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Query: UMLS:C0038454 (
stroke
)
147,016
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Anti-phospholipid syndrome, originally called anticardiolipin syndrome, is characterized by the presence of anti-phospholipid antibodies and a marked tendency to both arterial and venous thrombosis. The little information available on the implications of this syndrome for anesthesia derive from the recent description of the disease. We describe 2 patients, each with 1 of the 2 forms of antiphospholipid syndrome that have been described to date, and each needing surgery for a different reason. The first was a 24-year-old woman who was admitted to the hospital with
diarrhea
, fever and metrorrhagia in her fifth month of pregnancy. Blood tests revealed a weakly positive title of anti-cardiolipin antibodies. Steroid and antiplatelet therapy was begun. Delivery was at 35 weeks by elective cesarean with epidural anesthesia due to oligoamnios. The second patient was 52-year-old woman with a history of 13 miscarriages,
cerebrovascular accident
and deep venous thrombosis. She had been diagnosed as having systemic lupus erythematosus with anti-phospholipid syndrome and was receiving corticoid and antiplatelet therapy. She had been admitted on 2 occasions for epistaxis, purpura in the lower extremities and severe thrombocytopenia. The last condition did not respond well to immunosuppressant therapy and a splenectomy was therefore performed with the patient under general anesthesia. In both cases recovery was good in spite of the serious complications of anesthetic management.
...
PMID:[Anesthetic implications in antiphospholipid syndrome. 2 clinical cases]. 779 18
The "Health Transition" describes the medical consequences which accompany the demographic transition and development. In many Asian countries, as the infectious diseases of infancy decline, such as
diarrhea
, acute respiratory disease, measles and malaria, so too, do infant mortality rates. As a consequence of falling infant mortality rates and declines in fertility, the age pyramid has become more rectangular. No longer is nearly half of the population under the age of 15 years. Diseases of adults are beginning to become predominant: trauma, heart disease, cancer,
stroke
and diabetes. Life expectancy has increased along with costs of the health care system. As a fraction of per capita gross domestic product, health care is beginning to become a major national expense. It is ironic that the one vector-borne infectious disease likely to bridge the health transition in tropical countries is dengue. As evidenced by the experience of Singapore and Taiwan, modern housing and commercial development provide more, rather than fewer breeding places for Aedes aegypti. Greater affluence often means less compliance with mosquito control programs. Meanwhile, the dengue viruses, heeding some unknown genetic imperative, cause ever more severe disease. Modern Asian societies must count dengue as a real and enduring threat. To prevent costly hospitalizations and a sense of social disorder, effective measures must be adopted to achieve a significant reduction of Aedes aegypti populations. Sustained dengue control requires source reduction which, in turn depends upon imaginative leadership, skilled man power, legislative authority, an authentic national research program and intersectoral cooperation. A leadership role beckons for new actors in the control of Aedes aegypti: large municipalities, environmental agencies and the private sector.
...
PMID:Dengue in the health transition. 784 46
Gastrointestinal and liver disorders are often observed in high performance athletes, especially those training for the increasingly popular endurance sports including the marathon and the triathlon. The disorders often start with stress before competition or training, followed by dehydration during the event. Insufficient training is an aggravating factor as are certain environmental factors including hot climate, irregular terrain and high altitude. Athletes may also consume non-steroid anti-inflammatory drugs, for example after a minor bone lesion or joint sprain, in an attempt to maintain their highest level of performance. Gastric signs include epigastric pain known to be caused by ischaemic gastritis resulting from decreased splanchnic flow and increased vasoconstriction in the gastric mucosa. Gastrooesophageal reflux results from modifications in sphincter tone and gastric emptying. Drinking hyperosmolar liquids also plays a role. Abdominal pain,
diarrhoea
, melena and uncommonly ischaemic colitis are the main signs of colic disorders. Mesenteric ischaemia may occur due to lowered splanchnic blood supply (by as much as 80% in some cases). Mechanical trauma is another mechanism; in marathon runners the "caecal slap syndrome" is a repeated microtrauma of the caecum against a hypertrophied muscular wall. Waterborne infectious agents may also lead to colic lesions. Exertion heat
stroke
is an emergency situation which can cause multiple organ damage and usually occurs after long intense exercise, often, but not always in a hot environment. Uncompensated thermogenesis and excessive loss of water by perspiration leads to central hyperthermia and ischaemic hepatic necrosis. Fatal liver failure has been observed. More or less severe symptoms of gastrointestinal or hepatic disorders are observed in 30% of high performance athletes and the incidence may reach 40% in those who have trained insufficiently. Such disorders lead to reduced performance in 10% of these athletes.
...
PMID:[Hepato-digestive disorders in athletic practice]. 802 25
The plasma membrane Na/H exchanger plays an essential role in regulating intracellular pH and Na+ concentration and has been implicated in several pathophysiological conditions, including essential hypertension and congenital secretory
diarrhea
. Four isoforms of the Na/H exchanger encoded by separate genes have recently been identified by cDNA cloning. To map their locations in the human and rat genomes, rat isoform-specific cDNA probes were hybridized to Southern filters containing panels of somatic cell hybrids that segregate either human or rat chromosomes. The rat Nhe1 gene was assigned to Chromosome (Chr)5, extending the homology with human chromosome 1p that has previously been shown to contain the human NHE1 gene. The genes encoding the NHE-2 and NHE-4 isoforms were syntenic in the two species and assigned to rat Chr 9 and human Chr 2. A single Nhe3 gene was detected in rat and assigned to Chr 1. In contrast, although evidence to date has suggested a single human NHE3 gene on Chr 5, two NHE3 genes, NHE3A and NHE3B, were identified and assigned to Chrs 10 and 5, respectively. Interestingly, rat Chr 1 has recently been found to carry a gene controlling systolic blood pressure upon sodium loading in
stroke
-prone, spontaneously hypertensive rats. Thus, this and other evidence implicates rat Nhe3 as a possible candidate gene in this disease process.
...
PMID:Chromosomal assignment of four genes encoding Na/H exchanger isoforms in human and rat. 819 3
After DNA hybridization identified an isolate from an ill rhesus macaque (Macaca mulatta) as Arcobacter (Campylobacter) butzleri, we initiated a study to determine whether A. butzleri was associated with diarrheal disease in nonhuman primates at the Yerkes Primate Research Center. By using Campy-
CVA
medium incubated at 35 degrees C, 15 A. butzleri isolates were obtained from 14 macaques; 7 macaques were coinfected with Campylobacter coli and Campylobacter jejuni. A. butzleri was not isolated from normal feces, despite the fact that feces from 76 macaques were cultured at necropsy. Histologic evaluation of colonic specimens from three macaques from which A. butzleri had been isolated showed mild to moderately severe chronic, active colitis. Ribotype analysis of the 15 A. butzleri isolates revealed nine different strains; these data suggest that A. butzleri may be endemic in this primate population and that a point source of infection is unlikely. This is the first report of the presence of A. butzleri in juvenile and adult macaques with
diarrhea
, and it may present an opportunity to study the pathogenesis of this organism, which appears to be associated with persistent
diarrhea
in humans.
...
PMID:Arcobacter (Campylobacter) butzleri-associated diarrheal illness in a nonhuman primate population. 847 15
Endotoxemia occurs when intestinal ischemia allows bacterial lipopolysaccharide to translocate from colonic flora into the bloodstream, which triggers release of cytokines that can cause hypotension, rigors, fever, shock, and even death. Recently, blood endotoxin levels were shown to be higher in athletes needing medical attention (330 pg.ml-1) than in their competitors with similar performances (81 pg.ml-1). Though there were no data showing that these athletes had elevated core temperatures or severe illness, speculation followed that endotoxin may play a causal role in heat
stroke
. We examined the relationship between endotoxemia and mild post-exertional illness in 39 cyclists after a 100-mile ride. Thirteen cyclists had at least one of the following: orthostatic hypotension, rigors, nausea, vomiting,
diarrhea
, or syncope. Only 2/26 case-controls had any of these symptoms. Data were collected on vital signs, hemoglobin, sodium, creatine kinase, creatinine, and uric acid. Endotoxin titer was determined by chromogenic assay; tumor necrosis factor alpha (TNF-alpha) titer was determined by ELISA. One ill cyclist had an endotoxin level of 330 pg.ml-1, one control had an endotoxin level of 150 pg.ml-1, but endotoxin level was < or = 64 pg.ml-1 in all others. Comparison of pre- and post-ride data showed that controls increased creatine kinase activity (154 +/- 34 vs 561 +/- 191 IU.dl, P < 0.05), creatinine concentration (1.5 +/- 0.0 vs 1.6 +/- 0.0 mg.dl-1, P < 0.05), and uric acid concentration (5.4 +/- 0.3 vs 6.3 +/- 0.3 mg.dl-1, P < 0.05). Ill cyclists had lower serum sodium than post-ride controls (138 +/- 2 vs 142 +/- 0.6 mEq.l-1, P < 0.05), but there were no differences between groups in CK, creatinine, or uric acid. These findings suggest that endotoxemia may complicate, but does not cause mild post-exertional illness in cyclists.
...
PMID:Exercise-associated collapse in cyclists is unrelated to endotoxemia. 853 21
Ticlopidine is a thienopyridine derivative which reduces the risk of reversible ischaemia and
stroke
in patients who have previously experienced a cerebral ischaemic episode. In comparison with aspirin, ticlopidine produced a significant reduction in the risk of
stroke
in a multicentre clinical trial involving more than 3000 patients with previous transient or persistent minor ischaemia, and was superior to placebo for the prevention of
stroke
recurrence in more than 1000 patients who had experienced a major thrombotic
stroke
. The cost-utility ratio for ticlopidine in comparison with aspirin was estimated to be $US31 200 to 55,000 per quality-adjusted life-year gained.
Diarrhoea
is the most common adverse event in ticlopidine recipients (20 to 22% incidence versus about 10% with placebo), although skin rash, nausea, dyspepsia, bleeding events, abnormal liver function and haematological disturbances were also observed in clinical trials. Severe neutropenia is the most serious event: this developed in 0.85% of patients receiving ticlopidine in 2 large clinical studies (n = 4098) but resolved after treatment withdrawal. Fatal neutropenia, although rare, has been reported in some patients receiving ticlopidine. Thus, ticlopidine is effective in reducing the risk of recurrent cerebral ischaemia and
stroke
. It appears to provide a gain over aspirin for the prevention of
stroke
after reversible ischaemia, particularly during the first year of treatment (when the risk of
stroke
is greatest), although further data on its absolute relative benefit would be useful. The extent to which ticlopidine is prescribed will probably depend on individual clinicians' perception of its risk/benefit and cost-effectiveness profiles. Ticlopidine is likely to be particularly useful for
stroke
prophylaxis in patients who do not tolerate aspirin or who have an ischaemic episode during aspirin treatment, and for the prevention of
stroke
recurrence in patients who have previously experienced a major
stroke
.
...
PMID:Ticlopidine. A review of its pharmacology, clinical efficacy and tolerability in the prevention of cerebral ischaemia and stroke. 872 Jul 46
Clopidogrel is a thienopyridine that irreversibly inhibits platelet aggregation by selectively binding to adenylate cyclase-coupled ADP receptors on the platelet surface. In animal models, clopidogrel reduced the formation of both arterial and venous thrombi. After oral administration, clopidogrel is rapidly absorbed and undergoes metabolic activation in the liver. The principal circulating metabolite is SR 26334, an inactive carboxylic acid derivative. The active metabolite is not yet known. Findings of a large, well controlled study of clopidogrel versus aspirin in patients with atherosclerotic vascular disease (CAPRIE study) indicate that clopidogrel has superior efficacy in terms of prevention of ischaemic
stroke
, myocardial infarction and vascular death. Clopidogrel-treated patients experienced less frequent gastrointestinal upset, abnormal liver function and gastrointestinal haemorrhage than patients who received aspirin, but more frequent rash and
diarrhoea
. Neutropenia and thrombocytopenia occurred rarely and at similar rates in both groups.
...
PMID:Clopidogrel. 2642 34
We hypothesized that plasma nitric oxide (NO), generated via inducible NO synthase (iNOS) or endothelial constitutive NO synthase and measured via its by-products NO2- and NO3- (NO2- + NO3- = NOx) would increase and remain elevated during chronic peritoneal sepsis. We further hypothesized that treatment with aminoguanidine (AG; 50 mg/kg), a selective iNOS inhibitor, would decrease NO production and alter blood flow. Sprague Dawley rats were randomized to septic and nonseptic groups. Septic rats received an intraperitoneal cecal slurry (200 mg of cecal material/5 mL 5% dextrose-H2O/kg); control rats received sterile 5% dextrose-H2O (5 mL/kg) only. Plasma NOx and hemodynamics were measured 0, 4, 12, 24, and 48 h after sepsis or sham induction. We also examined the effect of AG, an iNOS inhibitor, on plasma NOx levels and tissue blood flow at 24 h. Septic rats uniformly displayed signs of sepsis, including lethargy, piloerection, and
diarrhea
. NOx levels were significantly elevated compared with controls at 4, 12, 24, and 48 h (p < or = .05). Septic rats also demonstrated hypotension (t = 12, 24, and 48 h) and tachycardia (t = 4, 12, 24, and 48 h). The infusion of AG (50 mg/kg intravenously for 30 min) at 24 h significantly decreased plasma NOx in septic animals. Plasma NOx concentrations returned to basal levels by 90 min after infusion of AG. In addition, blood flow studies demonstrated that AG treatment in nonseptic rats resulted in a significant decrease in blood flow to the stomach, skin, and adipose tissue, whereas AG infusion did not significantly alter the regional perfusion profile in septic animals. Furthermore, treatment with AG did not significantly alter mean arterial pressure in either group; however, nonseptic animals exhibited a decrease in
stroke
volume, and septic animals demonstrated an increase in heart rate. In contrast to the rise and fall of NOx levels in endotoxemia, this study demonstrates that the initial rise is sustained during 48 h of peritoneal sepsis. This sustained increase in NOx levels in this model correlated with the observable signs of systemic infection and may relate to enhanced iNOS activity. AG infusion demonstrated variable effects on regional tissue blood flow profiles in septic and nonseptic animals and attenuated the increase in plasma NOx levels in septic animals, an index of iNOS activity.
...
PMID:Effect of aminoguanidine on plasma nitric oxide by-products and blood flow during chronic peritoneal sepsis. 956 58
Fifteen healthy, colostrum-fed, male dairy calves, aged 2 to 7 d were used in a study to develop a
diarrhea
protocol for neonatal calves that is reliable, practical, and economical. After instrumentation and recording baseline data,
diarrhea
and dehydration were induced by administering milk replacer [16.5 mL/kg of body weight (BW), PO], sucrose (2 g/kg in a 20% aqueous solution, p.o.), spironolactone and hydrochlorothiazide (1 mg/kg, PO) every 8 h, and furosemide (2 mg/kg, i.m., q6h). Calves were administered sucrose and diuretic agents for 48 h to induce
diarrhea
and severe dehydration. Clinical changes after 48 h were severe watery
diarrhea
, severe depression, and marked dehydration (mean, 14% BW loss). Cardiac output,
stroke
volume, mean central venous pressure, plasma volume, thiocyanate space, blood pH and bicarbonate concentration, base excess, serum chloride concentration, and fetlock temperature were decreased. Plasma lactate concentration, hematocrit, and serum potassium, creatinine, phosphorus, total protein and albumin concentrations were increased. This non-infectious calf
diarrhea
protocol has a 100% response rate, while providing a consistent and predictable hypovolemic state with
diarrhea
that reflects most of the clinicopathologic changes observed in osmotic/maldigestive
diarrhea
caused by infection with rotavirus, coronavirus or cryptosporidia. Limitations of the protocol, when compared to infectious
diarrhea
models, include failure to induce a severe metabolic acidosis, absence of hyponatremia, renal instead of enteric loss of chloride, renal as well as enteric loss of free water, absence of profound clinical depression and suspected differences in the morphologic and functional effect on intestinal epithelium. Despite these differences, the sucrose/diuretic protocol should be useful in the initial screening of new treatment modalities for calf
diarrhea
. To confirm their efficacy, the most effective treatment methods should then be examined in calves with naturally-acquired
diarrhea
.
...
PMID:A reliable, practical, and economical protocol for inducing diarrhea and severe dehydration in the neonatal calf. 968 50
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