Department of Rheumatology, Stepping Hill Hospital, Stockport, UK
Correspondence to: C. B. Molloy, Department of Rheumatology, Stepping Hill Hospital, Poplar Grove, Stockport SK2 7JE, UK. E-mail: catherine_molloy{at}hotmail.com
SIR, We read with great interest the comprehensive review of chronic periaortitis (CP) by Jois and colleagues [1]. We wish to highlight another cause of this condition not mentioned in the review, as illustrated by a recent case.
A 36-yr-old Pakistani man resident in the UK for 13 yr presented with a 2-month history of intermittent pain in his epigastrium, myalgia, drenching night sweats and a non-productive cough. He also reported a 2-kg weight loss over 2 months. His previous medical history was of peptic ulcer disease with no known history of tuberculosis (TB). He was a market trader by profession and had not travelled abroad for at least 2 yr. He lived with his wife and two daughters, all of whom were in good health. Clinical examination revealed low-grade pyrexia and minimal epigastric tenderness without organomegaly. Cardiorespiratory and locomotor examinations were normal. His ESR was raised at 93 mm/h with CRP of 48 mg/l (normal range <10 mg/l). Autoantibody profiling showed the presence of anticardiolipin antibodies (IgG 28 IU; normal range 016 IU), but was otherwise normal. The following investigations were normal: full blood count, serum glucose and cholesterol, renal, liver, muscle and bone profiles, coagulation, electrocardiogram, chest radiograph, gastroscopy and cultures (of blood, stool and three early-morning urines for acid alcohol fast bacilli). An abdominal ultrasound revealed a fatty liver, but no other abnormality was noted.
MRI of the thorax and abdomen (Fig. 1a) showed circumferential encapsulation of the upper abdominal aorta with secondary aortic narrowing by an abnormal soft tissue mass. This extended 7 cm below the diaphragm and unfortunately was inaccessible for biopsy. A diagnosis of CP was made and the patient was commenced on 40 mg of prednisolone daily. However, following 3 months of treatment with only minor symptomatic improvement, repeat MRI scanning did not demonstrate any resolution of the periaortic mass.
|
We propose that this patient's CP be due to infection with M. tuberculosis, which, though resistant to corticosteroids, responded to antituberculous therapy. As highlighted by Jois et al. [1], chronic inflammation is the primary pathogenetic factor in the development of retroperitoneal fibrosis and periaortitis. A radiological diagnosis of CP is often made but determination of the exact aetiology may prove difficult [2, 3]. Chronic infections such as tuberculosis, actinomycosis and schistosomiasis can initiate this inflammatory reaction and are recognized causes of CP [4]. Even though microbiological confirmation of M. tuberculosis could not be made in this case, the patient's clinical history, radiological findings and therapeutic response were consistent with this being the causative organism. M. tuberculosis is a rare cause of retroperitoneal disease and when it does occur more commonly gives rise to tubercular pseudotumours and retroperitoneal abscesses [5, 6]. Confluent peritoneal lymphadenopathy may cause secondary oedema and thus ureteric obstruction, mimicking CP [6, 7]. CP may also occur secondary to spinal, peritoneal or haematogenous spread of distant M. tuberculosis infection [3, 8]. In this case the initial tubercular focus may have been pulmonary, with precipitation of overt clinical symptoms following systemic corticosteroid therapy. TB-related CP has a good outcome with adequate antitubercular therapy [3, 7], making this a treatable cause of CP.
The authors have declared no conflicts of interest.
References
|