Internal iliac artery embolisation for intractable bladder haemorrhage in the peri-operative phase.
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Intractable haemorrhage from the bladder wall during transurethral resection of bladder tumour is uncommon but potentially catastrophic. Internal iliac artery embolisation is a minimally invasive technique, which is now widely practised to stop bleeding from branches of these arteries is situations including pelvic malignancy, obstetric and gynaecological emergencies and trauma. We report its successful use peri-operatively, in an unfit, elderly patient with uncontrolled bleeding. (+info)
Severe pulmonary hemorrhage in patients with serious group A streptococcal infections: report of two cases.
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Severe pulmonary hemorrhage was observed in two patients who died of serious group A streptococcal infections. These two patients initially presented with fever and sore throat. This was followed by sudden onset of septicemia caused by the bacteria and by the subsequent development of severe pulmonary hemorrhage. Hemoptysis, cyanosis, and dyspnea were observed prior to death in both cases. This pulmonary lesion resulted in asphyxia and sudden death in one patient. Pathological examinations of the lung revealed severe intraalveolar hemorrhage, with no evidence of inflammation or necrosis of the pulmonary tissue. There was no evidence of aspiration of blood due to hemorrhage in the upper respiratory or alimentary tract. This visceral lesion appears to be an hitherto undescribed, novel clinicopathologic feature of patients with serious group A streptococcal infections. (+info)
Massive pulmonary hemorrhage due to cytomegalovirus infection in a Japanese patient with alpha-1-antitrypsin-deficient emphysema.
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Although alpha(1)-antitrypsin (AAT) deficiency is one of the most common hereditary diseases and a recognized cause of emphysema in Caucasians, variants of this deficiency are extremely rare among Orientals. We present here a Japanese emphysema patient with the AAT deficiency variant originally identified as S(iiyama). After an 8-year follow-up period, the patient suffered from repeated pulmonary Pseudomonas aeruginosa infection for 4 years. He died suddenly of massive pulmonary hemorrhage. The pathologic examination revealed a necrotic hematoma in the right S10 lobe, which exhibited pneumonia due to cytomegalovirus (CMV) infection. Pulmonary hemorrhage due to CMV can occur and be fatal in patients with emphysema and AAT deficiency. (+info)
Regional conductance changes during hemorrhage in pregnant and nonpregnant conscious rabbits.
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Late pregnant (P) conscious rabbits are less able to maintain arterial pressure during hemorrhage than nonpregnant (NP) animals. This study tested the hypothesis that the difference is due in part to less reflex vasoconstriction when the rabbits are P. Rabbits (n = 14) were instrumented with arterial and venous catheters as well as ultrasonic flow probes around the superior mesenteric, renal, and/or terminal aortic arteries. Pregnancy increased (P < 0.05) blood volume [235 +/- 5 (P) vs. 171 +/- 3 (NP) ml], terminal aortic conductance [1.88 +/- 0.11 (P) vs. 0.98 +/- 0.06 (NP) ml. min(-1). mmHg(-1)], mesenteric conductance [1.20 +/- 0.19 (P) vs. 0.80 +/- 0. 05 (NP) ml. min(-1). mmHg(-1)], and heart rate [191 +/- 4 (P) vs. 162 +/- 3 (NP) beats/min] and decreased arterial pressure [59 +/- 1 (P) vs. 67 +/- 2 (NP) mmHg; P < 0.05]. Renal conductance was unaltered. The rabbits were bled in both the NP and P states at 2% of the initial blood volume per minute until arterial pressure fell below 45 mmHg. Arterial pressure fell with less blood loss in P rabbits [28 +/- 2% (P) vs. 39 +/- 2% (NP) of initial blood volume; P < 0.001]. Terminal aortic conductance decreased (P < 0.001) before the pressure fall in both groups, but the response was reduced in P rabbits. Mesenteric and renal conductances did not change in either group before the blood pressure fall. During the pressure fall, terminal aortic conductance increased (P < 0.05) only in NP rabbits. Mesenteric conductance increased in both groups. In summary, rabbits in late gestation are less able to maintain arterial pressure during hemorrhage, at least in part because of reduced vasoconstriction in tissues perfused by the terminal aorta. (+info)
Subclinical alveolar bleeding in pulmonary vasculitides: correlation with indices of disease activity.
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Haemosiderin-laden alveolar macrophages are a common finding in patients with alveolar bleeding. Iron-positive macrophages, suggestive of subclinical alveolar bleeding, were found to be fairly common in bronchoalveolar lavage (BAL) fluid in primary systemic vasculitis but uncommon in collagen vascular diseases (CVDs) and rheumatoid arthritis (RA). To substantiate the impression that subclinical alveolar bleeding may be a feature distinguishing between these disorders, fibreoptic bronchoscopy and BAL were performed in 49 patients with active Wegener's granulomatosis or Churg-Strauss syndrome and 44 patients with CVDs or RA, all of them without clinically manifest alveolar bleeding. The percentage of iron-positive cells was compared with clinical and radiological findings. Only a minority of the CVD and RA patients had iron-positive alveolar macrophages; the 95th percentile of the median number of such cells was 5%. Fifty-three per cent of the patients in the vasculitis group had >5% iron-positive cells, with individual counts ranging up to 95%. Patients with iron-positive macrophages had more extensive disease, more frequent microhaematuria, a higher antineutrophil cytoplasmic antibody titre, a higher myeloperoxidase concentration in the BAL fluid and somewhat more frequent low-attenuation opacities in pulmonary high-resolution computed tomography than the patients with a low iron-positive cell count. In conclusion, subclinical alveolar bleeding was, indeed, a common finding in antineutrophil cytoplasmic antibody-associated vasculitis, which distinguished these disorders from lung disease due to collagen vascular diseases or rheumatoid arthritis. Its association with indices of disease activity, although weak in this cross-sectional study, merits a longitudinal study of its value for the long-term monitoring of vasculitis patients. (+info)
A prospective randomized trial of granulocyte colony-stimulating factor therapy after autologous blood stem cell transplantation in adults.
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In order to assess the potential clinical benefit of filgrastim (G-CSF) after peripheral blood stem cell (PBSC) autotransplantation a randomized study was begun in our center in July 1997: 62 patients were involved (30 received filgrastim after PBSC infusion and 32, the control group, received no cytokines). All were adults (median 40 years, range 18-65). Patients with one of three different pathologies were recruited: 28 had advanced breast carcinoma, 23 had lymphomas (12 Hodgkin's disease and 11 non-Hodgkin's lymphoma) and 11 had de novo AML. All of them were transplanted using myeloablative chemotherapy conditioning regimens. G-CSF was administered subcutaneously from day +5 in the treated group at a dose of 5 microg/kg body weight/day. The numbers of CD34+ and mononuclear (MNC) cells infused were similar in each group. Only minor differences regarding the use of G-CSF could be inferred from the analysis of the data. Faster granulocyte engraftment was evident in the treated group (mean of 10 vs 12 days to achieve >0.5 x 109/l granulocytes, P = 0.0008), without differences in incidence and severity of infections, days of fever or duration of antibiotic treatment between groups. There was slightly slower platelet engraftment (mean of 15 days in the group with G-CSF vs 12 days in the other group to achieve >20 x 109/l platelets, P = NS) in this series, but there were no differences in incidence and severity of haemorrhage or platelet transfusion support. Considering the economical costs, the median expenditure per inpatient stay was Eur5961 (range Eur4386-Eur17186) in the G-CSF group compared with Eur5751 (range Eur3676-Eur15640) in the control group (P = 0.47). From our data it could be concluded that for adult patients transplanted with PBSC there is no clear beneficial impact of post-infusion G-CSF administration. (+info)
An epidemic of enterovirus 71 infection in Taiwan. Taiwan Enterovirus Epidemic Working Group.
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BACKGROUND: Enteroviruses can cause outbreaks of hand-foot-and-mouth disease (characterized by vesicular lesions on the hands, feet, and oral mucosa) or herpangina, usually without life-threatening manifestations. In 1998 an epidemic of enterovirus 71 infection caused hand-foot-and-mouth disease and herpangina in thousands of people in Taiwan, some of whom died. METHODS: We assessed the epidemiologic aspects of this outbreak. Cases of hand-foot-and-mouth disease or herpangina in ambulatory patients were reported to the Taiwan Department of Health by a mean of 818 sentinel physicians. Severe cases in hospitalized patients were reported by 40 medical centers and regional hospitals. Viruses were isolated by 10 hospital laboratories and the department of health. RESULTS: The sentinel physicians reported 129,106 cases of hand-foot-and-mouth disease or herpangina in two waves of the epidemic, which probably represents less than 10 percent of the estimated total number of cases. There were 405 patients with severe disease, most of whom were five years old or younger; severe disease was seen in all regions of the island. Complications included encephalitis, aseptic meningitis, pulmonary edema or hemorrhage, acute flaccid paralysis, and myocarditis. Seventy-eight patients died, 71 of whom (91 percent) were five years of age or younger. Of the patients who died, 65 (83 percent) had pulmonary edema or pulmonary hemorrhage. Among patients from whom a virus was isolated, enterovirus 71 was present in 48.7 percent of outpatients with uncomplicated hand-foot-and-mouth disease or herpangina, 75 percent of hospitalized patients who survived, and 92 percent of patients who died. CONCLUSIONS: Although several enteroviruses were circulating in Taiwan during the 1998 epidemic, enterovirus 71 infection was associated with most of the serious clinical manifestations and with nearly all the deaths. Most of those who died were young, and the majority died of pulmonary edema and pulmonary hemorrhage. (+info)
Targeting myeloid leukemia with a DT(390)-mIL-3 fusion immunotoxin: ex vivo and in vivo studies in mice.
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The IL-3 receptor was expressed on a high frequency of myeloid leukemia cells and also on hematopoietic and vascular cells. We previously showed that a recombinant IL-3 fusion immunotoxin (DT(390)IL-3) expressed by splicing the murine IL-3 gene to a truncated diphtheria toxin (DT(390)) gene selectively killed IL-3R(+) expressing cells and was not uniformly toxic to uncommitted BM progenitor cells (Chan,C.-H., Blazar,B.R., Greenfield,L., Kreitman,R.J. and Vallera,D.A., 1996, Blood, 88, 1445-1456). Thus, we explored the feasibility of using DT(390)IL-3 as an anti-leukemia agent. DT(390)IL-3 was toxic when administered to mice at doses as low as 0.1 microg/day. The dose limiting toxicity appeared to be related to platelet and bleeding effects of the fusion toxin. Because of these effects, DT(390)IL-3 was studied ex vivo as a means of purging contaminating leukemia cells from BM grafts in a murine autologous BM transplantation. In this setting, as few as 1000 IL-3R-expressing, bcr/abl transformed myeloid 32Dp210 leukemia cells were lethal. An optimal purging interval of 10 nM/l for 8 h eliminated leukemia cells from 32Dp210/BM mixtures given to lethally irradiated (8 Gy) C3H/HeJ syngeneic mice. Mice given treated grafts containing BM and a lethal dose of 32Dp210 cells survived over 100 days while mice given untreated grafts did not survive (P < 0.00001). DT(390)IL-3 may prove highly useful for ex vivo purging of lethal malignant leukemia cells from autologous BM grafts. (+info)