Vascular lesions of malignant essential hypertension.
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The computed tomographic findings of three patients with cerebral syphilis, including cerebral gumma, which regressed completely under penicillin therapy, syphilitic angiitis with cerbral infarction, and syphilitic cerebral atrophy, are reported. CT is unable to provide specific diagnostic data for these conditions. The etiology can be clarified only by taking into consideration the clinical findings and course, the serological results, and the result of therapy.
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The clinical outcome in 12 late-diagnosed patients with homocystinuria is reported. Three children died: all were mentally damaged and were never treated effectively. Eight children have been treated with pyridoxine--or with a low-methionine diet with supplemental L-cystine--for 2 to 9 years. Follow-up of these patients shows a striking improvement in behaviour and intellectual development in close correlation to the biochemical normalisation. No thromboembolic episodes occurred in adequately treated patients. However, in one child thrombosis of the retinal artery developed during dietary failure. In another patient the characteristic symptoms of an endangiitis obliterans completely disappeared. Both the reversibility and the improvement of some of the main sequelae in homocystinuria emphasize the need to treat all patients, regardless of their age at diagnosis.
Out of 136 placentas with vascular obliterations, 25 cases were placentas of children born alive, in 92 cases the placentas belonged to children born dead. In 19 cases we had no data on the baby. In placentas of babies born alive, the same vascular changes (subtotal and total obliterations, septal partitions of vascular lumina) were found as in those of dead-born children, although considerably less severe. Vascular obliterations should not be considered as post-mortal alterations of the placenta blood vessels, since only quantitative differences could be proved. Septum-like partitions are hardly ever found in placentas of babies born alive, in dead-born babies they are more frequent. They seem to present recanalizations, and are understood as a compensation mechanism for a placental insufficiency caused by vascular obliterations. The accentuated collagenization of the placental periphery, noticed in placentas of babies born alive, is being interpreted as the consequence of an impaired blood circulation, caused by partial and total vascular obliterations. The high collagen rate in the placental periphery in placentas of the dead-born is probably a reaction to the diminished fetal circulation. Endangitis obliterations in 73 placentas out of 4600 pregnancies of cases with late abortions, premature deliveries, perinatal death, underweigh and small for gestational age babies, impaired adaptation in newborns of mothers with proteinuria and hypertension speak strongly for assuming that endangitis obliterans presents a form of placental insufficiency. Endangitis obliterans of the placental blood-vessels has, however, been discovered frequently after Rubella infection in early pregnancy. The etiological factors of the endovascular process can be multiple, the morphological and the pathophysiological reactions are the same.
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A 65-year-old woman died in sudden right heart failure caused by thrombendarteriitis pulmonalis carcinomatosa Ceelen 16 months after resection of a rectal carcinoma. Autopsy disclosed a complex picture of multiple tumour cell emboli in small pulmonary arteries associated with local thrombosis and thrombus-associated vessel wall reaction. This was characterized by movement of medial muscle cells into the thrombus. In addition, affected vessels showed a prominent perivascular tumour-related infiltration by lymphocytes which are identified immunohistochemically as CD3-reactive T-cells.
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With a graphic reconstruction on serial sections, performed with placentas which altogether showed so-called recanalisation, it is possible to work out the fact, that the recanalisation is an effect of the paravascular capillary network and with it to clarify the problem of the so-called recanalisation. It is proved, that the paravascular capillaries undertake compensatory hemodynamic functions and this undertaking of function prevents a complete occlusion of the cotyledonary vessels, so that you have to speak of restlumen and restflow but not of recanalisation. The endangitis obliterans of cotyledonary vessels is again unequivocally pointed out by this phenomenon as a intravital process.
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