Nyúltvelői neurovascularis kompresszió. A szekunder hypertonia ritka oka.

Compression of the rostral ventrolateral medulla oblongata is one of the rarely identified causes of refractory hypertension. In patients with severe, intractable hypertension caused by neurovascular compression, neurosurgical decompression should be considered. The authors present the history of a 20-year-old man with severe hypertension. After excluding other possible causes of secondary hypertension, the underlying cause of his high blood pressure was identified by the demonstration of neurovascular compression shown by magnetic resonance angiography and an increased sympathetic activity (sinus tachycardia) during the high blood pressure episodes. Due to frequent episodes of hypertensive crises, surgical decompression was recommended, which was performed with the placement of an isograft between the brainstem and the left vertebral artery. In the first six months after the operation, the patient's blood pressure could be kept in the normal range with significantly reduced doses of antihypertensive medication. Repeat magnetic resonance angiography confirmed the cessation of brainstem compression. After six months periodically increased blood pressure returned, but in smaller extent and less frequent. Based on the result of magnetic resonance angiography performed 22 months after surgery, re-operation was considerd. According to previous literature data long-term success can only be achieved in one third of patients after surgical decompression. In the majority of patients surgery results in a significant decrease of blood pressure, an increased efficiency of antihypertensive therapy as well as a decrease in the frequency of highly increased blood pressure episodes. Thus, a significant improvement of the patient's quality of life can be achieved. The case of this patient is an example of the latter scenario. Orv. Hetil., 2014, 155(21), 838-842

HIV Envelope gp120 Activates LFA-1 on CD4 T-Lymphocytes and Increases Cell Susceptibility to LFA-1-Targeting Leukotoxin (LtxA)

The cellular adhesion molecule LFA-1 and its ICAM-1 ligand play an important role in promoting HIV-1 infectivity and transmission. These molecules are present on the envelope of HIV-1 virions and are integral components of the HIV virological synapse. However, cellular activation is required to convert LFA-1 to the active conformation that has high affinity binding for ICAM-1. This study evaluates whether such activation can be induced by HIV itself. The data show that HIV-1 gp120 was sufficient to trigger LFA-1 activation in fully quiescent naïve CD4 T cells in a CD4-dependent manner, and these CD4 T cells became more susceptible to killing by LtxA, a bacterial leukotoxin that preferentially targets leukocytes expressing high levels of the active LFA-1. Moreover, virus p24-expressing CD4 T cells in the peripheral blood of HIV-infected subjects were found to have higher levels of surface LFA-1, and LtxA treatment led to significant reduction of the viral DNA burden. These results demonstrate for the first time the ability of HIV to directly induce LFA-1 activation on CD4 T cells. Although LFA-1 activation may enhance HIV infectivity and transmission, it also renders the cells more susceptible to an LFA-1-targeting bacterial toxin, which may be harnessed as a novel therapeutic strategy to deplete virus reservoir in HIV-infected individuals