Test–retest reliability of quantitative sensory testing for mechanical somatosensory and pain modulation assessment of masticatory structures

Assessing the reliability of medical measurements is a crucial step towards the elaboration of an applicable clinical instrument. There are few studies that evaluate the reliability of somatosensory assessment and pain modulation of masticatory structures. This study estimated the test–retest reliability, that is over time, of the mechanical somatosensory assessment of anterior temporalis, masseter and temporomandibular joint (TMJ) and the conditioned pain modulation (CPM) using the anterior temporalis as the test site. Twenty healthy women were evaluated in two sessions (1 week apart) by the same examiner. Mechanical detection threshold (MDT), mechanical pain threshold (MPT), wind‐up ratio (WUR) and pressure pain threshold (PPT) were assessed on the skin overlying the anterior temporalis, masseter and TMJ of the dominant side. CPM was tested by comparing PPT before and during the hand immersion in a hot water bath. anova and intra‐class correlation coefficients (ICCs) were applied to the data (α = 5%). The overall ICCs showed acceptable values for the test–retest reliability of mechanical somatosensory assessment of masticatory structures. The ICC values of 75% of all quantitative sensory measurements were considered fair to excellent (fair = 8·4%, good = 33·3% and excellent = 33·3%). However, the CPM paradigm presented poor reliability (ICC = 0·25). The mechanical somatosensory assessment of the masticatory structures, but not the proposed CPM protocol, can be considered sufficiently reliable over time to evaluate the trigeminal sensory function.     

Birth prevalence and characteristics of congenital toxoplasmosis in Sergipe,North‐east Brazil

Objectives To estimate, by neonatal screening, the birth prevalence of congenital toxoplasmosis among live‐born infants in Sergipe state, Brazil, and to investigate the clinical features of affected infants. Methods Dried blood spot specimens obtained from 15 204 neonates were assayed for the presence of anti‐T. gondii IgM antibodies. Duplicate retesting was done in infants with positive and borderline results. Confirmatory testing in peripheral blood samples consisted of testing for anti‐T. gondii IgG and IgM in infants and mothers. Those with possible congenital toxoplasmosis were evaluated and followed up to a median age of 20 months. Congenital infection was confirmed in the presence of persisting anti‐T. gondii IgG antibodies beyond 12 months of age. All infants with confirmed infection were treated with pyrimethamine, sulfadiazine and folinic acid for 1 year. Results Fifty‐three infants had detectable IgM in dried blood spot specimens. Confirmatory testing was reactive in 39/50, of which, 38 completed follow‐up. Six of 15 204 newborns were diagnosed with congenital toxoplasmosis, resulting in an estimated birth prevalence of four per 10 000 [CI 95% 1.4–8.0]. Four infants (67%) showed signs of congenital toxoplasmosis in their first year of life; three (75%) had retinochoroidal scars, and one had cerebral calcifications. Two infants remained asymptomatic until 20 months of age. Conclusions The birth prevalence of congenital toxoplasmosis is high in the Brazilian state of Sergipe, with most of the infants showing ocular lesions. Preventive measures are strongly warranted.     

Active avoidance from a crude oil soluble fraction by an Andean paramo copepod

Several oil spills due to ruptures in the pipeline oil systems have occurred at the Andean paramo. A sample of this crude oil was mixed with water from a nearby Andean lagoon and the toxicity of the soluble fraction was assessed through lethal and avoidance assays with a locally occurring copepod (Boeckella occidentalis intermedia). The integration of mortality and avoidance aimed at predicting the immediate decline of copepod populations facing an oil leakage. The 24-h median lethal PAH concentration was 42.7 (26.4–91.6) µg L^?1. In the 12-h avoidance assay, 30 % avoidance was recorded at the highest PAH concentration (19.4 µg L^?1). The mortality at this PAH concentration would be of 25 % and, thus, the population immediate decline would be of 55 %. The inclusion of non-forced exposure testing with the quantification of the avoidance response in environmental risk assessments is, therefore, supported due to underestimation of the lethal assays.     

Endoscopically proven case of rapid esophagogastric variceal progression and rupture as a result of portal hypertension with liver sarcoidosis

Sarcoidosis is a multi‐systemic disease of unknown etiology that results in the development of non‐caseating epithelioid granulomas. The liver is the third most frequently involved organ after the lymph nodes and the lungs. Most cases of liver sarcoidosis do not present with symptoms and involve minimal liver dysfunction, but some cases display progression to portal hypertension and liver cirrhosis, and finally to liver failure. The mechanism and the risk of progression in liver sarcoidosis are still unknown because of the diagnostic difficulty associated with this condition, and because follow‐up examinations can only be done in an invasive manner. Here, we present an informative case of liver sarcoidosis with rapid progression of esophagogastric varices. Four months prior to the definitive diagnosis, no signs of varices were observed on endoscopy, and developmentof esophagogastric varices, rapid progression, and eventual rupture occurred in a short period of time. A liver biopsy, carried out after endoscopic sclerotherapy, revealed that granulomas primarily affected the portal area without fibrotic and cirrhotic changes, which is considered a primary cause of portal hypertension and esophagogastric varices. Following the liver biopsy, the patient was given systemic steroids and is currently receiving outpatient care. Thus, we should consider the possibility that liver sarcoidosis, even in the absence of cirrhotic changes, can cause serious events such as esophagogastric variceal rupture following rapid progression as a result of portal hypertension.