Cardiogenic shock due to thrombotic thrombocytopenic purpura.

We report the case of a 49-year-old man with thrombotic thrombocytopenic purpura (TTP) leading to cardiogenic shock. Laboratory data were typical for TTP with thrombocytopenia and microangiopathic hemolytic anemia. The electrocardiogram recorded significant ST-segment elevations in the anterior and inferior leads. In addition' coronary angiography showed normal epicardial coronary arteries with slow flow. The patient died due to electromechanical dissociation six hours after admission. During autopsy typical features of thrombotic thrombocytopenic purpura were found. Histological preparation of the heart showed a diffuse myocardial necrosis due to microvascular thrombosis. Cardiac involvement is common in TTP but extended myocardial necrosis has been reported in only a few cases.

Comparative genomic hybridization (CGH) analysis of neuroblastomas--an important methodological approach in paediatric tumour pathology.

Comparative genomic hybridization (CGH) was applied to 35 neuroblastomas to obtain a global view of genetic imbalances. Results were validated by means of Southern blot hybridization (detection of N-myc amplification), loss of heterozygosity (LOH) studies (detection of deletion 1p), and interphase cytogenetics [dual labelling fluorescence in situ hybridization (FISH) of centromeric 17 and erbB-2]. CGH allowed sensitive detection of N-myc amplification and chromosome 1p deletion, representing the most established prognostic markers of neuroblastoma. In addition, a high rate of chromosome 17 aberrations (63 per cent) with possible prognostic relevance was observed. Previously unreported high level copy number increases indicating oncogene amplification were mapped to chromosome subbands 2p13-14 and 3q24-26. Other recurrent regional chromosomal aberrations were localized on 11q, 12q, 13q, 14q, and 15q. CGH results were fully consistent with data of Southern blot analysis and LOH study, as well as interphase cytogenetics. These results show that CGH is a sensitive method for the detection of all prognostically relevant genetic alterations in neuroblastomas; that CGH considerably simplifies the detection of these alterations, resulting in a single methodological approach; and that CGH is a powerful tool to elucidate previously unknown genetic changes in neuroblastomas.

Altered (oxidized) C1q induces a rheumatoid arthritis-like destructive and chronic inflammation in joint structures in arthritis-susceptible rats.

Previous studies have identified an altered C1q molecule in synovial fluids from the joints of rheumatoid arthritis patients. We therefore immunized arthritis-susceptible Lewis 1A.AVN rats with either native C1q (C1q nat), altered (oxidized) C1q (C1q ox), or type II collagen (CII, induces arthritis in these animals), in order to induce arthritis. Unlike C1q nat, both CII and C1q ox were able to induce swelling and erythema of joints consistent with an arthritis-like inflammatory reaction. Histopathological evaluation of individual joint sections revealed synovitis, bursitis and tendovaginitis, massive joint destruction, and severe pannus formation. In a time-course study, no differences in onset of arthritis or pathology were observed between C1q ox-induced arthritis and that induced by CII. High titers of antibodies recognizing CII, but not C1q (native or oxidized), were detected in rats immunized with CII. In contrast C1q ox, but not C1q nat, induced antibodies reactive with both C1q and CII. Antibodies from C1q ox-immunized animals contained an antibody subset that reacted with C1q but not CII and a subset that reacted with CII but not C1q, implying that induction of an immune response to CII does not require CII. These data support the hypothesis that C1q may provide one of the early antigens involved in induction of arthritis, before CII becomes available as antigen.

Pulmonary contusion: CT vs plain radiograms.

In experimentally induced pulmonary contusions, CT (n = 27) and chest X-ray (n = 24) findings were compared with the findings at autopsy. Twenty-seven of 27 (100%) pulmonary contusions were visible by CT immediately after trauma compared with 9 of 24 (37.5%) in the chest X-ray. After 30 min follow-up, 18 of 24 (75%) lesions were seen on the plain film. Five of 24 (21%) contusions escaped detection on conventional radiographs. Computed tomography underestimated lesion size in 5 of 60 (8%) measurements, conventional radiographs in 21 of 36 (58%) measurements. Pathological examination never revealed a pulmonary contusion that was not demonstrated by CT. Therefore, pulmonary contusion seems unlikely in a trauma patient with normal pulmonary CT.

[Computed tomography of lung contusion. An experimental study]. / Computertomographie der Lungenkontusion. Eine experimentelle Studie.

A new experimental model has been developed to determine whether computed tomography has any advantages for the investigation of lung contusions. In 27 dogs, chest wall deformation was produced at speeds varying from 17.3 m/sec to 45.7 m/sec, leading to lung contusion. After the injury, 27 out of 27 (100%) CT examinations demonstrated the contusions, but only nine out of 24 (37.5%) were seen on conventional radiographs. In contrast to conventional radiography, which either failed to show the presence of a contusion, or which under-estimated the extent by more than one cm, in more than half the cases CT agreed with the pathological findings in more than 90%. No lung contusions were found at autopsy which had not been demonstrated by CT.