resume jurnal gout dan resume bm osteoarthritis.docx

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 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

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

neutrofil dalam sendi, Proses ini melepaskan berbagai mediator peradangan area local

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 reportAbhijeet 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 - [email protected]

* Corresponding author

Published: 15 October 2008

Cases Journal 2008, 1:238 doi:10.1186/1757-1626-1-238

This article is available from: http://www.casesjournal.com/content/1/1/238

© 2008 Dhoble et al; licensee BioMed Central Ltd.

Received: 9 October 2008Accepted: 15 October 2008

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (h t t p :/ / creati v e c o mm o n s . org/l i cen s es/ b y / 2 .0 ), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

AbstractBackground: 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.

BackgroundGout is a metabolic disease, which is characterized byacute or chronic arthritis, and deposition of monosodium urate crystals in joint, bones, soft tissues, and kidneys [1-4]. In 18th century, Garrod proposed a causative relation- ship between elevated uric acid and urate crystal formation, which is underlying pathology for gout [4]. Gout can either manifest as acute arthritis or chronic arthropathy, which is also called tophaceous gout [1,2,5].

Case presentation

A 39-year-old African American male patient was admit-ted with one-day history of acute left lower quadrant pain, and was diagnosed with acute uncomplicated diverticulitis, confirmed by computed tomography (CT) of the abdomen. His medical and surgical 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 follow any particular diet. He had an average built with BMI of 29.6. He was started on intravenous antibiotics and pain medication, which led to significant clinical improvement within two days.

On the third day of hospitalization, he developed 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, erythematous, and swollen on examination (figure 1). Never investigated in the past, we also noted a firm 4 × 6 cm mass on each elbow, and another one surrounding the proximal inter-phalangeal 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

http://www.casesjournal.com/content/1/1/238

Figure 1Tophus at the back of right elbow. Figure 2 Tophi/tophus around the proximal inter-phalangeal

joint of right middle finger.

Plain radiography of left elbow showed joint 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 performed, and the results were unremarka- ble. Diagnostic arthocentesis was performed on both the elbows, and revealed negatively birefringent needle- shaped 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 deter- mine the etiology because patient had that swelling for a long time.

The patient responded partially to colchicine, but later had great relief with indomethacin. Colchicine 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.

DiscussionGout is a metabolic disease that can manifest as acute or

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 concentra-

Table 1: Laboratory values at admission.

Test Value Value range

Sodium 139 meq/l 135–145Potassium 3.5 meq/l 3.5–4.9Chloride 108 meq/l 96–110CO2 28 mmol/l 20–30BUN 18 mg/dl 6.0–23.0Creatnine 0.7 mg/dl 0.6–1.4Total protein 5.4 g/dl 6.0–8.0Albumin 3.4 g/dl 3.6–5.0Magnesium 1.6 meq/l 1.3–

2.2Phosphorus 3.3 mg/dl 2.5–4.5Calcium 8.2 mg/dl 8.0–10.5White blood count 12,400/mm3 4–

12Hemoglobin 11.6 g/dl 12.6–16.5Platelet count 133 000/mm3 150–400Uric acid 6.8 mg/dL 3.4–7.0

chronic arthritis, and deposition of urate crystals in con-




Table 2: Synovial fluid analysis.

Test ValueNormal

Investigational studies due to acute elbow joint pain deci- phered the underlying mystery of chronic swelling. Sys-

temic inflammatory response secondary to diverticulitis

Clarity Translucent TransparentColor Yellow Clear

WBC (per mm3) 2100 < 200

PMNs (%) 62 < 25

Gram stain No organisms No organisms

Culture NegativeNegative

Total protein (g/dL) 2 3.1LDH (IU/L) 440 105 –

333Glucose (mg/dL) 42 70–

110Crystal Monosodium urate crystals 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 when supported by vis- ualization of uric acid crystals in a sample of joint or bur- sal fluid, or demonstrated histologically in excised tissue. Synovial fluid analysis of our patient was consistent with inflammatory arthritis. Mild leucocytosis in this patient was due to systemic inflammatory response.

Visible or palpable tophi, as this patient exhibited, are usually noted only among those patients who are hyperuricemic and have had repeated attacks of acute gout, often over many years. However, presentation 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 inflammatory state prevails, such as in an acute infection, cytokines and chemokines triggers inflammation and cause arthritis in the presence of urate crystals [10,11]. Phagocytosis of these crystals by macrophages in the synovial lining cells precedes influx of neutrophils in the joint [9-11]. This process releases various mediators of inflammation locally [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 from 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 patient presented with tophi as an initial presentation of gout, which is very rare, but has been reported [5,8].

exposed the joints to the effects of urate.

First-line treatments for an acute flare are either oral colchicine and/or non-steroidal anti-inflammatory agents. Systemic or intra-articular corticosteroids can also be used, and are equally effective, but with more side effects [16,17]. Interleukin-1 inhibitors are still under investiga- tion, and are not approved for an acute attack of gout [18].

ConclusionGout usually flares up during an acute illness, and shouldalways 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 interestsThe authors declare that they have no competing interests.

Authors' contributionsAll authors contributed equally in collecting patient data,chart review, and editing medical images. All authors read and approved the final manuscript.

ConsentWritten informed consent was obtained from the patientfor 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-in-

Chief of this journal.

AcknowledgementsWe thank patient for giving us consent for the publication of the case report.

References1. Campion EW, Glynn RJ, DeLabry LO: Asymptomatic

hyperuricemia. 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 manifes-

tation 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 mech-anism of decreased serum uric acid concentrations duringacute gouty arthritis. J Rheumatol 2002, 29(9):1950-3.

7. Simkin PA: The pathogenesis of podagra. Ann Intern Med 1977,

86:230.8. Hollingworth P, Scott JT, Burry HC: Nonarticular gout: hyperuri-

cemia and tophus formation without gouty arthritis. ArthritisRheum 1983, 26:98-101.




9. Beutler A, Schumacher HR Jr: Gout and 'pseudogout': when are arthritic symptoms caused by crystal disposition? Postgrad Med 1994, 95:103-6.

10. Schumacher HR, Phelps P, Agudelo CA: Urate crystal induced inflammation in dog joints: sequence of synovial changes. J Rheumatol 1974, 1:102.

11. Gordon TP, Kowanko IC, James M, Roberts-Thomson PJ: Monoso- dium urate crystal-induced prostaglandin synthesis in the rat subcutaneous air pouch. Clin Exp Rheumatol 1985, 3:291.

12. Malawista SE, Duff GW, Atkins E, Cheung HS, McCarty DJ: Crystal- induced endogenous pyrogen production. A further look at gouty inflammation. Arthritis Rheum 1985, 28:1039.

13. 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.

14. 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.

15. Wallace SL, Singer JZ: Therapy in gout. Rheum Dis Clin North Am1988, 14:441.

16. Janssens HJ, Janssen M, Lisdonk EH van de, van Riel PL, van Weel C:Use of oral prednisolone or naproxen for the treatment ofgout arthritis: a double-blind, randomised equivalence trial.Lancet 371(9627):1854-60. 2008 May 31

17. 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, Zim-mermann-Gòrska I, EULAR Standing Committee for InternationalClinical Studies Including Therapeutics: EULAR evidence basedrecommendations for gout. Part II: Management. Report ofa task force of the EULAR Standing Committee for Interna-tional Clinical Studies Including Therapeutics (ESCISIT).Ann Rheum Dis 2006, 65(10):1312-24.

18. So A, De Smedt T, Revaz S, Tschopp J: A pilot study of IL-1 inhi-bition by anakinra in acute gout. Arthritis Res Ther 2007, 9:R28.

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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 keturunan

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

biasanya digunakan oleh dokter untuk menegakkan diagnosis, diantaranya2:

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

Ada beberapa cara dalam penanganan osteoarthritis non farmakologi, diantaranya2,3:

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 N-

acetygluosamine. 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 mengurangi rasa sakit.

8. Glucosamine dan chondroitin sulfate

Mengurangi pengobatan untuk pasien osteoarthritis pada lutut.

PENCEGAHAN

Ada beberapa hal yang perlu diperhatikan, agar kita terhindar dari osteoarthritis1:

1. menghindari olahraga yang bisa meyebabkan sendi 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=4ca6439313b991ed97f43906b994. 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

.

http://new.merapi.net/index.php?view=news/116&id=116&PHPSESSID=4ca6439313b991ed97f43906b994

http://new.merapi.net/index.php?view=news/116&id=116&PHPSESSID=4ca6439313b991ed97f43906b994

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