Pseudoephedrine and circadian rhythm interaction on neuromuscular performance

This study analyzed the effects of pseudoephedrine (PSE) provided at different time of day on neuromuscular performance, side effects, and violation of the current doping cut‐off threshold [World Anti‐Doping Agency (WADA)]. Nine resistance‐trained males carried out bench press and full squat exercises against four incremental loads (25%, 50%, 75%, and 90% one repetition maximum [1RM]), in a randomized, double‐blind, cross‐over design. Participants ingested either 180 mg of PSE (supra‐therapeutic dose) or placebo in the morning (7:00 h; AM_PLAC and AM_PSE) and in the afternoon (17:00 h; PM_PLAC and PM_PSE). PSE enhanced muscle contraction velocity against 25% and 50% 1RM loads, only when it was ingested in the mornings, and only in the full squat exercise (4.4–8.7%; P < 0.05). PSE ingestion raised urine and plasma PSE concentrations (P < 0.05) regardless of time of day; however, cathine only increased in the urine samples. PSE ingestion resulted in positive tests occurring in 11% of samples, and it rose some adverse side effects such us tachycardia and heart palpitations. Ingestion of a single dose of 180 mg of PSE results in enhanced lower body muscle contraction velocity against low and moderate loads only in the mornings. These mild performance improvements are accompanied by undesirable side effects and an 11% risk of surpassing the doping threshold.     

The prognostic value of blood lactate levels relative to that of vital signs in the pre-hospital setting: a pilot study

Introduction  

A limitation of pre-hospital monitoring is that vital signs often do not change until a patient is in a critical stage. Blood lactate levels are suggested as a more sensitive parameter to evaluate a patient's condition. The aim of this pilot study was to find presumptive evidence for a relation between pre-hospital lactate levels and in-hospital mortality, corrected for vital sign abnormalities.     

Contribution of polymerase chain reaction and radioimmunoprecipitation assay in the confirmation of human T-lymphotropic virus infection in French blood donors. Retrovirus Study Group of the French Society of Blood Transfusion

BACKGROUND: To verify the criteria for human T-lymphotropic virus (HTLV) seropositivity in Western blot (WB) proposed by the Retrovirus Study Group of the French Society of Blood Transfusion, 186 blood donations that were repeatedly reactive in HTLV enzyme-linked immunosorbent assay, selected according to their WB pattern, were tested by polymerase chain reaction (PCR) and radioimmunoprecipitation assay (RIPA). STUDY DESIGN AND METHODS: In two commercially available WBs, 12 samples were confirmed as positive (rgp21+p19+p24) and 174 were interpreted as indeterminate (one or two reactivities to these proteins). The primer pairs used for the PCR allowed the amplification of type I (HTLV-I) or type II (HTLV-II) (or both) sequences. The RIPA was performed with two 35S-labeled cell lines: HTLV-I infected HUT 102/B2 and HTLV-II-infected MoT. RESULTS: Of the 12 positive samples, 11 were classified as HTLV-I-positive and one as HTLV-II-positive. Among the 174 indeterminate samples, three (WB pattern: rgp21+, p19+, p24-) were HTLV-I positive in PCR (one of them was positive in RIPA also); the other 171 were HTLV negative. CONCLUSION: In the study of a population in which 97 percent of HTLV infections are due to HTLV-I, these data support the three-protein criteria (rgp21, p19, and p24) for a positive blot reading. No HTLV infection was observed when rgp21 did not react. Consequently, p19 and/or p24 band patterns represent false reactivity and do not require PCR or RIPA confirmation. To discriminate between false- and true-positive results in the absence of MTA-1 or K55 reactivity, PCR and/or RIPA is required only when rgp21 reactivity is associated with one gag band (p19 or p24).     

Nasal nitric oxide concentration is decreased in heart failure patients receiving nitrates

Summary— Nitric oxide (NO) is a free radical gas and a short-lived messenger which has many paracrine functions. Direct assessment of NO production is very difficult in vivo. However, the paranasal cavities generate a high amount of NO which diffuses in the nasal cavity where it can be easily measured. Several studies have suggested alterations of the NO production in heart failure. Thus, we assessed nasal NO concentration in normal subjects and in heart failure patients. The nasal NO concentration averaged 227 ± 10 ppb in the control group (n = 20), and 210 ± 10, 198 ± 20 and 159 ± 54 ppb in New York Heart Association (NYHA) class II (n = 30), III (n = 28) and IV (n = 7) patients, respectively (mean ± standard error [SE], not significant using analysis of variance [ANOVA]). Nasal NO level was not influenced by age, sex or etiology of the heart failure or by treatment with frusemide, angiotensin-converting enzyme inhibitor or digoxin. However, treatment with NO-releasing drugs (nitrates or molsidomine) significantly decreased the nasal NO level in heart failure patients. A two-way ANOVA revealed that treatment with a NO-releasing drug influenced nasal NO concentration (P = 0.0005), whereas NYHA class did not (P = 0.23), with a trend towards an interaction between the two parameters (P = 0.09): the inhibitory effect of NO-releasing drug on nasal NO concentration was more pronounced in severe heart failure. In an additional group of 12 patients (NYHA class II or III), the nasal NO concentration was 174 ± 19 ppb during NO-releasing drug treatment and increased to 231 ± 27 ppb 3 days after withdrawal of the nitrates (P = 0.0007 using paired t-test). Conversely, the nasal NO concentration in another group of seven patients (NYHA class II or III) was 219 ± 32 ppb without nitrate treatment and decreased to 188 ± 28 ppb 7 days after nitrate addition (P = 0.02 using paired (test). In contrast, the nasal NO concentration in another group of ten ischemic patients without heart failure was 203 ± 25 ppb without nitrate treatment and was similar (207 ± 28 ppb) 7 days after nitrate addition (not significant using paired t-test). In conclusion, nasal NO production is normal in heart failure, except in patients receiving NO-releasing drugs. Nasal NO concentration could be useful for investigating the mechanism(s) by which exogenous NO donors decrease endogenous NO production.     

Aortic bypass graft infection due to Aspergillus: report of a case and review.

Aspergillus is a rare cause of aortic graft infection. A recent case is reported and a review of seven other cases described in the literature since 1966 is presented. Infections of both thoracic and abdominal aortic grafts have been reported. Infection occurred from 5 weeks to 3 years after surgery. Underlying immunosuppressive disorders were not present. The most common presenting symptoms were back pain, fever, and embolic phenomena. Pseudoaneurysm of the vascular prosthesis with contiguous vertebral osteomyelitis was frequently seen. Blood cultures were always negative. Laboratory findings were nonspecific. The diagnosis was not anticipated in any case. Aspergillus was isolated in culture of specimens of the vertebral bone, excised graft, or peripheral emboli. Aspergillus fumigatus was the species most frequently isolated. Infection may have occurred intraoperatively as a result of contamination with airborne fungal spores. Optimal treatment included early removal of the graft with extraanatomical bypass plus prolonged antifungal therapy. Delayed surgical intervention and medical therapy alone were associated with high mortality rates. Aspergillar vascular infection should be suspected in patients with aortic grafts who develop persistent back pain, fever, or arterial embolization, and whose blood cultures are sterile.     

Experience with miltefosine for persistent or relapsing visceral leishmaniasis in solid organ transplant recipients: A case series from Spain

The incidence of visceral leishmaniasis (VL) after solid organ transplantation (SOT) is increasing. The optimal therapy for post‐transplant VL remains unclear, as relapses after liposomal amphotericin B (L‐AmB) are common. Miltefosine has been shown to be effective for treating VL in immunocompetent patients, although data in the specific population of SOT recipients are lacking. In the setting of an outbreak of leishmaniasis occurring in Southwest Madrid, we reviewed our experience in 6 SOT recipients with persistent or relapsing VL who received a 28‐day course of miltefosine (2.5 mg/kg/day) as salvage therapy. All patients had been treated previously with L‐AmB as first‐line therapy. The incident episode of VL occurred at a median of 14 months after transplantation. Two patients experienced persistent infection and the remaining 4 had a relapse after a median interval of 168 days since the completion of the course of L‐AmB. All the patients had an apparent initial clinical improvement with miltefosine. However, VL relapsed in 3 of them (after a median interval of 46 days), which required retreatment with L‐AmB‐based regimens. Miltefosine therapy was followed by a prolonged secondary prophylaxis with L‐AmB in the only 2 cases with sustained clinical response and ongoing immunosuppression. No adverse effects associated with miltefosine were observed. Albeit limited, our experience suggests that miltefosine monotherapy likely has a limited utility to obtain a long‐lasting clinical response in complicated (persistent or relapsing) forms of post‐transplant VL, although its role in association with L‐AmB‐based secondary prophylaxis may merit further investigation.