Quantitative ultrasound (QUS): a useful tool for monitoring bone health in preterm infants?

Preterm infants are at risk of osteopenia and metabolic bone disease (MBD) of prematurity. There is a need for simple, reliable methods to detect and monitor this condition. Aims: The aims were first to describe longitudinal changes in speed of sound (SOS) measured using quantitative ultrasound (QUS; Sunlight Omnisense, Israel) in preterm neonates: and second to determine whether SOS predicts the development of MBD. Methods: SOS was measured in the tibia in 99 preterm infants (mean (SD)) gestation 29.7 (3.6) weeks; birthweight 1340 (550) g, with longitudinal measurements in 75. SOS z‐scores were generated for gestation and sex. Clinical data were recorded. Results: Baseline SOS (but not SOS z‐score) was positively associated with gestational age. SOS and SOS z‐score fell with age. In multivariate models, peak ALP, minimum phosphate concentrations and markers of illness severity were not predictors of the fall in SOS z‐score, and baseline SOS measurements did not predict the development of high peak ALP or low phosphate. Interpretation: Speed of sound measurements fell with age in all infants, but we found no evidence that this measurement could predict biochemical indicators of MBD. We cannot exclude the possibility that this technique could be useful in monitoring the response to interventions designed to improve bone health in this population.     

A randomized double-blind, placebo-controlled trial of the EMLA® patch for the reduction of pain associated with intramuscular injection in four to six-year-old children

The effectiveness of a eutectic mixture lidocaine-prilocaine topical anaesthetic cream (EMLA) patch compared with a placebo patch in the reduction of pain associated with intramuscular immunization was evaluated. As part of the study, 161 children (aged 4-6-y) undergoing routine diphtheria, pertussis, tetanus and polio (DPTP) immunization in five urban and five rural private office settings were randomly assigned to an EMLA patch (n = 83) or a placebo patch control group (n = 78). Pain measurements included: child's self-report on a Faces Pain Scale; facial action on the Child Facial Coding System; the Children's Hospital of Eastern Ontario Pain Scale and parent and technician ratings on a Visual Analogue Scale. Parents also rated their own and their child's immunization-related anxiety on a Visual Analogue Scale. The EMLA patch group had significantly less pain on all four pain measures compared with the placebo group. Of the children in the placebo group, 43% had clinically significant pain, compared with 17% of children in the EMLA patch group. No severe adverse symptoms occurred as a result of either EMLA or placebo patch application. CONCLUSION: The EMLA patch reduced immunization pain in 4 to 6-y-old children during needle injection.     

A pragmatic randomized controlled trial on the effectiveness of low concentrated saline spa water baths followed by ultraviolet B (UVB) compared to UVB only in moderate to severe psoriasis

OBJECTIVE: To evaluate whether low concentrated saline spa water baths followed by ultraviolet B (LC-SSW-UVB) are superior to UVB alone in moderate to severe psoriasis. BACKGROUND: There is a lack of sufficiently large randomized controlled clinical trial evaluating the additional benefit of saltwater baths followed by UVB compared to UVB only in psoriasis. STUDY DESIGN: Partly evaluator blind, multicentre, pragmatic, randomized controlled trial. SETTING: Five German spa centres. SUBJECTS: One hundred and forty-three adults with stable psoriasis during the last month and a Psoriasis Area and Severity Index (PASI) of > 10 and/or an affected body surface area of > 15%. INTERVENTIONS: LC-SSW-UVB or UVB thrice a week until remission (PASI < 5) or for a maximum of 6 weeks. Sodium chloride concentrations of natural springs varied between 4.5% and 12%. Conventional UVB (broadband UVB or selective UVB phototherapy) was used as irradiation source. MAIN OUTCOME: Reduction of PASI and/or affected body surface area of 50% at the end of the intervention period (PASI-50). Only participants receiving at least one intervention were included in the primary analysis. RESULTS: Patients allocated to LC-SSP-UVB attained a statistically significantly higher rate of PASI-50 at the end of the intervention period than patients allocated to UVB [58/79 (73%) vs. 32/64 (50%); P = 0.01; NNT, 4.3, 95% CI, 2.4-18.1]. Benefit persisted until 3 months only for one of two secondary outcomes considered. CONCLUSIONS: In routine clinical practice balneophototherapy using conventional UVB is superior to conventional UVB only at the end of a 6-week treatment course.     

Oral manifestations of human T‐cell lymphotropic virus infection in adult patients from Brazil

Oral Diseases (2010) 16 , 167–171 Objective: Human T‐cell lymphotropic virus type 1 (HTLV‐1) was the first human retrovirus discovered and its pathogenesis is related to T cells infection. This study aimed to verify the presence of oral manifestations in a Brazilian population of patients who was seropositive for HTLV, and identify risk factors for oral manifestations. Subjects and methods: An assessment was made of 139 patients at the Emilio Ribas Institute of Infectious Diseases. Results: A total of 112 (80.5%) patients were HTLV‐1, 26 (18.7%) were HTLV‐2+. About 35.2% of patients had myelopathy/tropical spastic paraparesis (HAM/TSP), with 48 of them being HTLV‐1+ and one patient was seropositive for HTLV‐1 and ‐2. The most common oral manifestations were: xerostomia (26.8%), candidiasis (20.8%), fissured tongue (17.9%), and loss of tongue papillae (10.0%). A multivariate logistic regression analysis showed that HAM/TSP is an independent risk factor for xerostomia (P = 0.02). The patients who were HAM/TSP+ were three times more likely to develop xerostomia when compared with patients without HAM/TSP (odds ratio = 2.69, 95% confidence interval = 1.17–6.17). Conclusion: Despite the fact that the findings of this study suggest a relationship between xerostomia and HAM/TSP, more studies should be developed to show what the association would be between xerostomia presented by HTLV patients and pathogenesis of the virus.     

Efficacy of a 1‐week rabeprazole triple therapy for eradicating Helicobacter pylori and ulcer healing: an ‘in‐clinical‐practice’ study

OBJECTIVE: To determine the efficacy and tolerability of a 1‐week treatment regimen consisting of rabeprazole and two antibiotics, clarithromycin and amoxicillin, in the eradication of Helicobacter pylori in an ‘in‐clinical‐practice’ setting. METHODS: Patients selected had unequivocal evidence of H. pylori infection based on urease test and histology of antral and corpus biopsies obtained at endoscopy. Patients with complicated ulcers were not included. Patients received rabeprazole 10 mg b.i.d., clarithromycin 500 mg b.i.d. and amoxicillin 1 g b.i.d. for 1 week and were assessed for successful eradication at least 4 weeks after completion of therapy by repeat gastroscopy and gastric biopsies. Eradication was defined as absence of bacteria in both antral and corpus biopsies tested by histology and urease test. Ulcer patients did not receive continued acid suppression therapy following the 1‐week course of treatment. RESULTS: The study recruited 205 patients of whom 25 were not compliant with the medications or defaulted on follow‐up and were therefore not included in the per‐protocol analysis. Eradication of H. pylori was successful in 166/180 of patients on per‐protocol analysis (92.2% [95% CI: 87.3, 95.7]) and in 169/205 patients on intention‐to‐treat analysis (82.4% [95% CI: 80.5, 90.2]; P = 1.000). There were 47 patients with active ulcers: DU 27, GU 18, DU/GU 2. Overall, ulcer healing was achieved in 42 of 44 (95.5%) patients who had successful eradication of H. pylori infection, but ulcers did not heal in any of the three patients (DU 2, GU 1) who did not eradicate the infection. Of the total group, 199 were assessed for compliance and side‐effects of treatment. Side‐effects were in general mild and tolerable. Of 14 patients who were not compliant with medication, 4 (2.0%) attributed it to side‐effects of treatment (increased abdominal pain, dizziness and taste disturbances) and the remaining 10 did not give specific reasons. The most common side‐effect was bitter taste, reported by 39.2% of patients. Other side‐effects, such as giddiness, increased abdominal pain, lethargy, loose bowel motions and skin rash, were mild and found in only a small percentage of patients. CONCLUSIONS: The rabeprazole 1‐week triple therapy with amoxicillin and clarithromycin is effective in eradicating H. pylori in an ‘in‐clinical‐practice’ setting. The treatment was well tolerated by patients. Good ulcer healing was achieved with short‐course H. pylori eradication therapy without the need for continued acid suppression.     

Efficacy of short‐course lansoprazole with clarithromycin and amoxicillin in the eradication of Helicobacter pylori in South‐East Asian patients: 5‐day t.d.s. versus 7‐day b.d. treatment regimens

OBJECTIVE : To determine and compare the efficacy of 5‐day t.d.s and 7‐day b.d. treatment regimens comprising lansoprazole, clarithromycin and amoxicillin in the eradication of Helicobacter pylori. METHODS : Patients with unequivocal evidence of H. pylori infection based on histology and rapid urease tests of both antrum and corpus biopsies were recruited for the study. The study was a randomized, investigator‐blind, comparative study. Patients received either 500 mg clarithromycin t.d.s. and 500 mg amoxicillin t.d.s. for 5 days (LAC5) or 500 mg clarithromycin b.d. and 500 mg amoxicillin b.d. for 7 days (LAC7) together with 30 mg lansoprazole (both groups) daily for either 5 or 7 days, depending on the treatment group. Patients were assessed for the successful eradication of H. pylori, defined as the absence of bacteria based on histology and urease tests on both antral and corporeal biopsies, carried out at least 4 weeks after completion of the therapy. RESULTS : One hundred and eight patients were recruited for the study. In the LAC5 treatment group, four patients failed to return for follow up and in the LAC7 group, two failed to return for follow up and two were not compliant with medications. Eradication rates based on an intention‐to‐treat analysis were: 46/54 for LAC5 (85.2%; 95% CI = 72.9–93.4) and 47/54 for LAC7 (87.0%; 95% CI = 75.1–94.6). Based on a per protocol analysis, the rates were: 46/50 for LAC5 (92.0%; 95% CI = 80.8–97.8) and 47/50 for LAC7 (94.0%; 95% CI = 83.5–98.7). Both treatment regimens were convenient for patients and except for two patients in the LAC7 group, all patients reported taking 100% of all prescribed medications. The side‐effects encountered were uniformly mild and no patient discontinued treatment because of intolerance to medications. The most common side‐effects were altered taste (LAC5 64.7%; LAC7 78.8%). Diarrhea, nausea and anorexia were reported in a minority of patients. CONCLUSIONS : Both the LAC5 t.d.s. and the LAC7 b.d. treatment regimens were well tolerated by patients and were highly effective in the eradication of H. pylori.     

Neutrophil deactivation by influenza A viruses: mechanisms of protection after viral opsonization with collectins and hemagglutination-inhibiting antibodies

Bacterial superinfections are a major cause of morbidity and mortality during influenza A virus (IAV) epidemics. Depression of phagocyte functions resulting from attachment of the IAV hemagglutinin (HA) to cell surface sialo-glycoproteins is a likely contributory cause of these infections. We have proposed that the group of collagenous lectins (termed collectins) present in blood and pulmonary surfactant play a role in initial host defense against IAV. We used here several recombinant human surfactant protein D (RhSP-D) preparations to determine the mechanism through which opsonization of IAV with collectins protects neutrophils against the deactivating effects of IAV on cellular respiratory burst responses in vitro. RhSP-D was markedly more potent than antibodies that inhibited viral hemagglutination activity (anti-HA antibodies) at protecting neutrophils in this assay. Unlike the anti-HA antibodies, RhSP-D was protective at concentrations that minimally inhibited viral hemagglutination activity. Two related features of SP-D--the degree of multimerization and the ability to cause aggregation of IAV particles--were critical determinants of the ability of SP-D to protect neutrophils against deactivation. Similarly SP-D-induced viral aggregate formation resulted in enhanced IAV binding to neutrophils and potentiated the ability of the virus itself to trigger neutrophil respiratory burst responses. In contrast to the case of IAV-antibody complexes, SP-D-IAV complexes attached to and activated neutrophils through a neuraminidase-sensitive mechanism (ie, similar to unopsonized IAV). These results indicate that collectin-mediated viral aggregation per se may be an important host defense mechanism not only by virtue of reducing the number of infectious viral particles, but also by promoting phagocyte responsiveness.     

Determination of adhesion force between single cell pairs generated by activated GpIIb-IIIa receptors

A biophysical approach was used to directly determine the avidity of the junction between two Chinese hamster ovary (CHO) cells bearing recombinant GpIIb-IIIa in the presence and absence of fibrinogen. Micromanipulation was used to induce conjugation of the cell pairs with or without activating the GpIIb-IIIa molecules with monoclonal antibody (MoAb) 62. Activation of GpIIb-IIIa caused an increase in the force required to separate the conjugates. The molecular bonding force between cells bearing activated GpIIb-IIIa and fibrinogen molecules was found to be 2.1 x 10(-7) dyne, which is 3.7 times higher than that between nonactivated GpIIb-IIIa and fibrinogen (5.7 x 10(-8) dyne). The results provide a quantitative assessment of the molecular bonding force between fibrinogen and the GpIIb-IIIa expressed on cell surface. The findings indicate that the activation of GpIIb-IIIa leads to an increase in the adhesive force in CHO cell aggregation by increasing the strength of the GpIIb-IIIa-fibrinogen bonds rather than the number of these bonds.     

In vivo and in vitro suppression of primary B lymphocytopoiesis by tumor-derived and recombinant granulocyte colony-stimulating factor

Transplantation of a granulocytosis-inducing murine CE mammary carcinoma into mice suppresses primary B lymphopoiesis in the marrow. The mechanisms of this tumor-induced B-cell suppression were investigated using Whitlock-Witte-type lymphoid cultures. When seeded with normal marrow progenitors, stromal cells of tumor-bearing mice supported the production of B220+ cells as well as did either stomal cells derived from control mice or the stromal cell line S17. Cultured over normal stroma, marrow cells of tumor-bearing mice depleted of adherent cells and B220+ cells generated B220+ cells as effectively as a similar cell population from control mice. However, interleukin-7- responsive progenitors, were completely depleted from the marrow of tumor-bearing mice. When conditioned medium (CM) of cloned CE tumor cells known to produce granulocyte colony-stimulating factor (G-CSF) and macrophage-CSF, or recombinant murine G-CSF was added to the cultures established with S17 cells, B220+ cell production was significantly diminished. Antiserum to murine G-CSF blocked these effects. These in vitro observations were corroborated by the elimination of marrow B220+ cells in mice injected with G-CSF. These in vitro and in vivo studies suggest that G-CSF plays an inhibitory role in primary B lymphopoiesis by blocking stromal cell-mediated differentiation of early B-cell progenitors into phenotypically recognizable B220+ pre-B cells.