Nama : AGUS BUDI SETIAWAN NIM
: 20100320101 RESUME JURNAL GOUT
Gout adalah penyakit metabolik, yang ditandai dengan arthritis akut atau kronis, dan deposisi kristal monosodium urat pada sendi, tulang, jaringan lunak, dan ginjal.
Pada abad ke-18, Garrod berpendapat bahwa terdapat hubungan antara asam urat tinggi dan asam urat kristal forma-tion, yang mendasari patologi untuk gout.
Gout dapat bermanifestasi sebagai arthritis akut atau artropati kronis, yang juga disebut gout tophaceous
Semua pasien gout memiliki hyperuri-cemi Konsentrasi asam urat yang normal atau rendah dapat disebabkan oleh ekskresi berlebihan asam urat, pembentukan kristal, atau kondisi inflamasi sistemik. Namun mekanisme yang tepat masih belum sepenuhnya sepen uhnya dipahami Diagnosis gout yang paling akurat bila didukung oleh visualisasi kristal asam urat dalam sampel cairan sendi dan menunjukkan histologis pada sampel jaringan Analisis cairan synovial merupkan pemeriksaan penunjang yang dapat membantu menegkkan terjadinya gout, dnagn kriterika berikut: Synovial fluid analysis. Test
Value
Normal
penampakan
bening
Transparan
warna
kuning
bersih atau putih
WBC (per mm3)
2100
< 200
PMNs (%)
62
< 25
Gram stain
-
-
Kultur
Negative
Negative
Total protein (g/dL)
2
3.1
LDH (IU/L)
440
105 – 333
glukosa (mg/dL)
42
70 – 110 110
Serta terdapat Kristal monosodium urat jika terjadi kelainan
Rasa sakit dan peradangan terjadi ketika kristal asam urat mengaktifkan humoral dan seluler proses inflamasi
Pada penyakit gout akut, jika terjadi inflamasi sistemik, seperti infeksi akut, sitokin dan kemokin memicu peradangan dan menyebabkan arthritis dengan adanya kristal urat
Fagositosis kristal terjadi karena makrofag pada sel-sel lapisan sinovial yang mendahului masuknya
Pada pasien gout dilakukan pmeriksaan asam urat serum dan kadar asam urat urin 24 jam jika masih dalam batas normal sebelum pulang dari rumah sakit
Pasien disarankan untuk mengikuti pemeriksaan di klinik dalam dua minggu, sebelum memutuskan untuk meberikan terapi atau obat tertentu untuk mencegah serangan lebih lanjut dari arthritis akut.
Pengobatan lini pertama untuk gout akut adalah colchicines dan / atau non-steroid anti-inflamasi agen
Kortikosteroid sistemik atau intra-artikular juga dapat digunakan, dan sama-sama efektif, tetapi dengan efek samping yang lebih
Interleukin-1 inhibitor masih dalam penyelidikan, dan tidak disetujui untuk serangan akut gout
LAMPIRAN JURNAL GOUT:
Cases Journal
BioMed Central
Case Report
Open
Access
Chronic tophaceous gout presenting as acute arthritis during an acute illness: a case report Abhijeet Dhoble*, Vijay Balakrishnan and Robert Smith Address: Department of Internal Medicine, Michigan State University, East Lansing, Michigan, USA Email: Abhijeet Dhoble* -
[email protected]; Vijay Balakrishnan -
[email protected]; Robert Smith - robert.sm
[email protected] * Corresponding au thor
Published: 15 October 2008 Cases Journal 2008, 1:238
doi:10.1186/1757-1626-1-238
Received: 9 October 2008 Accepted: 15 October 2008
This article is available from: http://www.casesjournal.com/content/1/1/238 © 2008 Dhoble et al; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Abstract Background: Gout is a metabolic disease that can manifest as acute or chronic arthritis, and deposition of urate crystals in connective tissue and kidneys. It can either manifest as acute arthritis or chronic tophaceous gout. Case presentation: We present a 39-year-old male patient who developed acute arthritis during his hospital course. Later on, after a careful physical examination, patient was found to have chronic tophaceous gout. The acute episode was successfully treated with colchicines and indomethacin. Conclusion: Gout usually flares up during an acute illness, and should be considered while evaluating acute mono articular arthritis. Rarely, it can also present with tophi as an initial manifestation.
Background Gout is a metabolic disease, which is char acterized by acute or chronic arthritis, and deposition of monosodium urate crystals in joint, bones, soft tissues, and kidneys [1 4]. In 18 th century, Garrod proposed a causative relationship between elevated uric acid and urate crystal formation, which is underlying pathology for gout [4]. Gout can either manifes t as acute arthritis or chronic arthropathy, which is also called to phac eou s gout [1 ,2,5].
and was diagnosed with acute uncom plicated diverticuli- tis, confirmed by computed tomography (CT) of the abdomen. His medical and s urgical history was unre- markable, and he denied any medication use. He denied smoking or illicit drug use, but admitted occasional alco-
hol use on every other weekend. He did not follo w any particular diet. He had an average built with BMI of 29.6. He was started on intravenous antibiotics and pain medi- cation, which led to significant clinical improvement within two days . On the third day of hospitalization, he develope d acute, severe pain and swelling of the left elbow. Within next few hours, pain worsened and he was unable to move the elbow joint, which was tender,
erythe matous, and swollen on examination (figure 1). Neve r investigated in the past, we also noted a firm 4 × 6 cm mass on each elbow, a nd another one surrounding the proxim al inter-phala ngeal joint of right middle finger (figure 2). There was no over- lying edema or cellulitis. There were no other swellings or tophi noted especially on toes or ears. When asked partic- ularly, he denied similar episodes in the past. He also denied any episode of swelling of great toe in the past.
Page 1 of 4 (page number not for citation purposes)
Cases Journal 2008, 1:238
Figure 1 Tophus at the back of right elbow.
Plain radiography of left elbow showed join t effusion, and soft tissue swelling. Radiography of other joints including hands and feet was not performed. Laboratory values on the third day are given in table 1. Liver function test was also perfo rm ed, and the results were unremarka ble. Diagnostic arthocentesis was performed on both the elbows, and revealed negatively birefringent needleshaped crystals using polarized microscopy in both sam ples. Detailed analysis of synovial fluid is given in table 2. The swelling on the right elbow was aspirated to determine the etiology because patient had that swelling for a long time. The patient respo nded partially to colchicine, but later had great relief with indomethacin. Colch icine was used at the dose of 0.6 mg every two hourly. He received total of six doses, but it was stopped because he developed severe nausea and vomiting. He admitted that his pain was reduced to 4/10 in intensity from 9/10 before treatment, but swelling was persistent. We initiated indomethacin at 50 mg every eight hourly, and his pain and swelling was relieved to great extent in 48 hours.
Discussion Gout is a metabolic disease that can manifest as acute or
http://www.casesjournal.com/content/1/1/238
Figure 2 Tophi/tophus around the proximal inter-phalangeal joint of right middle finger.
nective tissue and kidneys. All patients have hyperuricemia at some point of their disease. But, either normal or low serum uric acid levels can occur at the time of acute attack; and asymptomatic hyperuricemic individuals may never experience a clinical event resulting from urate crystal deposition [1-4]. Low to normal uric acid concentr aTable 1: Laboratory values at admission. Test
Value
Value range
Sodium 145 Potassium Chloride CO2 BUN Creatnine Total protein Albumin Magnesium Phosphorus Calcium White blood count Hemoglobin 16.5
139 meq/l
135–
3.5 meq/l 108 meq/l 28 mmol/l 18 mg / dl 0.7 mg/dl 5.4 g / dl 3.4 g / dl 1.6 meq/l 3.3 mg/dl 8.2 mg/dl 12,400/mm 3 11.6 g / dl
3.5–4.9 96–110 20–30 6.0–23.0 0.6–1.4 6.0–8.0 3.6–5.0 1.3–2.2 2.5–4.5 8.0 –10.5 4–12 12.6–
Page 2 of 4 (page number not for citation purposes)
Cases Journal 2008, 1:238
http://www.casesjournal.com/content/1/1/238
Table 2: Synovial fluid analysis. Test Clarity Color WBC (per mm3) PMNs (%) Gram stain
Value
Translucent Yellow 2100 62 No organisms organism s Culture Negative Total protein (g/dL) 2 LDH (IU/L) 440 Glucose (mg/dL) 42 Crystal Monosodium urate crystals
Normal Transparent Clear < 200 < 25 No Negative 3.1 105 – 333 70–110 None
tion can be due to excessive excretion of uric acid, crystal formation, or systemic inflammatory state [6,7]; however, exact mechanism is still not completely understood. A diagnosis of gout is most accurate wh en supported by visualization of uric acid crystals in a sample of joint or bursal fluid, or demonstrated histologically in excised tissue. Synovial fluid analysis of our patient was consistent with inflammatory arthritis. Mild leucocytosis in this patie nt was due to systemic inflammatory respo nse. Visible or palpable tophi, as this patient exhib ited, are usually noted only among those patie nts who ar e hyperuricemic and have had repeated attacks of acute gout, often over many years. However, pr esentation of tophaceous deposits in the absence of gouty arthritis is also reported [5,8]. Pain and inflammation are manifested when uric acid crystals activate the humoral and cellular inflammatory processes [9 ]. During an acute illness, if systemic inflamm atory state prevails, such as in an acute inf ection, cytokines and chemokines triggers inflammation and cause arthritis in the presence of urate cr ystals [10,11]. Phagocytosis of these crystals by macro phages in the synovial lining cells pr ecedes influx of neutrophils in the joint [9-11]. This pr ocess releases various mediators of inflam mation lo cally [12 ,13 ].
Hyperuricemia is often present in patients with tophaceous gout, and they can benefit from uric acid lowering therapy early during the course [14,15]. In our patient, serum uric acid and 24-hour urine uric acid level was within normal limits when measured in the hospital before his discharge fro m the hospital. It was decided to follow him up in the clinic in two weeks, and measure these values again during 'interval gout' before deciding to start him on any particular medication to prevent further attacks of acute arthritis. Our patien t p resen ted with tophi as an initial presentation
Investigational studies due to acute elbow joint pain deci phered the underlying mystery of chr onic swelling. Systemic inflammatory response secondary to diverticulit is exposed the joints to the effects of urate. First-line treatments for an acute flare are either oral colchicine and/or non-steroidal anti-in f l ammato ry agents. Systemic or intra-articular cor ticostero ids can also be used, and are equally effective, but with more side effects [16,17]. Interleukin-1 inhibitors are still under investigation, and are not approved for an acute attack of gout [18 ].
Conclusion Gout usually flares up during an acute illness, and should always be considered while evaluating acute mono articular arthritis in hospitalized patients. Gout can present with tophi as an initial manifestation of the disease process.
Competing interests The authors declare that they have no com peting interests.
Authors' contributions All authors contributed equally in collecting pat ient da ta, chart review, and editing medical images. All authors read and approved the final manuscript.
Consent Written informed consent was obtained from the patie n t for publication of this case report and accompanying images in Journal of Medical Case Reports. A copy of the written consent is available for review by the Editor-inChief of this jou r n al.
Acknowledgements We thank patient for giving us consent for the publication of the case report.
References 1.
Campion EW, Glynn RJ, DeLabry LO: Asymptomatic hyperuri- cemia. Risks and consequences in the Normative Aging Study. Am J Med 1987, 82:421. 2. Hall AP, Barry PE, Dawber TR, McNamara PM: Epidemiology of gout and hyperuricemia: A long term population study. Am J Med 1967, 42:27. 3. Logan JA, Morrison E, McGill PE: Serum uric acid in acute gout. Ann Rheum Dis 1997, 56:696-7. 4. Garrod AB: The Nature and Treatment of Gout and Rheumatic Gout 2nd edition. 1863. 5. Wernick R, Winkler C, Campbell S: Tophi as the initial manifestation of gout. Report of six cases and review of literature. Arch intern med 1992, 152:873. 6. Urano W, Yamanaka H, Tsutani H, Nakajima H, Matsuda Y, Taniguchi A, Hara M, Kamatani N: The inflammatory process in the mechanism of decreased serum uric acid concentrations during acute gouty arthritis. J Rheumatol 2002, 29(9):1950-3.
Rheum 1983, 26:98-101.
Page 3 of 4 (page number not for citation purposes)
Cases Journal 2008, 1:238 http://www.casesjournal.com/conte nt/1/1/238
9.
10.
11.
12.
13.
14.
15. 16.
17.
18.
Beutler A, Schumacher HR Jr: Gout and 'pseudogout': when are arthritic symptoms caused by crystal disposition? Post grad Med 1994, 95:103-6. Schumacher HR, Phelps P, Agudelo CA: Urate crystal induced inflammation in dog joints: sequence of synovial changes. J Rheumatol 1974, 1:102. Gordon TP, Kowanko IC, James M, RobertsThomson PJ: Monoso- dium urate crystalinduced prostaglandin synthesis in the rat subcutaneous air pouch. Clin Exp Rheumatol 1985, 3:291. Malawista SE, Duff GW, Atkins E, Cheung HS, McCarty DJ: Crystal- induced endogenous pyrogen production. A further look at gouty inflammation. Art hritis Rheum 1985, 28:1039. Falasca GF, Ramachandrula A, Kelley KA, O'onnor CR, Reginato AJ: Superoxide anion production and phagocytosis of crystals by cultured endothelial cells. Arthritis Rheum 1993, 36:105. Sutaria S, Katbamna R, Underwood M: Effectiveness of interven- tions for the treatment of acute and prevention of recurrent gout – a systematic review. Rheumatology (Oxford) 2006, 45:1422. Wallace SL, Singer JZ: Therapy in gout. Rheum Dis Clin North Am 1988, 14:441. Janssens HJ, Janssen M, Lisdonk EH van de, van Riel PL, van Weel C: Use of oral prednisolone or naproxen for the treatment of gout arthritis: a double-blind, randomised equivalence trial. Lancet 371(9627):1854-60. 2008 May 31 Zhang W, Doherty M, Bardin T, Pascual E, Barskova V, Conaghan P, Gerster J, Jacobs J, Leeb B, Lioté F, McCarthy G, Netter P, Nuki G, Perez-Ruiz F, Pignone A, Pimentão J, Punzi L, Roddy E, Uhlig T, Zimmermann-Gòrska I, EULAR Standing Committee for International Clinical Studies Including Therapeutics: EULAR evidence based recommendations for gout. Part II: Management. Report of a task force of the EULAR Standing Committee for International Clinical Studies Including Therapeutics (ESCISIT). Ann Rheum Dis 2006, 65(10):1312-24. So A, De Smedt T, Revaz S, Tschopp J: A pilot study of IL-1 inhibition by anakinra in acute gout. Ar thritis Res Ther 2007, 9:R28.
Publish with Bio Med Central and ever y scientist can read your work free of charge "BioMed Central
will be
the most significant development for
disseminating the results of biomedical researc
h in our
lif etime."
Sir Paul Nurse, Cancer Research UK
Your research papers will be: available free of charge to the entire biom edical c omm unit y peer revi ewed and publ ished i mme diat ely upon acceptance cited in PubMed and archived on PubMed Central yours — you keep the copyright Submit your manuscript here:
BioMed central
http://www.biomedcentral.com/info/publishing_adv.asp
Page 4 of 4 (page number not for citation purposes)
NAMA: AGUS BUDI SETIAWAN (20100320101)
RESUME BM OSTEOARTHRITIS
DEFINISI
Osteoarthritis adalah penyakit yang merupakan bagian dari arthritis, penyakit ini meyerang sendi terutama pada tangan, lutut dan pinggul. Orang yang terserang osteoarthritis biasanya susah menggerakkan sendi-sendinya dan pergerakannya menjadi terbatas karena turunnya fungsi tulang rawan untuk menopang badan.
ETIOLOGI
Penyebab dari osteoarthritis adalah 1. adanya peradangan kronis pada persendian ditandai dengan pembengkakan pada jari-jari tangan, siku, dan lutut. Biasanya daereah yang mengalami pembengkakan, berwarna kemerah-merahan 2. pernah mengalami trauma dan radang pada sendi 3. karena faktor usia kebanyakan orang yang terkena osteoarthritis adalah orang dengan usia diatas 50 tahun. 4. keturunan ada beberapa orang yang mengalami osteoarthritis karena faktor ke turunan 5. berat badan yang berlebihan berat badan yang berlebihan, dapat memberatkan sendi dalam menopang tubuh. 6. stres pada sendi biasanya stres pada sendi ini terjadi pada olahragawan.
7. neurophaty perifer
TANDA-TANDA
Untuk mengetahui apakah kita terserang penyakit ini, ada beberapa hal yang perlu diperhatikan sebagai berikut: 1. biasanya, osteoarthritis terjadi secara perlahan, dimulai dari rasa sakit pada sendi setelah melakukan aktivitas, seperti olahraga, kemudian lama-kelamaan akan terasa lebih sakit dan kaku 2. pada tangan: jari-jari membesar, terasa sakit, kaku bahkan mati rasa 3. pada lutut: lutut terasa sakit dan kaku. Susah digunakan untuk berjalan dan dapat menyebabkan cacat 4. pada pinggul: terasa sakit dan kaku pada kunci paha dan dapat membatasi pergerakan 5. pada punggung/tulang belakang: terasa sakit dan kaku pada leher
DIAGNOSIS
Untuk mengetahiu apakah seseorang terkana penyakit osteoarthritis, ada beberapa cara yang 2
biasanya digunakan oleh dokter untuk mene gakkan diagnosis, diantaranya : 1. Riwayat penyakit Dokter menanyakan pada pasien tentang gejala yang dialami, kapan mulai terjadi, dan bagaimana hal itu terjadi untuk menegakkan diagnosis. Dan dokter juga menanyakan, apakah ada masalah dengan obat tertentu untuk alternatif pemberian obat jika ternyata pasien tidak cocok dengan jenis obat tertentu. 2. Pemeriksaan fisik Pada penderita osteoarthritis, pemeriksaan fisik ini biasanya dilakukan dengan memeriksa kemampuan berjalan. 3. X ray Xray untuk mengetahui sejauh mana sendi mengalami kerusakan. X ray dapat memperlihatkan rusaknya tulang. 4. MRI (Magnetic Resonance Imaging)
Magnetic resonance imaging dapat memberikan gambar-gambar seperti jaringan dalam tubuh dengan resolusi yang tinggi. MRI jika diduga ada penyakit dalam jaringan tubuh.
TERAPI NON FARMAKOLOGI 2,3
Ada beberapa cara dalam penanganan osteoarthritis non farmakologi, diantaranya : 1. Olahraga Olahraga dapat mengurangi rasa sakit dan dapat membantu mengontrol barat badan. Olahraga untuk osteoarthritis misalnya berenang dan jogging. 2. Menjaga sendi Menggunakan sendi dengan hati-hati dapat menghindari kelebihan stres pada sendi. 3. Panas/dingin Panas didapat, misalnya dengan mandi air panas. Panas dapat mengurangi rasa sakit pada sendi dan melancarkan peredaran darah. Dingin dapat mngurangi pembengkakan pada sendi dan mengurangi rasa sakit. Dapat didapat dengan mengompres daerah yang sakit dengan air dingin. 4. Viscosupplementation merupakan perawatan dari Canada untuk orang yang terkena osteoarthritis pada lutut, berbentuk gel. 5. Pembedahan Apabila sendi sudah benar-benar rusak dan rasa sakit sudah terlalu kuat, akan dilakukan pembedahan. Dengan pembedahan, dapat memperbaiki bagian dari tulang. 6. Akupuntur Dapat mengurangi rasa sakit dan merangsang fungsi sendi. 7. Pijat Pemijatan sebaiknya dilakukan oleh orang yang ahli di bidangnya. 8. vitamin D,C, E, dan beta karotin
untuk mengurangi laju perkembangan osteoarthritis. 9. Teh hijau Memiliki zat anti peradangan.
TERAPI FARMAKOLOGI
Semua obat memiliki efek samping yang berbeda, oleh karena itu, penting bagi pasien untuk membicarakan dengan dokter untuk mengetahui obat mana yang paling cocok untuk di konsumsi. Berikut adalah beberapa obat pengontrol rasa sakit untuk penderita osteoarthritis: 1. Acetaminophen Merupakan obat pertama yang di rekomendasikan oleh dokter karena relatif aman dan efektif untuk mengurangi rasa sakit. 2. NSAIDs (nonsteroidal anti inflammatory drugs) Dapat mengatasi rasa sakit dan peradangan pada sendi. Mempunyai efek samping, yaitu menyebabkan sakit perut dan gangguan fungsi ginjal. 3. Topical pain Dalam bentuk cream atau spray yang bisa digunakan langsung pada kulit yang terasa sakit. 4. Tramadol (Ultram) Tidak mempuyai efek samping seperti yang ada pada acetaminophen dan NSAIDs. 5. Milk narcotic painkillers Mengandung analgesic seperti codein atau hydrocodone yang efektif mengurangi rasa sakit pada penderita osteoarthritis. 6. Corticosteroids Efektif mengurangi rasa sakit. 7. Hyaluronic acid Merupakan glycosaminoglycan yang tersusun oleh disaccharides of glucuronic acid dan Nacetygluosamine. Disebut juga viscosupplementation.
Digunakan dalam perawatan pasien osteoarthritis. Dari hasil penelitian yang dilakukan, 80% pengobatan dengan menggunakan hyaluronic acid mempunyai efek yang lebih kecil dibandingkan pengobatan dengan menggunakan placebo. Makin besar molekul hyaluronic acid yang diberikan, makin besar efek positif yang di rasakan karena hyaluronic acid efektif m engurangi rasa sakit. 8. Glucosamine dan chondroitin sulfate Mengurangi pengobatan untuk pasien osteoarthritis pada lutut.
PENCEGAHAN 1
Ada beberapa hal yang perlu diperhatikan, agar kita terhindar dari osteo arthritis : 1. menghindari olahraga yang bisa meyebabkan se ndi terluka 2. mengontrol berat badan agar berat yang ditopang oleh sendi menjadi ringan 3. minum obat untuk mencegah osteoarthritis
DAFTAR PUSTAKA
1. Anonim.Osteoarthritis.http://new.merapi.net/index.php?view=news/116&id=116&PHPSESSID=4ca6 439313b991ed97f43906b994. 17 november 2007 2. Anonim. Handout of Health: Osteoarthritis. http://www.niams.nih.gov/Health_Info/Osteoarthritis/default.asp. 17 november 2007 4. Felson, D.T. 2006. Osteoarthritis of the Knee. NEJM 354: 841-848 5. Lane, N. E. 2007. Osteoarthritis of the Hip. NEJM 357: 1413-1421
.
