumor & lymphnode status

90. TESTICULAR CANCER

91. CA TESTIS Incidence USA : 3.7 / 100.000 Scandinavia : 6.7 / 100.000 Asia : low RSCM/RSKD : 13 pts/year (201 pts/15 year) Most common type : Seminoma

92. CA TESTIS

93. CA TESTIS Age Peak incidence in 20-40 yrs, > 60 years, and in infancy (0-10 years) Most common solid tumor in men age 20-34 years in USA & UK Tumor type Peak incidence Seminoma 35-39 years Spermatocytic seminoma > 50 years Embryonal & Teratocarcinoma 25-35 years Choriocarcinoma 20-30 years Lymphoma > 50 years

94. (Suprabawati TE & Umbas R, Indones J Cancer 2007)

95. CA TESTIS Risk factors: Race Undescended testis Klinefelter’s syndrome Familial history of testicular cancer Environment HIV-AIDS Usage of diethylstilbestrol (DES) or oral contraseptive during pregnancy

96. CA TESTIS Diagnosis: History Physical examination Tumor markers (AFP, β-hCG, LDH) Imaging

97. CA TESTIS History Painless, mass in the scrotum However, in 20% of patients, the first symptom is scrotal pain & in 27% may have local pain Undescended testis / orchydopexy Family history Neck mass Respiratory symptoms GI tract symptoms Back & flank pain Infertility

98. CA TESTIS Physical examination Scrotal examination Both testicles Abdominal mass Gynecomastia Supraclavicular lymphnode Respiratory tract involvement

99. CA TESTIS

100. CA TESTIS Tumor markers Should be measured before and after orchydectomy (± 1 week) The persistence of elevated serum tumour markers after orchidectomy might indicate the presence of metastatic disease (macro- or microscopically), while the normalisation of marker levels after orchidectomy does not rule out the presence of tumour metastases. Included in the AJCC TNM staging system

101. CA TESTIS Tumor markers α-Fetoprotein (AFP): - half life is between 5-7 days - elevated in hepatoma & testicular tumors - may be produced by pure embryonal carcinoma, teratocarcinoma, yolk sac tumor, or combined tumors - not produced by pure choriocarcinoma or pure seminoma

102. CA TESTIS Tumor markers β-human Chorionic Gonadotropin (β-hCG) - serum half life is between 24-36 hours - elevated with various malignancies(liver, pancreas, stomach, lung, breast, kidney, bladder) - elevated in 100% pts with choriocarcinoma, 40%-60% pts with embryonal carcinoma, and 5%-10% pts with pure seminoma

103. CA TESTIS Tumor markers Lactic Acid Dehydrogenase (LDH) - low specificity (high false-positive rate) - direct relationship with tumor burden - mostly elevated in stage III disease (81%) - recurrence rate in stage I and II disease were higher (77%) if pretreatment LDH were elevated

104. CA TESTIS Imaging Scrotal USG if suspicious for testicular mass Postero-anterior and lateral chest x-ray as initial imaging procedure CT Scan: - Abdominopelvis - Chest CT: In seminoma pts, if abnormal abdominal CT or suspiciuos lesion on chest x-ray; routinely done in all non-seminoma pts MRI & PET Scan were not superior to CT Scan

105. CA TESTIS: ROLE OF ULTRASONOGRAPHY EXAMINATION Seminoma of the right testicle Hyperechoic areas within the testicle

106. CHEST CT SCAN 5 mm tumor in the right cardiophrenic lymph node adjacent to the heart . www.kantrowitz.com/cancer/diagnosis.html

107. CA TESTIS: STAGING AT DIAGNOSIS EAU Guidelines 2010

108. CA TESTIS: DIAGNOSIS (1) Testicular ultrasound is mandatory (grade of recommendation: B). Orchidectomy and pathological examination of the testis are necessary to confirm the diagnosis and to define the local extension (pT category) (grade of recommendation: B). In a life-threatening situation due to extensive metastasis, chemotherapy must be started before orchidectomy.

109. CA TESTIS: DIAGNOSIS (2) Serum determination of tumour markers (AFP, hCG, and LDH in metastatic disease) must be performed before and after orchidectomy for staging and prognostic reasons (grade of recommendation: B). The state of the retroperitoneal, mediastinal and supraclavicular nodes and viscera must be assessed in testicular cancer. In seminoma, a chest CT scan is not necessary if the abdominal nodes are negative (grade of recommendation: B).

110. CA TESTIS Highlight of the management of primary tumor: No transcrotal biopsy High ligation orchydectomy (“radical orchyectomy”): with early clamping of the spermatic cord at the deep inguinal ring Testis sparing surgery Consider sperm banking In cases of disseminated disease and life-threatening metastases, it is current practice to start with up-front chemotherapy, and orchidectomy may be delayed until clinical stabilisation has occurred.

111. CA TESTIS: ORCHYDECTOMY High ligation

112. CA TESTIS: ORCHYDECTOMY High ligation The pathologist should record the T stage of the primary tumor & determine wether lymphatic or vascular invasion is seen within the tumor mass

113. CA TESTIS Staging system: AJCC TNMS Prognostic-based classification for metastatic germ cell cancer (International Germ Cell Cancer Collaborative Group, IGCCCG) Depend on: tumor type, imaging study, tumor markers (AFP, β-hCG, LDH)

114. CA TESTIS: TREATMENT Based on: Histopathological type Stage Risk factors Options: Surveillance Radiation therapy RPLND Chemotherapy

115. CA TESTIS: CHEMOTHERAPY

116. CA TESTIS: FERTILITY CONCERN ± 25% pts have defects in spermatogenesis at time of presentation Higher consentrations of anti-sperm antibodies ± 50% of pts are at least temporarily hypofertil after orchydectomy before any adjuvant therapy Fertility can be further impaired by adjuvant therapy (RPLND, radiation therapy, and chemotherapy) Only ± 35% of pts achieve paternity after chemotherapy; ± 76% paternity rate after RPLND

117. CA TESTIS One of the most curable cancer

118. CA TESTIS: Conclusion : Most common urological malignancy in young men & most curable cancer Tumor markers should be examined pre and post orchydectomy Avoid scrotal violation & do a high ligation orchydectomy Treatment option depend on histopathological type, stage, risk factors, and patients condition Follow up is mandatory

119. PENELITIAN RELEVAN

120. PENGABDIAN MASYARAKAT YANG RELEVAN (2021) Pemberdayaan Petugas Kesehatan Dalam Deteksi Dini Kanker Prostat Di Posyandu Lansia Wilayah Kerja Puskesmas Terminal Kecamatan Banjarmasin Timur Kota Banjarmasin Kalimantan Selatan (Eka Yuda dkk, 2021) Pemberdayaan Tenaga Kesehatan Posyandu Lansia di Wilayah Kerja Dinas Kesehatan Kota Banjarmasin Provinsi Kalimantan Selatan Dalam Deteksi Dini Kanker Prostat (Huldani dkk, 2021)

121. PENGABDIAN MASYARAKAT YANG RELEVAN (2024) PEMBERDAYAAN PETUGAS KESEHATAN POSYANDU LANSIA DI WILAYAH KERJA DINAS KESEHATAN KOTA BANJARBARU PROVINSI KALIMANTAN SELATAN DALAM DETEKSI DINI KANKER PROSTAT Eka Yudha Rahman, Nia Kania, Roselina Panghiyangani, Winardi Budiwinata, Hendra Sutapa, Deddy Rasyidan Yulizar,

122. TERIMA KASIH