News - Part 6

The most common origin of a right-to-left shunt is the patent foramen ovale (PFO). The PFO is an important feature of fetal circulation. The interatrial septum primum on the left side and the interatrial septum secundum on the right side maintain a central communication before birth, so that blood bypasses the pulmonary circulation. After birth, the pressure in the right atrium drops below the left atrial pressure, and this results into a functional closure. The latter may lead to fusion of the septum primum and secundum (anatomic closure). However, in 25% of the overall population, this fusion does not take place and the communication remains what is called probe patent, as it can open as a (one-way) valve when the right atrial pressure exceeds the left atrial pressure. This right-to-left shunt may be associated with paradoxical embolization of thrombi and has been postulated as a mechanism for cryptogenic stroke in young adults. Source
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The Relationship Between Migraine and Right-to-Left ShuntMigraine is a very common type of headache, affects the quality of life importantly, and has been ranked among the most disabling medical illnesses in the world. Migraine seems to be a complex disorder in which genetic, environmental, behavioral, and other as-yet unidentified factors interact to trigger the typical migraine attacks. A causal relationship between migraine and a right-to-left shunt has been proposed, particularly in patients with migraine with auraA However, the underlying pathophysiologic mechanism of this relationship is not well understood and remains hypothetical. In this review, we describe the relationship between both cardiac and pulmonary right-to-left shunts and the occurrence of migraine, and highlight observations that might support some pathophysiologic hypotheses of migraine. www.cheap-asthma-inhalers.com
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An Open-Label Trial of Granulocyte Macrophage Colony Stimulating Factor Therapy for Moderate Symptomatic Pulmonary Alveolar Proteinosis: ConclusionThe other factor that would argue in favor of a treatment effect for the observed clinical response is that many of these patients required frequent WLL for symptom relief before enrolling in our study, suggesting that they did not have many quiescent periods in their disease activity.
GM-CSF therapy was well tolerated, with minor side effects such as local skin reactions. The mean duration of follow-up was 39 months, and we did not see toxicity such as pulmonary fibrosis or bone marrow suppression with this therapy. The duration of follow-up may not be adequate to rule out longterm pulmonary or hematologic toxicity. Long-term follow-up of PAP patients treated with GM-CSF is ongoing.
All patients in our study had pretreatment anti-GM-CSF antibody, indicating an important diagnostic role for this antibody in the noninvasive diagnosis of PAP. In a study conducted at our institution, all adult patients (n = 40) with idiopathic PAP were found to have systemic and localized antibodies against GM-CSF, and the autoantibody response was specific for GM-CSF. The lowest serum end-titer for the PAP population was 1:400, and the highest titer was > 1:25,600. None of the healthy control subjects had end-titers > 1:10, and two of other pulmonary disease control subjects (beryllium lung disease) had end-titers at 1:100. The sensitivity of the serum anti-GM-CSF assay was 100%, and the specificity improved to 100% (using a cut-off end-titer of 1:400).

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Two plausible mechanisms for this observation in our patients are that both of these patients received escalating doses of GM-CSF for 26 weeks and 48 weeks, respectively, which may have overcome the inhibitory effect of the anti-GM-CSF antibody. The second mechanism could be that these two patients had a relatively lower anti-GM-CSF titer (1:3200 and 1:6400, respectively) compared to the other responders, which may have made them more susceptible to the stimulating effects of GM-CSF. birth control pills online
We have previously reported that the GM-CSF antibody titer is a predictor of response to GM-CSF therapy.” In 11 patients who completed the GM-CSF open-label clinical trial, it was demonstrated that the level of anti-GM-CSF titer is higher in patients with active disease and is lower in patients in remission. The anti-GM-CSF titer at baseline was lower and decreased further in responders to GM-CSF therapy. GM-CSF therapy did not induce or further increase the anti-GM-CSF titer. The data from this study indicate that the anti-GM-CSF titer correlates with PAP disease activity and also the response to therapy. There is also a case report of clinically successful treatment of PAP with GM-CSF that was associated with a profound reduction in GM-CSF-neutralizing autoantibodies (both serum and BAL) and improvement in alveolar macrophage morphology and function.
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The patients were followed up for a mean (± SD) duration of 39 ± 17.3 months. Of the 12 responders, 8 patients (67%) did not require WLL or home oxygen, and 4 patients (33%) required WLL for a mean of two occasions (range, one to five occasions). Of the nine nonresponders, four patients (44%) did not require WLL or home oxygen, and five patients (56%) required WLL once. Of four others screened initially, three required WLL. there
Overall, the drug was well tolerated. Table 5 lists the adverse events noted in the study participants. The majority of the side effects were minor and included injection-site edema, erythema, and malaise. Shortness of breath was noted in 10 patients. It is unclear whether the shortness of breath was related to PAP or the GM-CSF therapy. There were no bone marrow or lung toxicities.
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An Open-Label Trial of Granulocyte Macrophage Colony Stimulating Factor Therapy for Moderate Symptomatic Pulmonary Alveolar Proteinosis: DiscussionThe improvement in clinical parameters was not apparent until 8 to 12 weeks after initiation of therapy in our study. This was similar to the study by Seymour et al, in which improvement in P(A-a)O2 was not evident until 4 to 6 weeks, with maximal improvement achieved at approximately 6 to 10 weeks of therapy. These observed delays are consistent with published data that GM-CSF is required for immature precursor cells to be recruited to the lung and stimulated to differentiate into functional alveolar macrophages and, hence, help in surfactant clearance. In a trial of aerosolized GM-CSF in GM-CSF-deficient mice, improvement of the lung histology was first evident only after 4 to 5 weeks of therapy. avandia generic
One observation from our study is that several patients who were receiving GM-CSF treatment noted a response only after prolonged therapy (from 6 to 12 months). Four patients received therapy for 48 weeks, and two patients received therapy for 52 weeks. This is in contrast to the study by Seymour et al, in which only seven patients received treatment beyond 10 to 12 weeks and one patient for 26 weeks. Our study suggests that prolonged duration of therapy may be necessary in a subgroup of PAP patients to demonstrate clinical improvement. Whether there are any features that would identify a particular group of patients that would benefit from prolonged therapy is still unclear.
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An Open-Label Trial of Granulocyte Macrophage Colony Stimulating Factor Therapy for Moderate Symptomatic Pulmonary Alveolar Proteinosis: ResultsTwenty-seven patients with adult idiopathic PAP were screened, and 25 patients were enrolled in the trial. Figure 1 is a flow chart showing the disposition of all screened patients. Circulating anti-GM-CSF antibodies were present in all patients, measured in pretreatment sera as previously described. Among the 25 patients enrolled in the trial, 18 were men and 7 were women. The demographics and baseline characteristics are shown in Table 1. Of the 25 patients enrolled, 4 patients did not complete the study and were not evaluable. One patient withdrew due to arthralgia, one patient became pregnant and was withdrawn, one patient refused follow-up care, and one patient died of acute hypoxemic respiratory and multiorgan failure. so

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