Local and systemic cellular immunity in early renal artery atherosclerosis.

BACKGROUND AND OBJECTIVES: Modern imaging techniques have increased the incidental detection of renal atherosclerotic disease (RAD). Because immune activation may hasten RAD progression, identifying cellular immune markers might provide clues to clinical activity. In this study, cellular immune markers were assessed in early RAD. DESIGN, SETTING, PARTICIPANTS, & MEASUREMENTS: Immune cell markers in peripheral blood of two groups of hypertensive patients with normal carotid and coronary arteries were evaluated: 28 patients had incidental RAD and 22 patients had normal renal arteries; 21 renal arteries obtained at necropsy from individuals with history of hypertension and tissue evidence of RAD were examined and matched with 21 individuals with normal renal arteries. Cell subpopulations were measured by flow cytometry in peripheral blood and direct cell count, respectively, using T and dendritic cells monoclonal antibodies. RESULTS: Peripheral blood of RAD patients showed increased numbers of cells expressing CD3, CD4, CD83, and CD86. CD4 to CD8 ratio was 8.3 ± 1.4 (RAD) to 3.4 ± 0.9 (normal; P<0.001). No differences were found in CD25, CD8, and S100 among groups. Postmortem samples from RAD showed increased CD3+, CD4+, CD86+, and S100+ cells, whereas CD25+ and CD8+ were unmodified between groups. CD4+ to CD8+ ratio was higher in the RAD(PM) group. CONCLUSIONS: These results are consistent with an increased expression of immune cell markers in early RAD. Additional studies will explore if they may potentially turn into treatment targets to prevent disease progression.

Are plasma renin activity and aldosterone levels useful as a screening test to differentiate between unilateral and bilateral renal artery stenosis in hypertensive patients?

OBJECTIVE: To evaluate the serum aldosterone (Ald)/plasmatic renin activity (PRA) ratio as a surrogate marker of renin-angiotensin-aldosterone system status in unilateral (Uni)- and bilateral (Bi)-renal artery stenosis (RAS). METHODS: Seven hundred and eight hypertensive patients (HTP) were studied. Intermediate and high pretest risk of RAS was detected in 66 HTP who subsequently underwent renal gadolinium-enhanced magnetic resonance and arteriography. After application of exclusion criteria 51 HTP remained: 16 with Uni-RAS, 16 with Bi-RAS and 19 essential hypertensives with normal arteries. Nineteen normotensive individuals were also studied. Ald and PRA were determined before and after stenosis resolution by balloon angioplasty and stent implantation. RESULTS: Ald/PRA (ng/dl per (ng/ml per h(-1))) was markedly high in Bi-RAS (5.92 +/- 2.30, P < 0.001), and markedly low in Uni-RAS (0.38 +/- 0.17, P < 0.001) versus essential hypertensives (1.52 +/- 2.02). Multilevel likelihood ratios for Bi-RAS were positive for Ald/PRA higher than 3.6, negative for Ald/PRA lower than 0.2, and neutral for Ald/PRA at least 0.2 and 3.6 or less. ROC analysis identified Ald/PRA lower than 0.5 and Ald/PRA higher than 3.7 to have the best sensitivity and specificity to detect Uni-RAS and Bi-RAS, respectively. In Uni-RAS, but not in Bi-RAS, postinterventional PRA was significantly lower than basal PRA. In Uni-RAS and Bi-RAS, postinterventional Ald was approximately 30% and approximately three times lower than basal Ald, respectively. In essential hypertensives, PRA and Ald showed no changes in the same period. CONCLUSION: In the population studied, Ald, PRA and Ald/PRA were significantly different among essential hypertensives, and HTP with Uni-RAS or Bi-RAS. Studies with a higher number of patients will allow exploration of the usefulness of pharmacologic aldosterone blockade in Bi-RAS, and to assess the relevance of Ald/PRA to differentiate Uni-RAS from Bi-RAS.

Accidental intrathecal administration of vincristine.

We describe a case of accidental intrathecal administration of vincristine in a 33-year-old man with clinical diagnosis of acute lymphocytic leukemia. The patient died 20 days after receiving the drug. Clinically, the patient developed acute ascending paralysis with motor and sensory dysfunctions, and respiratory failure. Neuropathological investigation revealed lesions in spinal cord, roots, and cerebellum characterized by rarefaction of the neuropil, axonal, and myelin degeneration, accompanied by macrophagic infiltration.

Coronary intimal thickening in newborn babies and

We performed a morphological characterization of intimal thickenings in coronary arteries in the very early stages of life to obtain insights into initial coronary atherogenesis. We examined specimens from 67 infants who had died of noncardiac causes within their first year of life. Serially cut sections were stained with hematoxylin-eosin, Azan, Alcian blue, acetic orceine, and immunotypified for CD68, CD34, and alpha-smooth muscle (SM) actin. Substantial changes were detected in about 1 of 3 participants. Alterations ranged from focal areas with mild myointimal thickening to diffuse moderate thickening. In those lesions, smooth muscle cells (SMCs) showed loss of polarity, infiltrating the subendothelium, mostly with rupture of the internal elastic lamina and without neoangiogenesis. Morphometrically, in musculoelastic intimal thickenings, neointimal thickness averaged 58.3 +/- 17.8 microm, affecting 46% of the internal elastic membrane perimeter; lumen stenosis averaged 13.7% +/- 5.0%. These lesions can be present very early in life and SMCs seem to play an essential role.

Lesiones ateroscleróticas tempranas en el síndrome de muerte súbita infantil / Early Atherosclerotic Lesions in Sudden Infant Death Syndrome

Objetivo El presente estudio se llevó a cabo con el propósito de caracterizar morfológicamente lesiones ateroscleróticas precoces en arterias coronarias de víctimas del "síndrome de muerte súbita infantil" (SMSI) para conocer los mecanismos aterogénicos. Material y métodos Se efectuó el examen de 52 víctimas de SMSI y de 16 casos controles fallecidos de causas conocidas. Las principales arterias coronarias se cortaron serialmente y se tiñeron con hematoxilina-eosina, Azán, azul alciano, orceína acética, CD68, CD34 y α-SM-actina y se realizó histomorfometría de las lesiones. Resultados Se encontraron lesiones preateroscleróticas en el 44,2% del grupo SMSI (23/52) y en sólo el 6,3% del grupo control (1/16) (p = 0,0062). Las células musculares lisas perdieron la polaridad, infiltrándose en el subendotelio, en gran parte de los casos con rotura de la membrana elástica interna (MEI). No se observó neoangiogénesis. En el grupo SMSI con engrosamiento musculoelástico intimal, el espesor neointimal fue de 58,3 ± 17,8 mm, el perímetro de la MEI afectado fue del 45,6%, el área de proliferación neointimal fue de 0,03 ± 0,01 mm² y el área luminal fue de 0,21 ± 0,1 mm² con 13,8% ± 5% de estenosis luminal. Conclusiones Las lesiones preateroscleróticas se desarrollan temprano en víctimas del SMSI y son significativamente más frecuentes que en los controles. Las células musculares lisas tienen un papel fundamental en su génesis.

Objective The aim of the present study was to assess the morphology of early atherosclerotic lesions in coronary arteries from sudden infant death syndrome (SIDS) victims in order to recognize atherogenic mechanisms. Material and Methods We examined 52 victims of SIDS and 16 controls with known causes of infant death. The principal coronary arteries were serially cut and stained with hematoxilin-eosin, Azan, Alcian blue, acetic orcein, CD68, CD34 and α-SM actin, with subsequent histomorphometric analysis of the lesions. Results Preatherosclerotic lesions were found in 44.2% in SIDS group (23/52) and only in 6.3% in controls (1/16) (p=0.0062). Smooth muscle cells lost polarity, infiltrating the subedothelium, with rupture of the internal elastic membrane (IEM) in most cases. Angiogenesis was not observed. When muscular and elastic intimal thickening was present in the SIDS group, the results were as follows: neointimal thickness, 58.3±17.8 mm; affected perimeter of the EIM, 45.6%; area of neointimal proliferation, 0.03±0.01 mm²; and luminal area, 0.21±0.1 mm² with a luminal stenosis of 13.8±5%. Conclusions Preatherosclerotic lesions develop early in SIDS victims, and they are significantly more frequent than in controls. Smooth muscle cells are fundamental in its genesis.

Transformación maligna de la papilomatosis laringea juvenil / Malignant changes in juvenile laryngeal papillomatosis

La papilomatosis laríngea juvenil es una entidad generalmente benigna que debe ser considerada, no sólo por su eventual malignización, sino por su impredecible evolución local con compromiso respiratorio y séptico que pueden conducir a la muerte. Presentamos un paciente de sexo masculino con diagnóstico de esta enfermedad a los 9 meses de vida, que a los 15 años es internado con deterioro del estado general y alteraciones radiológicas pulmonares y vertebrales, lesiones que son biopsiadas com diagnóstico histopatológico de carcinoma epidermoide bien diferenciado con metástasis óseas. Este caso se suma a las escasas publicaciones de transformación carcinomatosa sin antecedentes de radioterapia (AU)

Transformación maligna de la papilomatosis laringea juvenil / Malignant changes in juvenile laryngeal papillomatosis

La papilomatosis laríngea juvenil es una entidad generalmente benigna que debe ser considerada, no sólo por su eventual malignización, sino por su impredecible evolución local con compromiso respiratorio y séptico que pueden conducir a la muerte. Presentamos un paciente de sexo masculino con diagnóstico de esta enfermedad a los 9 meses de vida, que a los 15 años es internado con deterioro del estado general y alteraciones radiológicas pulmonares y vertebrales, lesiones que son biopsiadas com diagnóstico histopatológico de carcinoma epidermoide bien diferenciado con metástasis óseas. Este caso se suma a las escasas publicaciones de transformación carcinomatosa sin antecedentes de radioterapia