We examined the blood lactate response, in terms of the maximal post-exercise concentration (La_max), time to reach La_max, and maximal lactate accumulation rate (VLa_max), to swimming sprints of 25, 35, and 50 m. A total of 14 highly trained and elite swimmers (8 male and 6 female), aged 14–32, completed the 3 sprints in their specialization stroke with 30 min of passive rest in between. The blood lactate was measured right before and continually (every minute) after each sprint to detect the La_max. The VLa_max, a potential index of anaerobic lactic power, was calculated. The blood lactate concentration, swimming speed, and VLa_max differed between the sprints (p < 0.001). The La_max was highest after 50 m (13.8 ± 2.6 mmol·L^–1, mean ± SD throughout), while the swimming speed and VLa_max were highest at 25 m (2.16 ± 0.25 m·s^–1 and 0.75 ± 0.18 mmol·L^–1·s^–1). The lactate peaked approximately 2 min after all the sprints. The VLa_max in each sprint correlated positively with the speed and with each other. In conclusion, the correlation of the swimming speed with the VLa_max suggests that the VLa_max is an index of anaerobic lactic power and that it is possible to improve performance by augmenting the VLa_max through appropriate training. To accurately measure the La_max and, hence, the VLa_max, we recommend starting blood sampling one minute after exercise.

Objectives: Vitamin D deficiency has been observed in autoimmune rheumatic diseases, such as rheumatoid arthritis. The aim was to study vitamin D in patients with systemic lupus erythematosus (SLE) and its relationship with disease activity. Methods: In a cohort of 45 patients with SLE, 41 females and 4 males, aged 47.07 ± 2.17 years (mean ± SEM), and range = 21–79 years, 25(OH)D₃ levels were determined by electrochemiluminescence. C₃ and C₄ levels were also analyzed. SLE disease activity was estimated by SLEDAI-2K. Observations were also performed in a control group matched for age and sex. Results: In this cohort of SLE patients, 25(OH)D₃ levels were 40.36 ± 2.41 nmol/L (mean ± SEM) as opposed to 60.98 ± 4.28 nmol/L in the control group ( p < 0.001, Student’s t test). Vitamin D levels were related to C₃ ( p < 0.001, linear regression analysis), correlation coefficient 0.106, r² = 0.011, and C₄ ( p < 0.001); correlation coefficient 0.316 and r² = 0.100; and inversely related to disease activity ( p < 0.001), correlation coefficient −0.572 and r² = 0.327. 25(OH)D₃ levels were 17.73 ± 1.20 nmol/L and 12.24 ± 0.93 nmol/L, in the groups without and with renal involvement, respectively ( p = 0.001, Student’s t test). Conclusions: Vitamin D levels are low in SLE patients and are inversely related to disease activity. Routine screening for vitamin D levels should be performed in SLE patients.

Background Systemic Lupus Erythematosus (SLE) patients are known to be prone to infections. In particular differential diagnosis between an acute infection or a disease flare should be performed in any SLE patient with fever or recurrent fever and signs of acute disease. Differential diagnosis becomes even more difficult in an SLE patient with central nervous system (CNS) involvement. The aim was to describe an SLE patient with CNS involvement and acute West Nile virus infection. Methods A female patient was diagnosed with SLE at the age of 32 with a light-sensitive face eruption, hair loss, fatigue, arthralgias, ANA 1/320 (+) and anti-dsDNA (+). At the age of 45 she developed CNS involvement with epileptic seizures, dysarthria, memory loss, concentration difficulties and an abnormal EEG. At the age of 53 she had an acute SLE flare and pulse cyclophosphamide iv was administered. Thereafter rituximab was given followed by hydroxychloroquine and prednisolone 10 mg/d. At the age of 54 years 3 months after the third rituximab cycle, while on therapy with hydroxychloroquine and prednisolone she developed diarrhea, vomiting and fever up to 40°C not responding to antipyretics. She presented to the emergency department with deteriorating renal function, fever and confusion. Results A brain MRI showed meningeal thickening and a lumbar puncture was performed. The diagnostic evaluation of the fluid aspirated showed a recent infection with the West Nile virus with IgM (+++) in serum and IgM (+) in the cerebrospinal fluid. Two weeks later the patient had improved, was oriented in place and time and had no focal neurological signs. Conclusions Patients with SLE are prone to infection, especially if they are on long-standing treatment with steroids. Whenever they present with signs of acute disease they should be carefully evaluated for the presence of an acute infection, as infections demand a different therapeutic approach to a disease flare. A patient with CNS involvement demands even more careful and extensive evaluation. The presence of West Nile virus in Europe in recent years along with other mosquito-borne viruses have created new diagnostic and therapeutic challenges in the management of immunosuppressed patients, as was the case in the patient presented herein.