123rc/medical_text huggingface dataset:
Monomicrobial nonneutrocytic bacterascites: a variant of spontaneous bacterial peritonitis. Spontaneous bacterial peritonitis is diagnosed when (a) the ascitic fluid culture is positive, (b) the ascitic fluid neutrophil count is greater than or equal to 250 cells/mm3 and (c) there is no evident intraabdominal surgically treatable source for infection. Few details are available regarding the variant of ascitic fluid infection in which the culture grows bacteria (pure growth of a single type of organism), but the neutrophil count is less than 250 cells/mm3. In this prospective study of 138 episodes of culture-positive spontaneously infected ascites detected in 105 patients, 44 (31.9%) were episodes of "monomicrobial nonneutrocytic bacterascites" compared with 94 (68.1%) episodes of spontaneous bacterial peritonitis. Seventeen patients had both types of infection. The infection-related mortality and hospitalization mortality were similar between the two groups. Patients with bacterascites appeared to have less severe liver disease. In 62% of bacterascites episodes in which a second paracentesis was performed before any treatment the fluid spontaneously became sterile without development of ascitic fluid neutrocytosis. Thirty-eight percent of patients with bacterascites (who underwent a second paracentesis before treatment was started) progressed to spontaneous bacterial peritonitis--sometimes within a few hours. The concentration of the chemoattractant C5a was not decreased in the ascitic fluid of the bacterascites patients; this excludes ascitic fluid C5a deficiency as the explanation of the lack of neutrocytosis. Monomicrobial nonneutrocytic bacterascites is a common variant of ascitic fluid infection that may resolve without treatment or may progress to spontaneous bacterial peritonitis.
Pulmonary function and cardiovascular risk factor relationships in black and in white young men and women. The CARDIA Study Pulmonary function is known to be related inversely to incidence of coronary heart disease, congestive heart failure, chronic obstructive lung disease, lung cancer, and death from all causes. Reasons for some of these associations are poorly understood. Relationships between cardiovascular disease risk factors and pulmonary function were examined in 5,115 18- to 30-year-old black and white male and female participants in the study of Coronary Artery Risk Development in Young Adults (CARDIA). Forced expiratory volume in 1 s adjusted for height (FEV1/Ht2) was significantly lower in smokers than nonsmokers and in persons who reported shortness of breath; FEV1/Ht2 was correlated positively with a history of strenuous physical activity, duration of exercise on the treadmill, and high-density lipoprotein cholesterol. It was associated negatively with skinfold thicknesses, serum triglycerides, fasting serum insulin, and the Cook Medley scale of hostility. The association between pulmonary function and heart disease risk may reflect associations with physical fitness, vigor, fatness, and lipid profiles, as well as with cigarette smoking.
Intraoperative electron beam radiation therapy for recurrent locally advanced rectal or rectosigmoid carcinoma. A multimodality approach of moderate-dose to high-dose preoperative radiation therapy, surgical resection, and intraoperative electron beam radiation therapy (IORT) has been used for patients with locally recurrent rectal or rectosigmoid carcinoma. The 5-year actuarial local control and disease-free survival for 30 patients undergoing this treatment program were 26% and 19%, respectively. The most important factor predicting a favorable outcome was complete resection with negative pathologic resection margins. The determinant local control and disease-free survival for 13 patients undergoing complete resection were 62% and 54%, respectively, whereas for 17 patients undergoing partial resection these figures were 18% and 6%, respectively. There did not appear to be a difference in local control or survival based on the original surgical resection (abdominoperineal resection versus low anterior resection). However, the likelihood of obtaining a complete resection after preoperative radiation therapy was higher in patients who had previously undergone a low anterior resection than patients undergoing prior abdominoperineal resection. For the 30 patients undergoing external beam irradiation, resection, and IORT, the most significant toxicities were soft tissue or sacral injury and pelvic neuropathy. Efforts to further improve local control are directed toward the concurrent use of chemotherapy (5-fluorouracil with and without leucovorin) as radiation dose modifiers during external beam irradiation and the use of additional postoperative radiation therapy.
Giant cell arteritis. A case with unusual neurologic manifestations and a normal sedimentation rate. Giant cell (temporal) arteritis is a serious inflammatory condition that can lead to blindness, stroke, or other adverse sequelae if not properly treated. An elevated erythrocyte sedimentation rate has traditionally been emphasized as a criterion for making this diagnosis. Delays in diagnosis and unnecessary testing may occur when a patient presents with a normal erythrocyte sedimentation rate and a clinical history consistent with this condition. We describe a patient with giant cell arteritis who presented with a normal erythrocyte sedimentation rate and who subsequently developed devastating central nervous system complications.
Morphological observations late (greater than 30 days) after clinically successful coronary balloon angioplasty. This report describes clinical, morphological, and histological findings late (1.6-24.1 months [average, 8.2 months]) after clinically successful coronary balloon angioplasty in 20 necropsied patients with coronary angioplasty restenosis. Clinical evidence of restenosis occurred in 14 (70%) of patients, including six patients with sudden coronary death. Of the 20 patients, 14 (70%) had cardiac causes of death and six (30%) had noncardiac causes of death. Two major subgroups of histological findings were observed: 1) intimal proliferation (60%) and 2) atherosclerotic plaques only. Of the eight sites with atherosclerotic plaques only, six were eccentric lesions and two were concentric lesions. No morphological evidence of previous angioplasty injury (cracks, breaks, or tears) was observed in the eight patients with atherosclerotic plaques only. Proposed mechanisms for the development of intimal proliferation involve the reaction of smooth muscle cells and platelets, whereas elastic recoil of overstretched eccentric or concentric atherosclerotic lesions represents the most likely explanation for the findings in the latter subgroup. On the basis of these morphological findings at angioplasty restenosis sites, specific treatment strategies for coronary artery balloon angioplasty restenosis are proposed.
Impaired production of tumor necrosis factor in breast cancer. Spontaneous and lipopolysaccharide (LPS)-induced production of tumor necrosis factor (TNF) by peripheral blood macrophages was investigated in breast cancer. Whereas spontaneous TNF production by macrophages derived from patients with breast cancer was comparable with the one found in healthy controls (P greater than 0.1), LPS-stimulated macrophages derived from patients in the disease-free interval as well as with metastatic breast cancer were found to produce significantly lower amounts of TNF, as compared with macrophages derived from healthy control individuals (P less than 0.0005). However, the production of TNF did not significantly differ between the two patient populations (P greater than 0.05). The impairment of LPS-induced TNF production did not depend upon such characteristics of the primary tumor as size, axillary lymph node and estrogen receptor status, or upon the fact of administration of adjuvant chemotherapy and, in patients with metastatic disease, hormone treatment. To further investigate cytokine production by macrophages, spontaneous and LPS-induced interleukin-1 (IL-1) production was investigated also. However, no difference was found between patients and controls concerning IL-1 generation. The authors thus conclude that LPS-induced TNF production was impaired in breast cancer independent of the presence of detectable metastatic disease, whereas IL-1 production remained unimpaired.
Evaluation and therapy of breakthrough bleeding in women using a triphasic oral contraceptive. This study was designed to investigate the incidence and pattern of breakthrough bleeding (BTB) in 1,259 women who were prescribed for the first time a triphasic oral contraceptive (OC, 7-7-7) and to evaluate a hypothesis of management for BTB persisting after three cycles. The new users were compared with a control group of 696 women who had used various OCs for at least 6 months. The incidence of BTB in the control group was 16.8% and in the new users was 24.9%, 17.5%, and 15.3% in the first 3 months, respectively. Breakthrough bleeding occurred late in the 7-7-7 package in 58% and early or midway through the package in 17% and 25%, respectively. We hypothesized that late-package BTB would improve if the patient was switched to a monophasic pill similar to the relatively estrogenic formulation of the beginning of the package and vice versa for early or midpackage BTB. Seventy women with BTB at 3 months were randomly given 0.5/35 or 1/35 for a further 3 months. Breakthrough bleeding was more likely (P less than 0.05) to improve in women switched to 1/35 compared with 0.5/35 regardless of where in the package BTB occurred.
The diagnosis and prognosis of autosomal dominant polycystic kidney disease. BACKGROUND. Autosomal dominant polycystic kidney disease is usually caused by a mutant gene at the PKD1 locus on the short arm of chromosome 16, but in about 4 percent of families with the disorder it is caused by unknown mutations elsewhere in the genome. The natural course of the disease in both genetic forms is not well characterized. METHODS. We studied 17 families with autosomal dominant polycystic kidney disease to compare presymptomatic diagnosis by ultrasonography with diagnosis by genetic-linkage studies and to relate clinical variation of the disease to whether the PKD1 mutation was implicated. RESULTS. In 10 families the disorder was found to cosegregate with polymorphic DNA markers flanking the PKD1 locus, in 2 families it did not, and in 5 families linkage could not be determined. In the 10 families with the PKD1 mutation, 46 percent of the members less than 30 years old who had a 50 percent risk of inheriting a mutation had renal cysts, as compared with 11 percent of the members of the two families without linkage (P less than 0.001). In the PKD1 families, all 67 diagnoses made by ultrasonography were confirmed by determination of the genotype as inferred from linkage. Forty of 48 members (83 percent) less than 30 years old who inherited the PKD1 mutation had renal cysts. All 27 members 30 years old or older who inherited the mutation had renal cysts, suggesting that the probability of a false negative diagnosis did not exceed 0.13 in this age group (P less than 0.05). The mean (+/- SE) age at the onset of end-stage renal disease among members of the PKD1 families was 56.7 +/- 1.9 years, as compared with 69.4 +/- 1.7 years among members with cysts in the families without linkage (P = 0.0025). Hypertension and renal impairment were less frequent and occurred later in the families without the PKD1 mutation. CONCLUSIONS. At present, in most persons with a 50 percent risk of autosomal dominant polycystic kidney disease, imaging techniques are the only mode of reaching a diagnosis before symptoms appear. In such persons a negative ultrasonographic study during early adult life indicates that the likelihood of inheriting a PKD1 mutation is small. In the few who inherit a non-PKD1 mutation for polycystic kidney disease, renal failure is likely to occur relatively late in life.
Electrocardiographic markers of ischemia during mental stress testing in postinfarction patients. Role of body surface mapping. In patients with coronary artery disease, radionuclide investigations have documented a high incidence of mental stress-induced myocardial ischemia in the absence of significant electrocardiographic changes and/or angina. To investigate the causes of the low electrocardiographic sensitivity, we recorded body surface maps during mental arithmetic in 22 normal volunteers and 37 postinfarction patients with residual exercise ischemia. Myocardial perfusion was studied with thallium-201 or technetium-99 (SESTAMIBI) planar scans. In 14 patients, body surface maps were also recorded during atrial pacing at the heart rate values achieved during mental stress. While taking the body surface maps, the area from J point to 80 msec after this point (ST-80) was analyzed by integral maps, difference maps, and departure maps (the difference between each patient's difference map and the mean difference map for normal subjects). The body surface mapping criteria for ischemia were a new negative area on the integral maps, a negative potential of more than 2 SD from mean normal values on the difference maps, and a negative departure index of more than 2. Scintigraphy showed asymptomatic myocardial hypoperfusion in 33 patients. Eight patients had significant ST segment depression. The ST-80 integral and difference maps identified 17 ischemic patients. Twenty-four patients presented abnormal departure maps. One patient presented ST depression and abnormal body surface maps without reversible tracer defect. In 14 of 14 patients, atrial pacing did not reproduce the body surface map abnormalities. The analyses of the other electrocardiographic variables showed that in patients with mental stress-induced perfusion defects, only changes of T apex-T offset (aT-eT) interval in Frank leads and changes of maximum negative potential value of aT-eT integral maps significantly differed from those of normal subjects. Our results confirm the low electrocardiographic sensitivity for detecting mental stress-induced myocardial hypoperfusion in postinfarction patients. ST analysis in the body surface map increases the information content of the electrocardiographic signal. T wave analysis appears to offer fewer diagnostic advantages.
Direct monitoring of capillary perfusion following normovolemic hemodilution in an experimental skin-flap model. The effects of normovolemic hemodilution on skin flap survival are studied in a recently developed skin-flap model (homozygous hairless mouse ear) in which nutritional capillary flow is monitored directly by means of intravital microscopy from the time of flap creation throughout the establishment of necrosis. Two diluting agents (dextran 60 and hydroxyethyl starch 200) are utilized. Our quantitative findings demonstrate that the amount of nonperfused tissue following flap creation in both the dextran (n = 23) and starch (n = 13) groups was significantly decreased as compared with controls (n = 19). Our qualitative observations suggest that improved hemorrheologic properties at the microcirculatory level are responsible for the observed decreased necrosis. Various mechanisms by which hemodilution may act to prevent necrosis are discussed.
The surgical pathologist's role in liver transplantation. Liver transplantation has become an option in treating a wide variety of diseases. The surgical pathologist, as a member of the transplantation team, is increasingly involved in the evaluation of allograft dysfunction. Interpretation of the liver allograft biopsy specimen requires integration of clinical history, biochemical data, and histologic patterns of a wide variety of lesions, including harvesting injury, vascular thrombosis, rejection, infection, and recurrent disease. This article reviews the varied histologic appearances of the more common forms of liver allograft injury, the contexts in which they arise, and their distinction from one another.
Nonsteroidal anti-inflammatory drugs and peptic ulcer disease. Evidence has accumulated that nonsteroidal anti-inflammatory drugs (NSAIDs) cause clinically important gastroduodenal ulcers. The pathogenesis, which involves the impairment of mucosal resistance to injury in an acid-peptic environment, is multifactorial and controversial. Ulcers caused by NSAIDs can occur either in mucosa inflamed because of infection with Helicobacter pylori or in histologically normal mucosa. The use of these drugs has been linked to an unexpectedly high incidence of ulcer complications, and a history of peptic ulcer disease is common in such cases. Nonsteroidal anti-inflammatory drugs thus appear both to exacerbate an underlying peptic diathesis and to cause de novo ulcers. The association between the use of these drugs and ulcer complications is supported by ulcer prevalence data from cross-sectional studies, and by data from case-controlled and cohort studies, and from randomized, experimental trials. Drug-induced gastric ulcers have been prevented by misoprostol, but not by H2 blocker therapy. Several therapies have been reported to promote ulcer healing despite continued use of NSAIDs, but adequate controlled trials have not been done. Small gastric and duodenal ulcers readily heal, whereas larger gastric ulcers require vigorous and prolonged therapy. The relative efficacies of various therapies in preventing ulcers, healing ulcers, or preventing complications remain to be established.
The Indian experience with hypertrophic pyloric stenosis. A study of 58 consecutive Indian infants operated for congenital hypertrophic pyloric stenosis revealed an accentuated male predominance in the incidence of the disease and far less preoperative hemetemesis as compared to that in their Western counterparts. 'Pyloric tumor' was palpable in 89% of cases. Only 34.5% of these infants were first born. Postoperative vomiting occurred in 13.8% of patients and wound sepsis was not encountered. Air contrast radiography confirmed the diagnosis in clinically doubtful cases.
Use of the variable-length intraluminal sutureless graft. From August 1987 to May 1988 we treated 4 patients with acute ascending aortic dissections with a variable-length intraluminal aortic prosthesis. This operation uses profound hypothermic circulatory arrest and represents a refinement of existing techniques. There was no mortality, and morbidity was minimal. Modifications of this technique can be used in performing proximal aortic root reconstruction with a composite valved conduit. The use of a variable-length intraluminal prosthesis and hypothermic circulatory arrest is illustrated. This is a safe and useful technique in select cases of acute ascending aortic dissection.
Localization of technetium-99m-glucarate in zones of acute cerebral injury. The potential structural similarity of technetium-99m-labeled glucaric acid (99mTc-glucarate) to that of fructose suggests that this agent may enter cells by a sugar transport system. Studies with LLC-PK1 cells demonstrated inhibition of 99mTc-glucarate uptake by fructose, confirming this potential relationship. Since anaerobic metabolism can use either glucose or fructose, we hypothesized that 99mTc-glucarate may concentrate in areas of acute ischemic injury. To test this hypothesis, 63 adult rats with middle cerebral artery (MCA) occlusion followed by reperfusion were injected with 99mTc-glucarate and in vivo and ex vivo images were acquired. Seven animals were also studied with 18FDG and high resolution PET imaging. The radionuclide images were compared to the results of triphenyl tetrazolium chloride (TTC) staining and conventional histopathology. Thirty-five rats had significant accumulation of 99mTc-glucarate and no TTC staining (indicating infarction) in the involved hemisphere. Of the remaining 28 rats with TTC staining (suggesting viability) of the involved hemisphere, 16 (57%) had 99mTc-glucarate accumulation. In the seven rats that were studied with both 99mTc-glucarate and 18FDG, 99mTc-glucarate accumulated at the center of the occluded MCA territory while 18FDG activity was decreased in this region. These results suggest that 99mTc-glucarate is a sensitive marker of acute severe cerebral injury, but its mechanism of localization is probably different from that of 18FDG.
Severity of cystic fibrosis in patients homozygous and heterozygous for delta F508 mutation. To assess the relation between genotype and severity of disease in cystic fibrosis (CF) the frequencies and extent of several features of its phenotypic expression were investigated in the 235 patients who attend the Danish CF Centre. 14 patients who attend irregularly and 3 who do not carry the delta F508 mutation at all were excluded. The case-reports of the remaining 218 patients (aged 4 months to 41 years) were carefully evaluated, and they were all analysed for the delta F508 mutation. 172 (79%) were homozygous for delta F508 and 46 (20%) were heterozygous. The mutation therefore occurs on 89% of the chromosomes analysed. There were no significant differences between the homozygous and heterozygous groups in the proportions with meconium ileus at birth, liver involvement, or chronic Pseudomonas aeruginosa infection. However, significantly more of the homozygous patients had onset of symptoms before the age of 6 months (p less than 0.025); they were significantly younger at diagnosis (p = 0.013) and centre referral (p = 0.006); they required greater pancreatic enzyme substitution (p = 0.0002) and had poorer lung function; and the calculated yearly incidence of chronic Ps aeruginosa infection and yearly mortality rates were greater than in heterozygous patients (p = 0.0001).
Studies of controlled reperfusion after ischemia. XX. Reperfusate composition: detrimental effects of initial asanguineous cardioplegic washout after acute coronary occlusion. This study tests whether initial asanguineous washout of potentially toxic substances that accumulate during ischemia improves recovery produced by blood cardioplegic reperfusion and evaluates the role of plasma versus whole blood cardioplegia. METHODS: Twenty-four dogs underwent 2 hours of occlusion of the left anterior descending coronary artery and 20 minutes of blood cardioplegic reperfusion on total vented bypass. In 13 dogs, a 5-minute infusion of either a crystalloid (n = 7) or plasma (n = 6) cardioplegic solution (containing the same pH, calcium potassium, and osmolarity as blood cardioplegia) was given immediately before reoxygenation with blood cardioplegia. Regional oxygen uptake and coronary vascular resistance were measured during controlled reperfusion, and segmental shortening (ultrasonic crystals), tissue water content, and histochemical damage (triphenyltetrazolium chloride stain) were assessed 1 hour after bypass was discontinued. RESULTS: Asanguineous cardioplegic washout before reoxygenation with blood cardioplegic solution resulted in a progressive (+42%) increase in coronary vascular resistances (from 123 to 176 units, p less than 0.05) and low oxygen utilization during 20 minutes of blood cardioplegic reperfusion (29 ml/100 gm, p less than 0.05); coronary vascular resistance remained low throughout blood cardioplegic reperfusion without washout (from 109 to 98 units), and oxygen utilization was 54 ml/100 gm (p less than 0.05). Neither plasma nor crystalloid washout restored substantial regional systolic shortening (3% systolic shortening versus 73% systolic shortening with blood cardioplegia), and asanguineous washout caused more myocardial edema (81.1% +/- 80.9% versus 79.5% water content, p less than 0.05) and produced extensive transmural triphenyltetrazolium chloride damage (48% +/- 41% versus 8% nonstaining in area at risk, p less than 0.05) than initial blood cardioplegic reperfusion. CONCLUSION: Asanguineous cardioplegic washout before blood cardioplegic reperfusion limits oxygen utilization during subsequent controlled reperfusion, restricts early recovery of systolic shortening, allows more myocardial edema, and produces extensive histochemical damage, which may be avoided by initial reoxygenation with blood cardioplegia. The red blood cells appear more important than the plasma components of blood cardioplegia.