Patients with unilateral renal/ureteral calculosis who had suffered a few painful attacks were examined. In the pain-free period, muscular, subcutaneous and cutaneous sensory thresholds to electrical stimulation were measured in the lumbar region (metamer L1) on both sides: (1) pain thresholds were lower on the affected side with respect to both the contralateral side and control thresholds recorded in normal subjects; (2) the greatest decrease in threshold was in the muscle (even the sensation of sustained contraction was no longer detectable), followed by subcutaneous tissue, and the smallest decrease was in the skin.

The effects of L-carnitine administration on maximal exercise capacity were studied in a double-blind, cross-over trial on ten moderately trained young men. A quantity of 2 g of L-carnitine or a placebo were administered orally in random order to these subjects 1 h before they began exercise on a cycle ergometer. Exercise intensity was increased by 50-W increments every 3 min until they became exhausted. After 72-h recovery, the same exercise regime was repeated but this time the subjects, who had previously received L-carnitine, were now given the placebo and vice versa. The results showed that at the maximal exercise intensity, treatment with L-carnitine significantly increased both maximal oxygen uptake, and power output. Moreover, at similar exercise intensities in the L-carnitine trial oxygen uptake, carbon dioxide production, pulmonary ventilation and plasma lactate were reduced. It is concluded that under these experimental conditions pretreatment with L-carnitine favoured aerobic processes resulting in a more efficient performance. Possible mechanisms producing this effect are discussed.

Background: This article summarizes the outcome from an international consensus meeting, which took place in Vienna on 4 November 2014.

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Eccentric muscle effort is known to induce delayed muscle soreness (DOMS) and muscle damage which are not responsive to medical treatment with the most common analgesic agents. The aim of the study was to investigate the effects of oral L-carnitine supplementation on pain (VAS scale), tenderness (pain thresholds) and CK release induced by a 20-min eccentric effort of the quadriceps muscle. A single-blind study was carried out on 6 untrained subjects (mean age: 26 +/- 3.8 yrs; mean height: 173 +/- 4.6 cm; mean body weight, 68.3 +/- 4.5 kg) over 7 weeks during which each subject: a) was given 3 g/day of placebo for 3 weeks and, after a week's interval, 3 g/day of L-carnitine for 3 weeks: b) performed 2 step tests on the first day of the 3rd and 7th week inverting the order of the exercising limb. In a separate set of experiments carried out 8 months later, the possible effects of training on pain parameters and CK levels were also investigated in the same subjects who performed 2 step tests at a 4-weeks' interval, without medication. L-carnitine significantly reduced pain, tenderness and CK release after the effort with respect to placebo. In contrast, no significant difference was found in the parameters measured between the two tests performed without medication. It is concluded that L-carnitine has a protective effect against pain and damage from eccentric effort. This effect is mainly attributed to the vasodilatation property of the compound, which both improves energetic metabolism of the hypoxic/damaged muscle and enhances wash-out of algogenic metabolites.

The hypothesis of a relationship between sarcoidosis and malignancy was firstly formulated in 1972 by Brincker. He documented an association of sarcoid reactions or sarcoidosis with 19 lymphomas and associated malignancies. Based on various epidemiological studies, for more than 20 years sarcoidosis has been considered as a condition at increased risk for cancer, particularly lymphoproliferative disorders. The existence of a sarcoidosis-lymphoma syndrome was therefore proposed, highlighting, as a potential mechanism, the uncontrolled lymphocyte proliferation and mitotic activity. A reduced ability to eliminate an antigen and chronic inflammation have been suggested as triggering events. Leading to a reduced tumor immune surveillance, a diminished myeloid dendritic cells (mDC) function, despite up-regulated co-stimulatory and maturation markers, was also raised as potential mechanism. However, some subsequent studies have questioned the presence of a close association between the two entities and have explained those previously published as the result of selection bias and misclassification. Recently, a Swedish population-based cohort study documented a significant overall excess incidence of cancer among sarcoidosis patients, especially those with multiple hospitalizations or admission in older age, emphasizing again a potential neoplastic risk. Therefore, currently, whether these patients have an increased risk of developing malignant lesions is still debated. Larger and unbiased studies are needed before drawing definite conclusions.

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