123rc/medical_text huggingface dataset:
Vaginal bleeding in childhood and adolescence. Vaginal bleeding in early childhood, regardless of its duration and quantity, is always of clinical importance. This article discusses the examination of the child and adolescent and reviews the various causes of vaginal bleeding in these patient groups.
A prospective clinical evaluation of autogenous vein grafts used as a nerve conduit for distal sensory nerve defects of 3 cm or less. The purpose of this study was to determine the efficacy of autogenous vein grafts as nerve grafts (AVNC) for bridging of small peripheral sensory nerve gaps as compared with direct repair and with conventional nerve grafting techniques (ANG). Patients with painful neuroma or segmental nerve injury of 3 cm were chosen as the test group. Those amenable to direct repair were classified as controls. Between 1982 to 1988, a total of 22 patients were enrolled in this study. A total of 34 nerves were repaired, 15 with a venous nerve conduit, 4 with a sural nerve graft, and 15 with direct repair. Significant symptom relief and satisfactory sensory function return were uniformly observed. The two-point discrimination measurements indicated superiority of direct repair and probably of conventional nerve grafting. However, the universally favorable patient acceptance and the return of measurable two-point discrimination indicates the effectiveness of autogenous vein grafts as nerve conduits when selectively applied to bridge a small nerve gap (less than or equal to 3 cm) on nonessential peripheral sensory nerves.
Premature alveolar bone loss in Erdheim-Chester disease. Erdheim-Chester disease is a rare histiocytosis also known as lipoid granulomatosis. Oral findings have not been reported previously to our knowledge. This case report documents evidence of oral sequelae of Erdheim-Chester disease. A patient whose course was followed for 10 years at the National Institutes of Health had premature alveolar bone resorption. He underwent full-mouth extraction at age 29 years because of severe periodontitis. Histopathologic evidence of Erdheim-Chester disease was demonstrated in the periodontal soft tissues. In the ensuring years, accelerated resorption of the residual ridges precluded the use of conventional dentures. We recommend early preventive dental management for patients with Erdheim-Chester disease.
Changes in cardiovascular homeostasis after injury are mediated by tissue damage and not haemorrhage. During treatment of the injured patient it is assumed that the cardiovascular responses follow recognized physiological principles. Studies in humans have shown that injury causes a profound suppression of arterial baroreflex function which alters the normal relationship between heart rate and blood pressure and casts doubt on this assumption. To investigate the mechanism of baroreflex suppression, we have studied the effects of the two major components of injury, blood loss and tissue damage, on baroreflex function in healthy volunteers. Baroreflex function was assessed using suction stimulation of the carotid sinus. The loss of 500 ml blood had no effect on baroreflex sensitivity. A human laboratory model of tissue injury reduced the ability of the baroreflex to compensate for a rise in blood pressure (P less than 0.05, Wilcoxon signed rank test). We conclude that tissue damage, rather than hypovolaemia, appears to mediate the effect of injury on baroreflex function in the injured. Blockade of neural signals from damaged tissue may have a role in the treatment of injury.
Malignant melanoma of the oral cavity. A case report. The oral cavity is a rare location for the development of primary malignant melanoma. Less than 2% of all malignant melanomas develop in the region. A case report is presented, illustrating the management in the site of the palate, together with a review of the relevant literature.
Can heart failure be prevented, delayed, or reversed? A review of the clinical course of chronic heart failure demonstrates that current outcomes remain highly unsatisfactory both in mortality and perhaps more important in morbidity. The extraordinary satisfactory functional responses seen in patients who undergo cardiac transplantation clearly identify the primary cause as the status of the heart itself, whatever the pathophysiologic adjustments of the neuroendocrine system, and interventions of the wide variety of drugs. Since donor hearts are unlikely to be available even from younger sufferers of these clinical syndromes, prevention must be the hallmark. Protection of the viability of myocytes, such as in acute myocarditis and acute infarction, is essential. Myocardial collagen undergoes continual synthesis, and production is greatly stimulated in the presence of hypertrophy caused by increased wall stress. It is possible that excess collagen is intimately involved with diastolic ventricular dysfunction, but that this may be a reversible process if the collagen-producing stimulus is removed. Thus reduction in wall stress and reversibility of ventricular hypertrophy appear to be promising directions. However, to limit the catastrophic effects of chronic heart failure, early recognition of the precursors of these syndromes, prevention of progression, and surgical intervention in valvular heart disease at an optimal point in time are essential.
Coronary angiographic patterns in hypertensive compared with normotensive patients. Patients in this study were assessed by coronary angiography because of classic effort angina and a positive exercise test. Of these patients, 320 had untreated primary hypertension and 320, similar in age and gender distribution, were normotensive. In all patients coronary angiography documented that at least one major epicardial branch was restricted by 50% or more. Prevalence of single- and double-vessel disease in the fourth and fifth decades of life was similar in the two populations and in both tended to decline with age. Prevalence of triple-vessel disease was also similar in the two populations in the fourth and fifth decades; in either population it rose with age and reached a peak at the seventh decade of life. The percentages of hypertensive patients in the sixth and seventh decades with triple-vessel disease was significantly (p less than 0.01) greater (40% and 50%, respectively) than the corresponding values in normotensive individuals (25% and 31%, respectively). The left main coronary artery was not significantly more involved in the high blood pressure group. Pressure was moderately and similarly raised at any age in hypertension; serum cholesterol and triglyceride levels, blood glucose, and smoking habits were comparable in the two populations. These results suggest that hypertension does not accelerate the appearance of significant coronary narrowing or multiple vessel involvement. Starting from the sixth decade, the natural age-related evolution of coronary disease seems to be aggravated in hypertensive subjects, as reflected by an augmented number of diseased vessels. This process is probably related to high blood pressure in itself; whether the severity of hypertension might also exert an influence is not deducible from this study.
Limb-body wall complex with complete absence of external genitalia after in vitro fertilization. The first case of limb-body wall complex (a combination of a body wall defect, neural tube defect, and limb abnormalities) after IVF is described. This is the third reported patient with this complex anomaly associated with complete absence of external genitalia. The possible pathogenic mechanisms are discussed.
Myocardial protein turnover in patients with coronary artery disease. Effect of branched chain amino acid infusion. The regulation of protein metabolism in the human heart has not previously been studied. In 10 postabsorptive patients with coronary artery disease, heart protein synthesis and degradation were estimated simultaneously from the extraction of intravenously infused L-[ring-2,6-3H]phenylalanine (PHE) and the dilution of its specific activity across the heart at isotopic steady state. We subsequently examined the effect of branched chain amino acid (BCAA) infusion on heart protein turnover and on the myocardial balance of amino acids and branched chain ketoacids (BCKA) in these patients. In the postabsorptive state, there was a net release of phenylalanine (arterial-cardiac venous [PHE] = -1.71 +/- 0.32 nmol/ml, P less than 0.001; balance = -116 +/- 21 nmol PHE/min, P less than 0.001), reflecting protein degradation (142 +/- 40 nmol PHE/min) in excess of synthesis (24 +/- 42 nmol PHE/min) and net myocardial protein catabolism. During BCAA infusion, protein synthesis increased to equal the degradation rate (106 +/- 24 and 106 +/- 28 nmol PHE/min, respectively) and the phenylalanine balance shifted (P = 0.01) from negative to neutral (arterial-cardiac venous [PHE] = 0.07 +/- 0.36 nmol/ml; balance = 2 +/- 25 nmol PHE/min). BCAA infusion stimulated the myocardial uptake of both BCAA (P less than 0.005) and their ketoacid conjugates (P less than 0.001) in proportion to their circulating concentrations. Net uptake of the BCAA greatly exceeded that of other essential amino acids suggesting a role for BCAA and BCKA as metabolic fuels. Plasma insulin levels, cardiac double product, coronary blood flow, and myocardial oxygen consumption were unchanged. These results demonstrate that the myocardium of postabsorptive humans is in negative protein balance and indicate a primary anabolic effect of BCAA on the human heart.
Management of aortobronchial fistula with graft replacement and omentopexy. Massive hemoptysis due to a recurrent aortobronchial fistula after repair of a thoracic aortic aneurysm developed in a 64-year-old woman. The infected aortic tissue was resected and replaced with an in situ Dacron graft covered by omentum. The patient is alive and well 15 months later.
Tuberculous psoas muscle abscess following chemoprophylaxis with isoniazid in a patient with human immunodeficiency virus infection. A 34-year-old man with human immunodeficiency virus infection and disseminated Mycobacterium avium and Mycobacterium intracellulare infection developed a right psoas muscle abscess due to Mycobacterium tuberculosis. The abscess occurred 18 months after completion of a 12-month course of chemoprophylaxis with isoniazid that was given because of a positive reaction with purified protein derivative of tuberculin. The adjacent vertebrae did not appear to be involved. The abscess was drained with a percutaneously inserted catheter, and he received standard antituberculous chemotherapy. Three weeks into therapy, a second drainage with a catheter was required. The isolation of two mycobacteria in this patient and the apparent failure of chemoprophylaxis with isoniazid are noted.
Clinical evaluation of high-frequency (ultrasonic) mechanical debridement in the surgical treatment of calcific aortic stenosis. Repair of aortic valve stenosis due to calcific degeneration may lead to hemodynamic and clinical improvement without the problems inherent with prosthetic valves. We have evaluated the use of a device capable of debriding calcium, the Cavitron ultrasonic aspirator (CUSA), as an adjunct to mechanical debridement in the repair of calcific aortic stenosis. Ten patients (five women), ages 63 to 83 years, were studied by M-mode, two-dimensional, and Doppler echocardiography before and an average of 26 (range 3 to 124) days after this procedure. The degree of calcification of the valve cusps was clearly reduced. The maximal cusp excursion increased from 0.7 +/- 0.1 cm preoperatively to 1.5 +/- 0.4 cm postoperatively (p = 0.006). The peak aortic gradient fell from 80 +/- 36 mm Hg to 28 +/- 10 mm Hg (p = 0.0007). The mean aortic gradient fell from 53 +/- 20 mm Hg to 16 +/- 5 mm Hg (p less than 0.0001). Aortic valve area calculated by the continuity equation increased from 0.6 + 0.2 cm2 to 1.6 +/- 0.6 cm2 (p = 0.0009). No patient had more than mild aortic insufficiency preoperatively. Postoperatively, color Doppler flow mapping revealed severe aortic insufficiency in two patients. Seven patients had further echocardiographic evaluation 99 (range 33 to 196) days after the procedure. These studies revealed the development of severe aortic insufficiency in an additional four patients. Four patients with severe symptomatic aortic insufficiency eventually underwent aortic valve replacement. Pathology revealed scarring and retraction of the aortic cusps. Widening of the commissures was responsible for the severe aortic insufficiency.
Antitumor activity of liposome-encapsulated doxorubicin in advanced breast cancer: phase II study. Previous studies in animals have demonstrated liposome-encapsulated doxorubicin (LED) has substantially less cardiac toxicity than free doxorubicin but retains antitumor activity. In a phase I clinical study of LED, the maximum tolerated dose was 90 mg/m2 and dose-limiting toxicity was considered to have been reached when granulocytopenia was produced. We used LED to treat 20 patients with advanced, measurable breast cancer. LED was given at doses of 60-75 mg/m2 every 3 weeks as an intravenous infusion. Regression of disease was objectively measured in nine patients; in five of these patients, complete regression of the index lesion occurred. The mean duration of the responses was 7 months. Hematologic toxicity consisted of grade 1-2 leukopenia in some patients. Gastrointestinal toxicity and mucositis were generally mild and tolerable. Alopecia occurred in all patients and usually was complete. Twelve patients received cumulative doses of LED of greater than 400 mg/m2 and were evaluated with radionuclide ventriculograms. In eight patients, the cumulative dose was greater than 500 mg/m2, and five had endomyocardial biopsies. Four of these biopsy results were Billingham grade 0, while one (cumulative LED dose, 750 mg/m2) showed grade 1 changes with mild myofibrillar loss and dilatation of the sarcoplasmic reticulum involving less than 5% of cardiac myocytes. Two patients had decreases in left ventricular ejection fraction. One of these patients had received a total dose of LED of 630 mg/m2 and had a decline of 13% in left ventricular ejection fraction, but had no clinical evidence of congestive heart failure and had a Billingham grade 0 endomyocardial biopsy.
An unusual venous anomaly of the placenta. The authors present an unusual vascular anomaly of the placenta. The placenta was very large, weighing 1,490 g. On the fetal surface, numerous dilated and tortuous vessels were observed on and under the chorionic membrane, of which three branches arose from a vein that was connected to the umbilical vein. One of them had a 5 x 2.5 cm aneurysmal dilatation, where three secondary branches arose. These venous channels were dilated and tortuous. The longest secondary branch was 133 cm in length and 1.2 cm in mean diameter and led into the placenta. Multiple, severely coiled or straight small branches arising from these vessels were also observed as vascular tangles. Some of these smaller vessels also led into the placenta. All abnormal vessels were veins. The umbilical cord was also normal except for a membranous insertion, and the placenta was unremarkable except for its large size.