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Kikuchi-Fujimoto disease (KFD) is a rare cause of lymphadenopathy, most often cervical. It has been mainly described in Asia. There are few data available on this disease in Europe. We conducted this retrospective, observational, multicenter study to describe KFD in France and to determine the characteristics of severe forms of the disease and forms associated with systemic lupus erythematosus (SLE). We included 91 cases of KFD, diagnosed between January 1989 and January 2011 in 13 French hospital centers (median age, 30 ± 10.4 yr; 77% female). The ethnic origins of the patients were European (33%), Afro-Caribbean (32%), North African (15.4%), and Asian (13%). Eighteen patients had a history of systemic disease, including 11 with SLE. Lymph node involvement was cervical (90%), often in the context of polyadenopathy (52%), and it was associated with hepatomegaly and splenomegaly in 14.8% of cases. Deeper sites of involvement were noted in 18% of cases. Constitutional signs consisted mainly of fever (67%), asthenia (74.4%), and weight loss (51.2%). Other manifestations included skin rash (32.9%), arthromyalgia (34.1%), 2 cases of aseptic meningitis, and 3 cases of hemophagocytic lymphohistiocytosis. Biological signs included lymphocytopenia (63.8%) and increase of acute phase reactants (56.4%). Antinuclear antibodies (ANAs) and anti-DNA antibodies were present in 45.2% and 18% of the patients sampled, respectively. Concomitant viral infection was detected in 8 patients (8.8%). Systemic corticosteroids were prescribed in 32% of cases, hydroxychloroquine in 17.6%, and intravenous immunoglobulin in 3 patients. The disease course was always favorable. Recurrence was observed in 21% of cases. In the 33 patients with ANA at diagnosis, SLE was known in 11 patients, diagnosed concomitantly in 10 cases and in the year following diagnosis in 2 cases; 6 patients did not have SLE, and 4 patients were lost to follow-up (median follow-up, 19 mo; range, 3-39 mo). The presence of weight loss, arthralgia, skin lesions, and ANA was associated with the development of SLE (p < 0.05). Male sex and lymphopenia were associated with severe forms of KFD (p < 0.05). KFD can occur in all populations, irrespective of ethnic origin. Deep forms are common. An association with SLE should be investigated. A prospective study is required to determine the risk factors for the development of SLE.

Objective: HIV infection is associated with an atherogenic lipoprotein profile, and ritonavir-boosted protease inhibitors exacerbate this phenotype. We evaluated the effect of 45 days of rosuvastatin versus pravastatin on the low-density lipoprotein (LDL) size and the distribution of LDL subfractions in HIV-1 patients receiving boosted protease inhibitors with elevated LDL levels., Design: Substudy of the randomized double-blind multicentre ANRS 126 VIHstatine trial., Setting: Twenty clinical centres in France., Patients: HIV-infected patients receiving boosted protease inhibitors with dyslipidaemia (LDL cholesterol > 4.1 mmol/l and triglycerides < 8.8 mmol/l)., Intervention: Rosuvastatin 10 mg/day (n = 39) or pravastatin 40 mg/day (n = 37) for 45 days., Main Outcome Measure(s): LDL size and distribution of LDL subfractions blindly assessed by gradient gel electrophoresis at baseline and at day 45., Results: Rosuvastatin was more effective than pravastatin in increasing the diameter of the LDL peak. The LDL diameter change was 0.33 ± 0.59 nm in the rosuvastatin group versus -0.01 ± 0.52 nm in the pravastatin group (P = 0.021). Rosuvastatin was also more effective in increasing significantly the percentage of large LDL (LDL1, P = 0.038; LDL2, P = 0.031) and in decreasing the percentage of small LDL (LDL3, P = 0.009)., Conclusion: Rosuvastatin was more effective than pravastatin in normalizing LDL size and LDL subfraction distributions, leading to a less atherogenic phenotype.

We describe the main characteristics and treatment of urogenital manifestations in patients with Wegener granulomatosis (WG). We conducted a retrospective review of the charts of 11 patients with WG. All patients were men, and their median age at WG diagnosis was 53 years (range, 21-70 yr). Urogenital involvement was present at onset of WG in 9 cases (81%), it was the first clinical evidence of WG in 2 cases (18%), and was a symptom of WG relapse in 6 cases (54%). Symptomatic urogenital involvement included prostatitis (n = 4) (with suspicion of an abscess in 1 case), orchitis (n = 4), epididymitis (n = 1), a renal pseudotumor (n = 2), ureteral stenosis (n = 1), and penile ulceration (n = 1). Urogenital symptoms rapidly resolved after therapy with glucocorticoids and immunosuppressive agents. Several patients underwent a surgical procedure, either at the time of diagnosis (n = 3) (consisting of an open nephrectomy and radical prostatectomy for suspicion of carcinoma, suprapubic cystostomy for acute urinary retention), or during follow-up (n = 3) (consisting of ureteral double J stents for ureteral stenosis, and prostate transurethral resection because of dysuria). After a mean follow-up of 56 months, urogenital relapse occurred in 4 patients (36%). Urogenital involvement can be the first clinical evidence of WG. Some presentations, such as a renal or prostate mass that mimics cancer or an abscess, should be assessed to avoid unnecessary radical surgery. Urogenital symptoms can be promptly resolved with glucocorticoids and immunosuppressive agents. However, surgical procedures, such as prostatic transurethral resection, may be mandatory in patients with persistent symptoms.

HIV-infected patients are at an increased risk of developing cardiovascular disease. Elevated levels of C-reactive protein (CRP) are associated with an increased risk of cardiovascular disease in the general population and are reduced by statin therapy. We examined the effect of pravastatin and rosuvastatin on CRP levels in 58 dyslipidemic HIV-infected patients. A 45-day course of either statin reduced the median CRP level from 3.0 to 2.4 mg/l (P < 0.001) with no correlation with changes in lipid parameters.

Background: HIV infection and its treatment with protease inhibitors, especially when boosted with ritonavir, can cause lipid disorders. Statins, with the exception of fluvastatin, pravastatin and rosuvastatin, interact with protease inhibitor metabolism via CYP450. Pravastatin is recommended for patients with protease inhibitor-associated dyslipidemia. Rosuvastatin is the statin most effective on low-density lipoprotein cholesterol (LDL-c) in non-HIV patients., Methods: HIV-1-infected patients treated with boosted protease inhibitor were randomized to receive either rosuvastatin 10 mg/day or pravastatin 40 mg/day for dyslipidemia (LDL-c >4.1 mmol/l and triglycerides <8.8 mmol/l). The percentage change in LDL-c, triglyceride and high-density lipoprotein-cholesterol levels, measured in a central laboratory, was determined after 45 days of statin treatment., Results: Eighty-eight patients were randomized and 83 took the study drugs, 41 rosuvastatin and 42 pravastatin. The median duration of prior antiretroviral treatment was 9 years. At baseline, the median LDL-c level was 4.93 mmol/l, the triglyceride level 2.29 mmol/l, and the high-density lipoprotein-cholesterol level 1.27 mmol/l. The median percentage changes in the rosuvastatin and pravastatin arms were -37 and -19% for LDL-c (P < 0.001), respectively, and -19 and -7% for triglycerides (P = 0.035), respectively. The change in the high-density lipoprotein-cholesterol level was not significantly different between the two arms. None of the four severe adverse events was attributed to the statins; in particular, there were no renal, hepatic or muscular events., Conclusion: Rosuvastatin 10 mg/day was more effective than pravastatin 40 mg/day on LDL-c and triglyceride levels in HIV-1-infected patients receiving a boosted protease inhibitor.

Tenofovir is a nucleoside reverse transcription inhibitor used to treat human immunodeficiency virus patients with early treatment failure. Increasing numbers of cases of tubular dysfunction and Fanconi syndrome have been reported in patients treated with tenofovir, after the detection of biochemical abnormalities during routine assessments. Some patients have acute renal failure, and bone involvement is observed in rare cases. We describe a case of chronic metabolic complications with bone fractures related to tenofovir treatment. Several factors that increased the renal toxicity of tenofovir included low body mass index, concomitant use of nonsteroidal anti-inflammatory agents, and other antiretroviral drugs, including ritonavir.