En la etapa postcontractual

complicated by agitation despite higher doses of midazolam. Several attempts to cannulate the common bile duct were undertaken, but nevertheless unsuccessful. The next day, the patient experienced considerable painless scrotal swelling (figure 1). An abdominal X-ray was also performed (figure 2).

W H a t i s y o U r d i a G n o s i s ?

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The affected dermatomal pattern on one side of the body, in conjunction with the immunosuppressive treatment, made us think of an opportunistic infection with varicella zoster virus (VZV). The haemorrhagic aspect was suggested to be caused by the underlying thrombocytopenia, which initially persisted despite therapy with rituximab. A polymerase chain reaction on the bullous fluid was positive for VZV DNA, indicating an active VZV infection.

ITP treatment with corticosteroids results in a complete response in 20% of adult patients. Most of the patients, however, will require a second-line treatment. For the clinical management of ITP we refer to a recent paper

in this journal.1 _{Rituximab, a chimeric anti-CD20}

monoclonal antibody, depletes CD20+ B-cells which results in low or even undetectable levels for two to six months,

returning to pre-treatment levels within a year. Rituximab also induces complement-mediated cytotoxicity and dysfunction of CD4 T cells leading to abnormal cytotoxic

T-cell-mediated responses.2 _{The above predisposes the}

patient to opportunistic infections. Data from 356 patients receiving rituximab monotherapy showed a 30% incidence rate of infectious events; 19% of patients had a bacterial infection, 10% viral infections, 1% fungal infections and

6% infections of unknown aetiology.3 _{One randomised}

controlled trial showed opportunistic viral infections which included three dermatomal herpes zoster infections and four localised herpes simplex infections. Isolated cases of other viral infections have been associated with rituximab, such as cytomegalovirus, West Nile virus, JC virus, BK

virus and parvovirus.4

Our patient was treated with valaciclovir 1000 mg twice a day. He responded very well to drug therapy and there was a major reduction of the bullae and herpes zoster rash. Additionally, after the third rituximab infusion, a

significant increase in the platelet count to 70 x 109 _cells/l

was seen.

r e f e r e n C e s

1. Schipperus M, Fijnheer R. New therapeutic options for immune thrombocytopenia. Neth J Med. 2011;69:480-5.

2. Kelesidis T, Daikos G, Boumpas D, Tsiodras S. Does rituximab increase the incidence of infectious complications? Int J Infect Dis. 2011;15:e2-16. 3. Kimby E. Tolerability and safety of Rituximab (MabThera). Cancer Treat

Rev. 2005;31:456-73.

4. Aksoy S, Harputluoglu H, Kilickap S, et al. Rituximab-related viral infections in lymfoma patients. Leuk Lymphoma. 2007;48:1307-12. a n s W e r t o P H o t o Q U i Z ( P a G e 1 8 9 )

a P a t i e n t W i t H H a e M o r r H a G i C b U l l a e

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The chest CT shows a deep atheromatous ulcer in the descending aorta. A small intramural haematoma was also observed throughout the complete thoracic aorta (thickened aortic wall with slightly increased Hounsefield units). No evidence was found for aortic dissection or pulmonary embolism. Thus, the diagnosis was penetrating aortic ulcer (PAU), which is an ulceration of an atherosclerotic lesion leading to a disruption of the internal elastic lamina of the aortic wall and, subsequently,

the development of an intramural haematoma.1 _Diagnosing

PAU may be challenging as chest pain has a wide range of differential diagnoses. Sudden onset of severe chest pain in the elderly hypertensive patient is the classical

presentation, although symptoms vary greatly.2 _{PAU is}

often overlooked due to its low incidence and the fact that an aortic dissection is considered unlikely if the blood pressure is equal in both arms and vascular murmurs are absent. Unfortunately, other acute aortic syndromes besides aortic dissection, such as PAU or intramural haematoma, are often forgotten. The diagnosis is made by

imaging studies, mostly by contrast-enhanced chest-CT.3

Since PAU has a high risk for progression into a fatal rupture of the aorta, emergent treatment is required. Both invasive (surgical or endovascular) and conservative

treatments are considered appropriate.4 _{Our patient was}

treated conservatively (as a ‘hypertensive emergency’) with labetalol intravenously. His blood pressure decreased quickly and the pain dissolved. Six months later, the blood pressure was normal (using four antihypertensive drugs) and the patient no longer complained of pain. Control CT scans after 24 hours, seven days and six months showed no further progression of the aortic ulcer.

r e f e r e n C e s

1. Stanson AW, Kazmier FJ, Hollier LH, et al. Penetrating atherosclerotic ulcers of the thoracic aorta: natural history and clinicopathologic correlations. Ann Vasc Surg. 1986;1:15-23.

2. Troxler M, Mavor AI, Homer-Vanniasinkam S. Penetrating atherosclerotic ulcers of the aorta. Br J Surg. 2001;88:1169-77.

3. Salvolini L, Renda P, Fiore D, Scaglione M, Piccoli G, Giovagnoni A. Acute aortic syndromes: Role of multi-detector row CT. Eur J Radiol. 2008;65:350-8.

4. Sundt TM. Intramural hematoma and penetrating atherosclerotic ulcer of the aorta. Ann Thorac Surg. 2007;83:S835-41; discussion S46-50.

a n s W e r t o P H o t o Q U i Z ( P a G e 1 9 2 ) a n U n e x P e C t e d C a U s e o f C H e s t P a i n