The laboratory results revealed no elevated inflammatory markers, normal hepatic directly enzymes, and normal LDH; creatinine clearance according to MDRD formula was 42mL/mn/1,73m2 and tacrolimus trough level was 5��g/l. Analyses for EBV and CMV viruses by plasmatic PCR were negative. A lumbar puncture was performed; it revealed 8 cellular elements/mm3. The bacteriological, virological, mycological, and parasitological tests of the cerebrospinal fluid were all negative. The CT scan of the head without contrast injection was normal. The MRI performed 3 days later detected diffuse periventricular cerebral and cerebellar contrast-enhanced lesions (hypersignal Flair) (Figure 1). In view of these findings, the diagnosis of cerebral toxoplasmosis was considered.

A reduction of immunosuppression (MMF 1g/d) was performed and an antitoxoplasma treatment (malocide+sulphadiazine) was started. One month later, due to the absence of any clinical improvement with the treatment, a stereotactic cerebral biopsy was carried out. Figure 1 Cerebral MRI: (a) coronal view T1 with gadolinium injection: left cerebellar nodular lesion with central necrotic zone and peripheral contrast enhancement. (b) Coronal view T1 without gadolinium injection: periventricular localization of multiple cerebral … The histological study (Figure 2) showed a heterogeneous necrotising lesion, with cellular remnants, granulomatous clusters of giant cells, with circumvented nuclei and well visible nucleoli, which looked like lymphoplasmocyte cells. The cells created dense castings on the meninges and were infiltrating the wall of several vessels.

The immuno-histochemical study showed granulomatous cells stained by antibodies (ab) anti-CD68 (macrophages), anti-CD20 (B cells), and anti-CD30. The reaction to anti-EBV ab (anti-LMP1) was positive; conversely, the reaction to antitoxoplasma ab was negative. In view of these results, we concluded a grade III lymphomatoid granulomatosis according to LIPFORD classification [3, 4]. A complete workup including chest and abdominal CT was carried out. The CT scan of the thorax showed 6 pulmonary nodules of tissular density in the left lung and one pulmonary nodule in the right lung (Figure 3(a)). The CT of the abdomen was free. The bronchial endoscopy revealed purulent secretions with severe inflammatory reaction. Bronchoalveolar lavage was negative for Koch’s bacillus.

The histological study showed unsteadily scraped bronchial mucous membrane. The subjacent chorion was composed of an inflammatory polymorphic infiltrate, rich in polynuclear eosinophils with small Brefeldin_A growing granulomas. The diagnosis of grade III LYG with pulmonary and cerebral localization was considered. So, the immunosuppression was again minimized. MMF was discontinued; tacrolimus was reduced to 1mg/d, to achieve trough levels around 3ng/mL, whereas prednisone was increased to 0.5mg/kg/d.