PUSKESMAS BABANA, dalam kenangan

Puskesmas Babana, tempat tugasku pertama kali ketika menjadi dokter PTT. Puskesmas yang sangat berkesan, menyenangkan sekaligus dengan kenangan menyedihkan. Puskesmas Babana, riwayatmu kini. Aku gak tahu apa aku mau kembali.

Sebenarmu tempatmu sangat indah, berhadapan dengan lapangan sekaligus pantai. Sungguh asik buat menenangkan diri. Setiap pagi dan sore hari, selalu ramai

Tetapi sayang, dibalik semuanya, ada kisah sedih yang tak bisa kulupakan, yang membuatku sulit kembali dan menimba pengalaman. Tetapi jauh di lubuk hatiku yang paling dalam, kau kan selalu menjadi kenangan yang tak mungkin aku lupakan.

Semoga Puskesmas Babana semakin maju menjadi yang terdepan di Mamuju, Sulawesi Barat dan juga di Indonesia. Tetapi entah itu kapan

MDR-TB epidemiology

Andi Cahyadi

Multidrug-resistant tuberculosis (MDR-TB) and extensively-drug resistant Tuberculosis (XDR TB) has become an emerging diseases and health problems of the world. (1-5) Presence of Mycobacterium tuberculosis (M.tb) antituberculosis drug-resistant (OAT) to investigate the basis of the importance of contact with rifampicin-resistant strain (RMP) and isoniazid (INH) in the prevention of tuberculosis (TB) (2,6,7) according to WHO recommendations. (2,5) Children at high risk of contracting TB from household contacts with MDR-TB so that the identification of both TB infection (latent TB) or TB disease must be done systematically. (5) Incidence of TB illness and M.tb resistance patterns in children with MDR-TB contacts in Indonesia is still not well known.

Incidence of drug resistance has increased since TB treatment was first introduced in 1943. MDR-TB cases emerged after widespread use of rifampicin in the 1970's through the use of second-line anti-tuberculosis. (5) The problem that then arises is Mycbacterium tuberculosis resistant to antituberculosis drugs such as fluoroquinolon and second generation antituberculosis injection, known as XDR (Extended drug resistant). (5) Cases of MDR-TB is a major issue which, according to WHO, the prevalence of MDR-TB was 5.5% while the control is right with the implementation of directly observed treatment short course (DOTS), the prevalence of MDR-TB only 1.6%. (5) In regions with high TB ​​incidence, prevalence of MDR-TB are recorded in the DOTS program varies between 4.4 to 26.9% where 20% of cases are from India and China. (5) The data of MDR-TB official in Indonesia until now not currently exist.

Global Project Based on data from WHO (2008), data from 16 countries, acquired 2,509,545 new TB cases, 17% (95% CI 13.6 to 20.4) resistance M.tb, 10.3% (95% CI 8, 4 to 12.1) INH-resistant, 2.9% (95% CI 2.2 to 3.6) of MDR-TB. Global incidence of resistance to the patients who had been treated were: 35% resistance M.tb (95% CI 24.1 to 45.8), 27.7% (95% CI 18.7 to 36.7) and 15 INH-resistant, 3% (95% CI 9.6 to 21.1) of MDR-TB. Incidence of resistance of all TB cases are: 20% (95% CI 16.1 to 23.9) resistesi M.tb, 13.3% (95% CI 10.9 to 15.8) and 5.3% resistant to INH (95% CI 3.9 to 6.6) of MDR-TB. Based on data from 116 countries, the estimated amount of resistance M.tb 489 139 (95% CI 455093-614215) occurred in 2006. China and India of MDR-TB cases accounted for approximately 50% Russia 7%. (5)

TB incident in the world (2009)

 http://wwwnc.cdc.gov/travel/yellowbook/2012/chapter-3-infectious-diseases-related-to-travel/tuberculosis.htm

Drug resistance is related to previous treatment. In people who have received treatment for tuberculosis, four times the likelihood of resistance and the presence of MDR-TB as much as ten times greater than those that have not been previously treated tuberculosis. In countries with high TB ​​incidence, the incidence of resistance in people who have been treated between 4.4% to 26.9% of all persons registered in the DOTS program (5)

Incidence of active TB in children with MDR-TB contacts by 4% in Brazil and 8% in Peru as an area with high TB ​​prevalence. (7) Incidence of active TB in people with non-MDR TB contacts by 4% in Brazil, while a systematic review by Morrison et al., (2008) showed the incidence of active TB in people with TB in contact with the country's economic income is low to moderate at 4.5% 8. Four percent of children with MDR-TB contacts and 4% of children with non-MDR TB contacts progress to active TB but oddnya ratio of 2.1 in Brazil.

Global map of MDR-TB proportion (2009)

http://wwwnc.cdc.gov/travel/yellowbook/2012/chapter-3-infectious-diseases-related-to-travel/tuberculosis.htm

In areas with high TB ​​incidence, Van Rie et al. (2000) through analysis of restriction fragment length polymorphism (RFLP) successfully demonstrated that M.tb MDR strains have been transmitted to the contact. (9) Kritsky et al. (1996), transmission of MDR-TB in Brazil reached 7.8% of 218 patients with positive contact (1.6 cases per 1000 months of contact). As many as 46% of cases with identical strains of M.tb contact, 31% and 23% different from all the drug resistant one. Sekuencing DNA analysis indicates some genes determine the identity of the gene of Mycobacterium tuberculosis complex, rpoB, katG, rpsL, and gyrA. Resistant bacteria that have been OAT-mediated changes in gene katG, and rpoB Inha .

DAFTAR PUSTAKA                                                                            

1. Kritski AL, Marques MJ, Rabahi MF, Vieira MA, Werneck-Barroso E, Carvalho CE, et al. Transmission of tuberculosis to close contacts of patients with multidrug-resistant tuberculosis. Am J Respir Crit Care Med 1996;153(1):331-5.

2. Becerra MC, Appleton SC, Franke MF, Chalco K, Arteaga F, Bayona J, et al. Tuberculosis burden in households of patients with multidrug-resistant and extensively drug-resistant tuberculosis: a retrospective cohort study. Lancet 2011;377(9760):147-52.

3. Schaaf HS, Shean K, Donald PR. Culture confirmed multidrug resistant tuberculosis: diagnostic delay, clinical features, and outcome. Arch Dis Child 2003;88(12):1106-11.

4. Rahajoe NN, Basir D, Makmuri, Kartasasmita CB. Pedoman nasional tuberkulosis anak. 2 dengan revisi ed. Jakarta: UKK Respirologi PP IDAI, 2008.

5. WHO. Guidelines for the programmatic management of drug-resistant tuberculosis. Emergency update 2008 ed. Geneva: World Health Organization, 2008.

6. Mohle-Boetani JC, Flood J. Contact investigations and the continued commitment to control tuberculosis. JAMA 2002;287(8):1040-2.

7. Bayona J, Chavez-Pachas AM, Palacios E, Llaro K, Sapag R, Becerra MC. Contact investigations as a means of detection and timely treatment of persons with infectious multidrug-resistant tuberculosis. Int J Tuberc Lung Dis 2003;7(12 Suppl 3):S501-9.

8. Morrison J, Pai M, Hopewell PC. Tuberculosis and latent tuberculosis infection in close contacts of people with pulmonary tuberculosis in low-income and middle-income countries: a systematic review and meta-analysis. Lancet Infect Dis 2008;8(6):359-68.

9. Van Rie A, Warren R, Richardson M, Gie RP, Enarson DA, Beyers N, et al. Classification of drug-resistant tuberculosis in an epidemic area. Lancet 2000;356(9223):22-5.

TROMBOSITOSIS

Peningkatan jumlah trombosit pada sebagian besar pasien tidak memberikan gejala dan tidak memerlukan terapi spesifik tetapi beberapa kasus dapat menimbulkan komplikasi serius bahkan kematian.^{1 2} Sebagian besar peningkatan jumlah trombosit >450x109/L terjadi secara insidentil dan transien. Pemeriksaan trombosit ulang sebaiknya dilakukan dalam beberapa minggu berikutnya.²

Jumlah trombosit yang tinggi lebih disebabkan oleh reaksi terhadap proses inflamasi, infeksi dan keganasan. TRombositosis juga dapat disebabkan oleh kelainan myeloproliferatif seperti trombositosis esensial dan polisitemia vera yang terjadi karena kelainan klonal dari system hematopoetik.²

Secara normal jumlah trombosit berkisar antara 150-450x10⁹/L.¹ Studi lain menunjukkan, trombosit normal berkisar antara 100-400x10⁹/L pada individu sehat dan hanya kadang pada angka 400-450x10⁹/L.³ Trombosit antar 350-450x109/L memerlukan follow up dan evaluasi lebih lanjut.³

Batasan trombositosis secara klinis bervariasi, banyak literature menyepakati jumlah trombosit darah tepi >450x10⁹/L,⁴ atau jumlah trombosit >2 SD diatas rata-rata.¹ Trombositosis pada dewasa didefinisikan apabila jumlah trombosit >450x10⁹/L.^3-5 Trombositosis diklasifikasikan dalam beberapa hal tergantung kepentingan penelitian diantaranya primer dan sekunder,^{4 6 7} familial, klonal dan reaktif (sekunder)² serta pembagian trombositosis familial/ herediter, trombositosis dikaitkan kelainan myeloproliferatif/myelodisplasia (trombositosis klonal) dan trombositosis reaktif (sekunder).³ Pada studi ini dipakai beberapa terinologi pembagian trombositosis.  

 

Klasifikasi trombosit berdasarkan jumlah trombosit adalah:¹

1.      Trombositosis ringan   :  500-700x10⁹/L

2.      Trombositosis sedang :  700-900x10⁹/L

3.      Trombositosis berat      :  >900x10⁵/L

4.      Trombositosis ekstrim   :  >1000x10⁹/L

Berdasarkan etiologinya, trombositosis dibedakan menjadi dua kelompok yaitu:¹

1.      Trombositosis  primer/autonom  (esensial)

2.      Trombositosis sekunder (reaktif)

Trombositosis primer terjadi apabila peningkatan jumlah trombosit disebabkan oleh gangguan sel hematopoetik sedangkan trombositosis reaktif atau sekunder terjadi akibat factor luar seperti inflamasi kronis, kanker, defisiensi besi, paska splenektomi.⁴ Pada sebagian besar kasus, trombositosis pertama kali terdeteksi pada pemeriksaan darah lengkap. Trombositosis sekunder lebih sering ditemukan daripada trombositosis sekunder.⁴

 Daftar pustaka

1.    Sutor AH. Thrombocytosis. Dalam: Lilleymen JS, Hann IM, Blanchette VS, penyunting . Pediatric Hematology: Edisi ke- 2. London: Churchill Livingstone; 2000. h 455-62

2.    Lanzkowsky P. Disorder of Platelet. Dalam: Lanzkowsky P. penyunting. Manual of Pediatric Hematology and Oncology: Edisi ke-.2. New York: Churchill Livingstone; 1995.h 219-20

3.    Diuna SB. Thrombocytosis. Disorder with Increases Platelet. Dalam: Nathan DG. Oski FA, penyunting, Hematology of Infancy and Childhood: Edisi ke- 5. Philadelphia:  Saunders ; 1998. h.1607

4.    Schwartz CL dan Cohen HJ. Mycloproliferative and Myclodysplatia Syndromes. Dalam: Pizzo PA dan Poplack DG. penyunting. Principles and Practice of Pediatric Oncology: Edisi ke- 3. Philadelphia: Lippincont-Raven; 1997. h 505-17

5.    J Marilyn dan J Mauco. Hemostasis and bleeding disorders. Dalam : Rudolph, MA , Hoffman JIE dan Rudolph DC. penyunting. Rudolph’Pediatrics: Edisi ke- 20. London : Prentice Hall International ( UK ); 1996 . h 1244.

6.    Corrigan JJ. Trombotic disorders. Dalam : Behrman RE, Kliegman RM dan Arvin AM. penyunting. Nelson Textbook of Pediatrics: Edisi ke-15. Philadelphia:  Saunders .; 1996  h. 1434.

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Yang selalu terpendam dalam hati.