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Saudi Journal of Kidney Diseases and Transplantation
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CASE REPORT Table of Contents   
Year : 2007  |  Volume : 18  |  Issue : 4  |  Page : 603-608
Multi-Drug-Resistant Tuberculosis in a Patient Presenting with Bilateral Gluteal Abscesses and Right Leg Swelling with End-Stage Renal Disease


1 Department of Medicine, King Abdulaziz University, Jeddah, Saudi Arabia
2 Department of Medicine, King Faisal Specialist Hospital and Research Center, Jeddah, Saudi Arabia
3 Department of Surgery, King Faisal Specialist Hospital and Research Center, Jeddah, Saudi Arabia
4 Department of Radiology, King Faisal Specialist Hospital and Research Center, Jeddah, Saudi Arabia

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   Abstract 

This is a 40-year-old woman with end-stage renal disease (ESRD). She received empirical treatment for presumed TB of the right knee joint. The arthritis and the constitutional symptoms resolved despite the patient's poor compliance. One year later, she presented with TB abscesses involving the upper end of right tibia and bilateral gluteus muscles, which proved to be resistant to isoniazid, rifampicin and ethambutol. The patient was successfully treated with pyrazinamide, ofloxacin and amikacin.

Keywords: ESRD, Multi-Drug Resistant TB, gluteal abscess

How to cite this article:
Al-Shehri AM, Al-Ghamdi SM, Khalil A, Al-Amoudi A, Baslaim A, Mamoun I. Multi-Drug-Resistant Tuberculosis in a Patient Presenting with Bilateral Gluteal Abscesses and Right Leg Swelling with End-Stage Renal Disease. Saudi J Kidney Dis Transpl 2007;18:603-8

How to cite this URL:
Al-Shehri AM, Al-Ghamdi SM, Khalil A, Al-Amoudi A, Baslaim A, Mamoun I. Multi-Drug-Resistant Tuberculosis in a Patient Presenting with Bilateral Gluteal Abscesses and Right Leg Swelling with End-Stage Renal Disease. Saudi J Kidney Dis Transpl [serial online] 2007 [cited 2020 Oct 31];18:603-8. Available from: https://www.sjkdt.org/text.asp?2007/18/4/603/36520

   Case report Top


A 40-year-old woman who developed end­stage renal disease (ESRD) secondary to hypertension, and had received hemodialysis for one year before, presented to another hospital with a 4-week history of fever, night sweats and increasing right knee swelling and was unable to ambulate. She underwent joint aspiration, and a turbid fluid was drained, which did not grow any micro­organism. No Ziehl Neelsen's stain or myco­bacterial culture was done. Cell counts were not available. The patient underwent multiple courses of antibiotics and non-steroidal anti­inflammatory agents, and in spite of this, remained symptomatic with worsening knee pain and swelling.

Eventually, she received empirical quadruple anti-tuberculous drugs that included isoniazid, rifampicin, ethambutol and pyrazinamide for 12 months, which resulted in complete resolution of the knee swelling and her constitutional symptoms. However, she was noncompliant and had frequently stopped her medications for days to weeks.

The patient presented to our hospital 18 months later with a 4-month history of wor­sening fever, night sweats and a 15 kg weight loss. She complained of a new, and a much larger swelling, on the medial and lateral aspects of the upper one third of the right tibia, however, with minimally decreased ability to move the joint or ambulate. The patient also complained of small painless lumps on both buttocks that did not interfere with her sleep or daily activity. She reported no cough, hemoptysis, history of travel, or tuberculosis contact. On physical examination, the patient was alert, pale, emaciated, and weighed 40 kg. Her temperature was 37.8 °C; respiratory rate 20/min, and blood pressure 146/78 mmHg. The exam was unremarkable for lymphadenopathy or organomegaly. The examination of the right lower limb revealed two large cystic swellings on the medial and lateral aspect of the upper third of the tibia and the knee joint. They were slightly tender with shiny skin and dilated superficial vessels; no redness or warmth could be appreciated [Figure - 1]. There was no knee effusion and the swelling was adjacent to the knee joint, however, apparently not communicating with the joint space. Passive and active movements of the joint were minimally restricted. There were two small rounded deep, non-tender fluctuating cysts on gluteal muscles on both sides that measured 2-3 cm each in the largest diameter.

Laboratory investigations revealed: WBC 10.2 x10 3 /µL; Hb 92 gm/L, platelets 319 x10 3 /µL ; ESR 120 mm/hr; C-reactive protein 34 mg/dl; ALT 7 u/L; total bilirubin 6 pmol/L serum albumin 33 gm/l; alkaline phosphatase 104 u/l; calcium 2.96 mmol/l; phosphorus 2.37 mmol/L; intact PTH 12ngm/ L; glucose 6 mmol, urea 19.2 mmol/L; s. creatinine 991 μmol/L; and PT and PTT were within normal range. Hepatitis screen for both types B and C was non-reactive as well as human immunodeficiency virus (HIV). Tuberculin test revealed a significant induration of 10 mm.

Chest X-ray was normal and right knee MRI revealed multi-loculated areas with high signal intensity on T2- weighted images in the medial and postro-lateral aspect of the right knee [Figure - 2],[Figure - 3]. There was evidence of debris of different signal intensities within the swelling. There was a destruction of the tibial plateau as well as the articular cartilage, with diffuse bone marrow signal changes. Both swellings were neither communicating with each other nor with the joint space. There were multi-loculated different signal masses invol­ving the gluteal area on the right side together with similar findings at a lower location on the left side [Figure - 4]. Intra-operatively, multi­loculated abscesses, yellowish brown in color with lots of debris, corresponding to MRI signal changes were drained. Acid fast bacilli stains of the knee debridement and abscesses were negative. The drained fluid was inocu­lated on Lowenstein-Jensen media. Histo­pathologic examination revealed multiple areas of caseating granuloma with areas of necrosis.

Accordingly, the patient was started on iso­niazid, rifampicin, pyrazinamide, and etham­butol adjusted for her renal function.

Eight weeks later, the mycobacterial culture grew mycobacterium tuberculosis, which was resistant to isoniazid, rifampicin, ethambutol, and streptomycin but sensitive to pyrazinamide, quinolones, and amikacin. Hence, the anti­TB regimen was modified to include pyra­zinamide, ofloxacin, and amikacin. The patient improved clinically with resolution of her fever three weeks later. Both gluteal abscesses resolved on therapy four months later. Pyra­zinamide and ofloxacin were maintained for one year, while amikacin was discontinued after two months as the patient developed ototoxicity despite stringent drug monitoring. A keen relative closely monitored her treat­ment to ensure compliance to therapy. Repeat MRI revealed complete resolution of the initial lesions. Follow-up for more than three years after completion of her therapy did not disclose any reactivation or relapse.


   Discussion Top


Patients with chronic kidney disease (CKD) are at increased risk to develop or reactivate tuberculosis. [1],[2],[3],[4],[5] The calculated risk is in the range of 7-52 fold compared to the general population. [5] This wide range probably reflects the nature of the published data as mostly were retrospective reported from different geogra­phical areas with varied prevalence rate. In a population-based study in British Columbia, Canada, the relative risk was found to be 25-fold more than that in the general popu­lation. [6]

In the Saudi dialysis population, tuberculosis is commonly seen and often successfully treated on empirical bases pending further ancillary tests. [2],[3],[4],[5] The cause of this increased risk is probably the result of a multitude of deranged immunologic mechanisms in uremic patients. [7] Extra-pulmonary tuberculosis is an increasingly observed entity that may account for more than 50% of the cases of TB in patients with CKD. [1],[2],[3],[4],[5],[8] However, other studies reported predominance of pulmonary involvement. [9] Common extra-pulmonary locations usually involve the lymph nodes, peritoneum and pericardium. [2],[3],[4],[5] Tuberculous peritonitis is commonly seen in patients on peritoneal dialysis more than hemo-dialysis.[5],[8],[9] Rare locations have been described including, kidneys, [1] meninges, [1] intestine, [10] joints, [11] bones, [4] spine, [12] and muscles. [13],[14] Our patient presented with extrapulmonary TB resistant to the conventional therapy. Abdelwahab et al [13] and Ergin et al [14] reported two cases with tuberculous gluteal abscesses without any bony involvement that resolved on anti­TB medications. Trochantric bursitis with spread to form gluteal abscesses was postu­lated. [12] This may explain our case too. The leg swelling could have resulted from previous tuberculous arthritis or bursitis of the right knee, which formed a sinus tract that sealed off to be reactivated at a later time. There were some speculative reports of TB transmission via injection. Shafer et al [15] reported 464 HIV­infected patients with extra pulmonary TB, two cases of intravenous drug users were presumed to have developed TB arm muscle abscesses at the site of previous intravenous drug injections. To our knowledge, this is the first reported case of extra pulmonary TB with combined leg and gluteal involvement in a hemodialysis patient.

Multidrug-resistant TB (MDR-TB) is defined as strain resistant to isoniazid and rifampicin, with or without resistance to other drugs. [16] MDR-TB is an increasing health problem especially in HIV patients. [15],[16],[17] This problem is not peculiar to HIV-positive patients as there are an increasing number of HIV-negative patients who were reported to have multi­drug resistance TB. [18] In the global surveillance for anti-tuberculous drug-resistance, 12.6 % of the mycobacterium TB strains were found to be resistant to at least one drug [19] and 2.2% of the strains had multidrug-resistance.

The resistance is dependent on prior use of medication. The prevalence of primary MDR­TB was 1.4% compared to 13% in patients who had previous drug exposure. [19] There is geographical variability in MDR-TB preva­lence in Kingdom of Saudi Arabia from 2.8% and 19.4%. [20],[21],[22],[23] Drug resistance is multifac­torial in origin, which may be due to poor compliance of the patient, monotherapy, shorter duration of therapy and failure to supervise therapy. However, exogenous infec­tion rather than reactivation could be respon­sible for some of the cases. [24]

Morbidity, length of hospitalization and mortality of patients infected with MDR-TB is significantly more than in non-resistant cases. Selecting therapy of MDR-TB is sometimes a difficult task as second line therapy is usually required for longer duration and may involve surgical debridement of infected tissues. [25],[26]

In one study, the mortality rate attributed to TB resistance was 22% and overall response rate to prolonged therapy with second line therapy was only 56%. [25] In other more recent and obviously optimistic study from Turkey, the overall response rate after 24 months of therapy was 77%. In this study, many of the cases had undergone surgical debridement, which could be responsible for the better outcome. [26] Our patient received therapy for only one year of pyrazinamide and ofloxacin, and for two months of isonaizid, rifampicin, and amikacin. This is contrary to previous reports where patients with MDR-TB were treated with 4-6 drugs for up to two years. [25],[26] The surgical drainage of the knee abscess might have been responsible for the good outcome.

Finally, the patient was not enrolled in a directly observed therapy (DOT) program, she had a close observation by a relative who supervised her treatment. DOT is more cost­effective than self-administered treatment and MDR-TB is less likely to develop. [27] This case highlights the importance of establishing the diagnosis of TB and directly observing the prescribed medication in order to prevent resistance.

 
   References Top

1.Al Shohaib S. Tuberculosis in chronic renal failure in Jeddah. J Infect 2000;40(2):150-3.  Back to cited text no. 1    
2.Al-Homrany M. Successful therapy of tuberculosis in hemodialysis patients. Am J Nephrol 1997;17(1):32-5.  Back to cited text no. 2    
3.Shohaib SA, Scrimgeour EM, Shaerya F. Tuberculosis in active dialysis patients in Jeddah. Am J Nephrol 1999;19(1):34-7.  Back to cited text no. 3    
4.Malik GH, Al-Harbi AS, Al-Mohaya S, et al. Eleven years of experience with dialysis associated tuberculosis. Clin Nephrol 2002; 58(5):356-62.  Back to cited text no. 4    
5.Hussein MM. Mooij M, Roujouleh H. Tuberculosis and chronic renal disease. Semin Dial 2003;16(1):38-44.  Back to cited text no. 5    
6.Chia S, Karim M, Elwood RK, FitzGerald JM. Risk of tuberculosis in dialysis patients: A population-based study. Int J Tuberculosis Lung Dis 1998;2(12):989-91  Back to cited text no. 6    
7.Murphy BV, Pereira BJ. A 1990s perspective of hepatitis C, human immune deficiency virus, and tuberculosis infections in dialysis patients. Semin Nephrol 1997;17 (4):346-63.  Back to cited text no. 7    
8.Lui SL, Tang S, Li FK, et al. Tuberculosis infection in Chinese patients undergoing continuous ambulatory peritoneal dialysis. Am J Kidney Dis 2001;38(5):1055-60.  Back to cited text no. 8    
9.Vachharajani T, Abreo K, Phadke A, Oza U, Kirpalani A. Diagnosis and treatment of tuberculosis in hemodialysis and renal transplant patients. Am J Nephrol 2000; 20(4): 273-7  Back to cited text no. 9    
10.Feriozzi S, Meschini L, Costantini S, et al. Fatal intestinal tuberculosis in a uremic patient with renal transplant. J Nephrol 2002;15(5):593-6  Back to cited text no. 10    
11.Fukasawa H, Suzuki H, Kato A, et al. Tuberculous arthritis mimicking neoplasm in a hemodialysis patient. Am J Med Sci 2001;322(6):373-5  Back to cited text no. 11    
12.el-Shahawy MA, Gadallah MF, Campese VM. Tuberculosis of the spine (Pott's disease) in patients with end-stage renal disease. Am J Nephrol 1994;14(1):55-9  Back to cited text no. 12    
13.Abdelwahab IF, Kenan S, Hermann G, Klein MJ. Tuberculous gluteal abscess without bony involvement. Skeletal Radiol 1998;27: 36-9.  Back to cited text no. 13  [PUBMED]  [FULLTEXT]
14.Ergin F, Arslan H, Bilezikci B, Agildere AM, Ozdemir N. Primary tuberculosis in the gluteal muscle of a patient with chronic renal failure. A rare presentation. Nephron 2001;89(4):463-6.  Back to cited text no. 14    
15.Shafer RW, Kim DS, Weiss JP, Quale JM. Extrapulmonary tuberculosis in patients with HIV infection. Medicine 1991;70(6): 384-97.  Back to cited text no. 15    
16.Iseman MD. Treatment of multidrug resistant tubeculosis. N Engl J Med 1993; 329:784-91.  Back to cited text no. 16  [PUBMED]  [FULLTEXT]
17.Vareldzis BP, Grosset J, de-Kantor I, et al. Drug-resistant tuberculosis: laboratory issues. World Health Organization recommen­dations. Tuber Lung Dis 1994;75:1-7  Back to cited text no. 17    
18.Telzak EE, Sepkowitz K, Alpert P, et al. Multidrug-resistant tuberculosis in patients without HIV infection. N Engl J Med 1995;333(14):907-11.  Back to cited text no. 18    
19.Pablo-Mendez A, Raviglione MC, Laszlo A, et al. Global surveillance for the Anti­tuberculosis-Drug Resistance, 1994-1997. N Engl J Med 1998;338(23):1641-9.  Back to cited text no. 19    
20.Schiott Cr, Engbaek HC, Vergmann B, Al- Motez M, Kassim I. Incidence of drug resistance among isolates of Mycobacterium Tuberculosis recovered in Gizan area. Saudi Arabia. Saudi Med J 1985;6:375-8.  Back to cited text no. 20    
21.Al-Orainy IO, Saeed ES, El-Kassimi FA, Al-shareef N. Resistance to antituberculosis drugs in Riyadh. Saudi Arabia. Tubercle 1989;70:207-10.  Back to cited text no. 21    
22.Ellis ME, Al-Hajjar S, Bokhari H, Qadri SH. High proportion of multi-drug resistance Mycobacterium Tuberculosis in Saudi Arabia. Scand J Infect Dis 1996;28:591-5.  Back to cited text no. 22    
23.Kinsara A, Gilipin CM, Osoba AO. Review of tuberculosis at King Khalid National Guard Hospital, Jeddah. Saudi Arabia. Saudi Med J 1997;19:212-4.  Back to cited text no. 23    
24.van Rie A, Warren R, Richardson M, et al. Exogenous reinfection as a cause of recurrent tuberculosis after curative treatment. N Engl J Med 1999;341(16): 1174-9.  Back to cited text no. 24    
25.Goble M, Iseman MD, Madsen LA, Waite D, Ackerson L, Horsburgh CR Jr. Treatment of 171 patients with pulmonary tuberculosis resistant to isoniazid and rifampin. N Engl J Med 1993;328(8):527-32  Back to cited text no. 25    
26.Tahaoglu K, Torun T, Sevim T, et al. The treatment of multidrug-resistant tuberculosis in Turkey. N Engl J Med 2001;345(3):170-4  Back to cited text no. 26    
27.Burman WJ, Dalton CB, Cohn DL, Butler JR, Reves RR. A cost-effectiveness analysis of directly observed therapy vs self-admi­nistered therapy for treatment of tuberculosis. Chest 1997;112:63-70.  Back to cited text no. 27  [PUBMED]  [FULLTEXT]

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Correspondence Address:
Saeed M.G Al-Ghamdi
Department Medicine, King Faisal Specialist Hospital and Research Center, P.O. Box 40047, Jeddah 21499
Saudi Arabia
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