Shoulder pain due to cervical radiculopathy: an underestimated long-term complication of herpes zoster virus reactivation?

Purpose To evaluate if herpes zoster virus (HZV) reactivation may be considered in the aetiology of cervical radiculopathy. Methods The study group was composed of 110 patients (52 M-58F;mean age ± SD:46.5 ± 6.12; range:40-73) with a clinical diagnosis of cervical radiculopathy. Patients with signs of chronic damage on neurophysiological studies were submitted to an X-ray and to an MRI of the cervical spine in order to clarify the cause of the cervical radiculopathy and were investigated for a possible reactivation of HZV; HZV reactivation was considered as “recent” or “antique” if it occurs within or after 24 months from the onset of symptoms, respectively. Data were submitted to statistics. Results Thirty-eight patients (34,5%,16 M-22F) had a history of HZV reactivation: four (2 M-2F) were “recent” and 34 (14 M-20F) were “antique”. In 68 of 110 participants (61,8%,30 M-38F), pathological signs on X-ray and/or MRI of the cervical spine appeared; in the remaining 42 (38,2%,22 M-20F) X-ray and MRI resulted as negative. Among patients with HZV reactivation, seven (18,4%) had a “positive” X-ray-MRI while in 31 (81,6%) the instrumental exams were considered as negative. The prevalence of “antique” HZV reactivations was statistically greater in the group of patients with no pathological signs on X-ray/MRI of the cervical spine with respect to the group with a pathological instrumental exam (p < 0.01). Conclusions It may be useful to investigate the presence of a positive history of HZV reactivation and to consider it as a long-term complication of a cervical root inflammation especially in patients in which X-ray and MRI of the cervical spine did not show pathological findings

Mannose-binding lectin genotypes: lack of association with susceptibility to thoracic empyema

<p>Abstract</p> <p>Background</p> <p>The role of the innate immune protein mannose-binding lectin (MBL) in host defence against severe respiratory infection remains controversial. Thoracic empyema is a suppurative lung infection that arises as a major complication of pneumonia and is associated with a significant mortality. Although the pathogenesis of thoracic empyema is poorly understood, genetic susceptibility loci for this condition have recently been identified. The possible role of MBL genotypic deficiency in susceptibility to thoracic empyema has not previously been reported.</p> <p>Methods</p> <p>To investigate this further we compared the frequencies of the six functional <it>MBL </it>polymorphisms in 170 European individuals with thoracic empyema and 225 healthy control individuals.</p> <p>Results</p> <p>No overall association was observed between MBL genotypic deficiency and susceptibility to thoracic empyema (2 × 2 Chi square = 0.02, <it>P </it>= 0.87). Furthermore, no association was seen between MBL deficiency and susceptibility to the Gram-positive or pneumococcal empyema subgroups. MBL genotypic deficiency did not associate with progression to death or requirement for surgery.</p> <p>Conclusions</p> <p>Our results suggest that MBL genotypic deficiency does not associate with susceptibility to thoracic empyema in humans.</p

Mannose-Binding Lectin 2 Polymorphisms Do Not Influence Frequency or Type of Infection in Adults with Chemotherapy Induced Neutropaenia

BACKGROUND: Mannose-binding Lectin protein (MBL) has been suggested to be relevant in the defence against infections in immunosuppressed individuals. In a Swedish adult cohort immunosuppressed from both the underlying disease and from iatrogenic treatments for their underlying disease we investigated the role of MBL in susceptibility to infection. METHODS: In this cross sectional, prospective study, blood samples obtained from 96 neutropaenic febrile episodes, representing 82 individuals were analysed for single nucleotide polymorphism (SNP) in the MBL2 gene. Concurrent measurement of plasma MBL protein concentrations was also performed for observation of acute response during febrile episodes. FINDINGS: No association was observed between MBL2 genotype or plasma MBL concentrations, and the type or frequency of infection. Adding to the literature, we found no evidence that viral infections or co-infections with virus and bacteria would be predisposed by MBL deficiency. We further saw no correlation between MBL2 genotype and the risk of fever. However, fever duration in febrile neutropaenic episodes was negatively associated with MBL2 SNP mutations (p<0.05). Patients with MBL2 SNP mutations presented a median febrile duration of 1.8 days compared with 3 days amongst patients with wildtype MBL2 genotype. INTERPRETATION: We found no clear association between infection, or infection type to MBL2 genotypes or plasma MBL concentration, and add to the reports casting doubts on the benefit of recombinant MBL replacement therapy use during iatrogenic neutropaenia