Concomitant pulmonary tuberculosis and tuberculous appendicitis in a recipient of a renal transplant: A case report

Tuberculosis and Lung Disease Research Center, Tabriz University of Medical Sciences, Tabriz, Iran. .
Journal of Medical Case Reports 05/2011; 5(1):191. DOI: 10.1186/1752-1947-5-191
Source: PubMed


Tuberculosis is still a serious infection among recipients of renal transplants. Although the ileocecal region is the most affected part in intestinal tuberculosis, acute tuberculous appendicitis is quite a rare entity. We report a case of concomitant pulmonary tuberculosis and tuberculous appendicitis in a recipient of a renal transplant.
A 27-year-old Iranian woman, who had been the recipient of a renal transplant five years earlier, presented with a two-week history of coughing, fever and weight loss. The cause of her end-stage renal disease was chronic pyelonephritis. There were fine crackles noted during a chest examination, and a plain chest radiography showed fine miliary nodules throughout her entire lung fields. Sputum and bronchial aspirate examination was positive for acid-fast bacilli, suggestive of Mycobacterium tuberculosis infection. A chest computed tomography scan revealed widespread miliary nodules, compatible with miliary tuberculosis. She developed severe abdominal pain and abdominal surgery disclosed a perforated appendicitis. Histopathological examination of the resected appendix revealed widespread caseating epithelioid granulomas, suggestive of tuberculosis.
Our case report highlights a rare presentation of tuberculosis in a patient who has undergone renal transplant. Such unusual presentation of tuberculosis, particularly among patients receiving potent immunosuppressive protocols, should be considered by clinicians.

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Available from: Mohammadali M Shoja, May 25, 2014
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    • "The prevalence of GITB in RT patients is about 0.2–0.6% (in developing countries), occurring about 50 times more frequently than in general population [8] [10]. It has a higher frequency during the first post-transplant year (32–57% of all cases) [1] [9] and may be related to higher doses of IS used in initial period and during episodes of acute rejection [9]. "
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    ABSTRACT: Tuberculosis is a disease relatively frequent in renal transplant patients, presenting a wide variety of clinical manifestations, often involving various organs and potentially fatal. Gastrointestinal tuberculosis, although rare in the general population, is about 50 timesmore frequent in renal transplant patients. Intestinal tuberculosis has a very difficult investigational approach, requiring a high clinical suspicion for its diagnosis.Therapeutic options may be a problem in the context of an immunosuppressed patient, requiring adjustment of maintenance therapy. The authors report two cases of isolated gastro-intestinal tuberculosis in renal transplant recipients that illustrates the difficulty of making this diagnosis and a brief review of the literature on its clinical presentation, diagnosis, and therapeutic approach.
    Full-text · Article · Jan 2013 · Case Reports
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    • "Our patient was on isoniazid as a prophylactic treatment of tuberculosis; renal transplantation increases the risk of tuberculosis infection [14]. One of the earliest known side effects of isoniazid is peripheral neuropathy characterized by paresthesia and weakness. "
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    ABSTRACT: Neurological complications leading to morbidity and mortality are not frequent in renal transplant recipients. Here, we report a renal transplant recipient who presented with diminished strength in his limbs probably due to multiple etiologies of axonal sensorimotor polyneuropathy, which resolved with intravenous immunoglobulin. A 49-year-old Iranian male renal transplant recipient with previous history of autosomal dominant polycystic kidney disease presented with diminished strength in his limbs one month after surgery. Our patient was on cyclosporine A, mycophenolate mofetil and prednisone. Although a detected hypophosphatemia was corrected with supplemental phosphate, the loss of strength was still slowly progressive and diffuse muscular atrophy was remarkable in his trunk, upper limb and pelvic girdle. Meanwhile, his cranial nerves were intact. Post-transplant diabetes mellitus was diagnosed and insulin therapy was initiated. In addition, as a high serum cyclosporine level was detected, the dose of cyclosporine was reduced. Our patient was also put on intravenous ganciclovir due to positive serum cytomegalovirus immunoglobulin M antibody. Despite the reduction of oral cyclosporine dose along with medical therapy for the cytomegalovirus infection and diabetes mellitus, his muscular weakness and atrophy did not improve. One week after administration of intravenous immunoglobulin, a significant improvement was noted in his muscular weakness. A remarkable response to intravenous immunoglobulin is compatible with an immunological basis for the present condition (post-transplant polyneuropathy). In cases of post-transplant polyneuropathy with a high clinical suspicion of immunological origin, administration of intravenous immunoglobulin may be recommended.
    Full-text · Article · Oct 2011 · Journal of Medical Case Reports
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    ABSTRACT: Cytomegalovirus is the most common viral infection after kidney transplantation. Clinical presentations of cytomegalovirus infection range from asymptomatic infection to organ-specific involvement. Most symptomatic infections manifest as fever and cytopenia. The gastrointestinal tract is the most common site of tissue-invasive infection, often presenting as diarrhea or gastrointestinal bleeding. Gastrointestinal obstruction, perforation, thrombosis of large gastrointestinal veins, splenic artery thrombosis, and pancreatitis are rare gastrointestinal presentations of cytomegalovirus infection. Renal-allograft ureteral stricture and skin involvement are other rare presentations of cytomegalovirus infection. hemophagocytic syndrome, thrombotic microangiopathy, adrenal insufficiency, and renal allograft artery stenosis are other rare symptoms of cytomegalovirus infection.
    Full-text · Article · Mar 2012
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