Posttransfusion thrombocytopenia associated with passive transfusion of a platelet-specific antibody

A transfusion reaction in a 76-year-old man was followed by severe but transient thrombocytopenia after infusion of whole blood. A high-titer platelet-specific antibody (anti-PLA) was demonstrated in the plasma of the implicated unit and in the serum of the blood donor. In addition, three previous recipients of blood from the implicated donor had posttransfusion episodes of unexplained thrombocytopenia. These cases represent the first reported clinical examples of posttransfusion thrombocytopenia caused by passively transfused platelet-specific alloantibodies.     

Influence of anesthetic management on quality of magnetoencephalography scan data in pediatric patients: a case series

Background:  Magnetoencephalography (MEG) is increasingly used in the presurgical evaluation of pediatric seizure patients. Many pediatric patients require sedation or anesthesia to tolerate these exams. However, the available literature on anesthetic management in this population is very limited.
Methods:  We retrospectively reviewed the records of all patients who underwent MEG scanning at our institution with regard to the interaction of anesthetic management and quality of scan data.
Results:  High-dose propofol infusions (≥200 μg·kg⁻¹·min⁻¹) were associated with high frequency artifacts that interfered with the identification of epileptiform discharges. Lower-dose propofol infusions (≤100 μg·kg⁻¹·min⁻¹) did not produce artifacts but required co-administration of fentanyl to prevent patient motion. Dexmedetomidine infusions were not associated with signal artifacts and prevented patient motion very well in our initial patients and became our standard technique.
Conclusion:  In our experience, dexmedetomidine infusions are preferable to propofol-based techniques for pediatric MEG scans due to the absence of adverse effect on interictal activity.     

Chronic mercury exposure impairs the sympathovagal control of the rat heart

Mercury is known to cause harmful neural effects affecting the cardiovascular system. Here, we evaluated the chronic effects of low‐dose mercury exposure on the autonomic control of the cardiovascular system. Wistar rats were treated for 30 days with HgCl₂ (1st dose 4.6 μg/kg followed by 0.07 μg/kg per day, intramuscular) or saline. The femoral artery and vein were then cannulated for evaluation of autonomic control of the hemodynamic function, which was evaluated in awake rats. The following tests were performed: baroreflex sensitivity, Von Bezold‐Jarisch reflex, heart rate variability (HRV) and pharmacological blockade with methylatropine and atenolol to test the autonomic tone of the heart. Exposure to HgCl₂ for 30 days slightly increased the mean arterial pressure and heart rate (HR). There was a significant reduction in the baroreflex gain of animals exposed to HgCl₂. Moreover, haemodynamic responses to the activation of the Von Bezold‐Jarisch reflex were also reduced. The changes in the spectral analysis of HRV suggested a shift in the sympathovagal balance toward a sympathetic predominance after mercury exposure, which was confirmed by autonomic pharmacological blockade in the HgCl₂ group. This group also exhibited reduced intrinsic HR after the double block suggesting that the pacemaker activity of the sinus node was also affected. These findings suggested that the autonomic modulation of the heart was significantly altered by chronic mercury exposure, thus reinforcing that even at low concentrations such exposure might be associated with increased cardiovascular risk.     

Detection of chromosome 20q deletions in bone marrow metaphases but not peripheral blood granulocytes in patients with myeloproliferative disorders or myelodysplastic syndromes

Myeloproliferative disorders and myelodysplastic syndromes arise in multipotent progenitors and may be associated with chromosomal deletions that can be detected in peripheral blood granulocytes. We present here seven patients with myeloproliferative disorders or myelodysplastic syndromes in whom a deletion of the long arm of chromosome 20 was detectable by G-banding and/or fluorescence in situ hybridization in most or all bone marrow metaphases. However, in each case, microsatellite polymerase chain reaction (PCR) using 15 primer pairs spanning the common deleted region on 20q showed that the deletion was absent from most peripheral blood granulocytes. The human androgen receptor clonality assay was used to show that the vast majority of peripheral blood granulocytes were clonal in all four female patients. This represents the first demonstration that the 20q deletion can arise as a second event in patients with pre-existing clonal granulopoiesis. Microsatellite PCR analysis of whole bone marrow from two patients was consistent with cytogenetic studies, a result that suggests that cytogenetic analysis was not merely selecting for a minor subclone of cells carrying the deletion. Furthermore, in one patient, the deletion was present in both erythroid and granulocyte/monocyte colonies. This implies that the absence of the deletion in most peripheral blood granulocytes did not reflect lineage restriction of the progenitors carrying the deletion but may instead result from other selective influences such as preferential retention/destruction within the bone marrow of granulocytes carrying the deletion.     

Plasmacytoid Dendritic Cells (pDCs) From HIV Controllers Produce Interferon-α and Differentiate Into Functional Killer pDCs Under HIV Activation

Background.Human immunodeficiency virus (HIV) controllers spontaneously control viremia and CD4 T-cell depletion in contrast to viremic patients. After HIV exposure, plasmacytoid dendritic cells (pDCs) produce high levels of interferon alpha (IFN-α) and express the apoptotic ligand TRAIL (tumor necrosis factor-related apoptosis inducing ligand). Simian models have shown that prolonged high levels of IFN-α production could be responsible for AIDS progression. Methods.We studied pDC activation in response to human immunodeficiency virus (HIV) using flow cytometry and 3D microscopy. Results.We show here that pDCs from controller patients produced higher levels of IFN-α in response to HIV than pDCs from viremic patients but similar levels to pDCs from healthy donors. Because binding of HIV to CD4 is essential for pDC activation, the low CD4 expression by pDCs from viremic patients may explain the weak IFN-α response to HIV. Three-dimensional microscopy revealed that pDCs from controllers and healthy donors expressed intracellular TRAIL that is relocalized to the membrane after HIV exposure. In contrast, pDCs from viremic patients expressed membrane TRAIL without any stimulation. Conclusions.We demonstrate that, in response to HIV, pDCs from controller patients produce IFN-α, express membrane TRAIL, and induce apoptosis of T-cell lines.     

Visual system dysfunction in migraine: a review of clinical and psychophysical findings

This paper reviews both clinical and experimental literature relating to visual dysfunction in migraine, starting with the eye and progressing via the retina and visual pathways to the visual cortex. Migraine is associated with (i) a pupillary sympathetic hypofunction, and (ii) a cortical hypersensitivity to visual stimuli (perhaps only in migraine with aura), the pathogenesis of which remains to be determined. Various hypotheses are discussed, and it is proposed that the methods of visual psychophysics may represent a useful approach in the future study of cortical hyperexcitability in migraine. Paradoxically, little research has been directed towards understanding (i) the photophobia of migraine attacks, and (ii) how migraine may be triggered by visual stimuli. Research aimed at elucidating the mechanisms of these phenomena may enhance understanding of the pathogenes is of migraine.