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Biomedical subjects

L L Sanders

Publications and source records attributed to L L Sanders.

At least 19 recordsLinked to original sources
PubMed1995

Carcinoid heart disease. Correlation of high serotonin levels with valvular abnormalities detected by cardiac catheterization and echocardiography.

BACKGROUND: Although serotonin has been postulated as an etiologic agent in the development of carcinoid heart disease, no direct evidence for different ambient serotonin levels in cardiac and noncardiac patients has been reported to date. METHODS AND RESULTS: The present study reviews our experience with 604 patients in the Duke Carcinoid Database. Nineteen patients with proven carcinoid heart disease (by cardiac catheterization and/or echocardiogram) were compared with the remaining 585 noncardiac patients in the database with regard to circulating serotonin and its principal metabolite, 5-hydroxyindole acetic acid (5-HIAA). No significant demographic differences existed between the cardiac and noncardiac groups; however, typical carcinoid syndrome symptoms (ie, flushing and diarrhea) were almost threefold more common in the cardiac group (P < .001). Compared with the noncardiac group, heart disease patients demonstrated strikingly higher (P < .0001) mean serum serotonin (9750 versus 4350 pmol/mL), plasma serotonin (1130 versus 426 pmol/mL), platelet serotonin (6240 versus 2700 pmol/mg protein), and urine 5-HIAA (219 versus 55.3 mg/24 h) levels. The spectrum of heart disease among the 19 patients showed a strong right-sided valvular predominance, with tricuspid regurgitation being the most common valvular dysfunction (92% by cardiac catheterization; 100% by echocardiogram). CONCLUSIONS: These data suggest that serotonin plays a major role in the pathogenesis of the cardiac plaque formation observed in carcinoid patients.

Carcinoid Heart Disease↗
PubMed1995

Physician attitudes about anticoagulation for nonvalvular atrial fibrillation in the elderly.

BACKGROUND: Our goal was to determine whether patient age affects a physician's reported likelihood of using anticoagulant therapy or the intensity of anticoagulant therapy for patients with nonvalvular atrial fibrillation. METHODS: We surveyed a nationwide sample of 1189 randomly selected office-based practitioners in three strata: primary care (geriatrics, internal medicine, family practice, and general practice), cardiology, and neurology. A vignette-based questionnaire was used to measure attitudes and beliefs regarding anticoagulation risks and effectiveness, barriers to anticoagulation in clinical practice, and likelihood of using anticoagulation and target intensity of anticoagulation at three patient ages (55, 65, and 75 years) for four clinical scenarios (chronic non-valvular atrial fibrillation with mild left atrial enlargement, intermittent or paroxysmal atrial fibrillation, recent-onset atrial fibrillation, and atrial fibrillation with recent [3 months] embolic stroke). RESULTS: The overall response rate was 38%. The mean likelihoods of using anticoagulation for the three ages were unequal (P < .0001) for each scenario. Most physicians were "very" or "somewhat" likely to use anticoagulant therapy for a 65-year-old with left atrial enlargement (71%), intermittent or paryoxysmal atrial fibrillation (68%), recent-onset atrial fibrillation (86%), or embolic stroke (96%). Fewer physicians were likely to use anticoagulant therapy for a 75-year-old with left atrial enlargement (63%), intermittent or paroxysmal atrial fibrillation (56%), recent-onset atrial fibrillation (80%), or embolic stroke (93%). Among physicians equally likely to use anticoagulation for 65- and 75-year-old patients, intensity of anticoagulant therapy (target international normalized ratio or prothrombin time ratio) was lower (P < .04) for the 75-year-old. CONCLUSION: Anticoagulant therapy may be less often and less intensively used for elderly patients with nonvalvular atrial fibrillation.

Aged↗
PubMed1987

Chancroid in the United States. Reestablishment of an old disease.

For 30 years, chancroid has been an uncommon and geographically localized disease in the United States; a mean of 878 cases were reported annually between 1971 and 1980. Since 1981, however, numerous outbreaks have established chancroid as an endemic disease in many additional areas and, in 1986, 3418 cases, the largest number since 1952, were reported. Cases are occurring preponderantly among men who patronize prostitutes, and infected individuals who have traveled from outbreak areas or from outside the United States are suspected of having contributed to the spread of disease. Efforts to eradicate disease in outbreak areas have been only occasionally effective and have been hampered by difficulty in locating potentially infected individuals and by travel by infected individuals. The failure to eradicate outbreaks leaves residual sources for new disease transmission into yet additional areas.

Black or African American↗
PubMed1987

Chlamydia trachomatis infections in the United States. What are they costing us?

Chlamydia trachomatis has emerged as the most common sexually transmitted bacterial pathogen in the United States and is now recognized to cause substantial morbidity. To determine the economic consequences of chlamydial infections in the United States, we analyzed data from local, state, and national sources. We estimate that C trachomatis infections cost Americans over $1.4 billion per year in direct and indirect costs. Chlamydial infections in women account for 79% of this cost, although men and infants are also affected. Three fourths of the total cost is due to sequelae of untreated, uncomplicated infections. If the current rate of chlamydial infection persists, the projected annual costs will exceed $2.18 billion by 1990. Reducing the incidence of personal suffering and heavy economic burden imposed by C trachomatis infections requires establishment and maintenance of effective prevention/control programs.

Chlamydia Infections↗
PubMed1987

Inhibitor of calmodulin and cAMP phosphodiesterase activity in BB rats.

Diabetes mellitus in humans is associated with increased plasma and tissue levels of cAMP and decreased cAMP phosphodiesterase (PDE) activity. Calmodulin (CM) is a low-molecular-weight protein essential for activation of cAMP PDE. The inhibitor (INH) is a low-molecular-weight substance that inhibits the activity of CM in multiple systems, including PDE. Spontaneously diabetic BB rats (SDR) and their nondiabetic littermates (NDR) were used in this study. Holtzman rats were rendered diabetic by streptozocin (STZ). STZ-induced diabetic rats (STZ-DR) and BB rats were studied with and without the benefit of insulin therapy. Calmodulin was assayed both by bioassay and by specific radioimmunoassay. The inhibitor was bioassayed by its ability to inhibit CM-activated PDE. Results showed that both spontaneous and STZ-induced diabetes are associated with a decrease in activity of the low-Michaelis constant (Km) cAMP PDE in the liver (39%, SDR; 70% STZ-DR). Calmodulin activity was also decreased in the livers of both animals (13%, SDR; 68%, STZ-DR). Similar data were obtained for NDRs. The inhibitor, on the other hand, was increased in the livers of untreated SDRs and STZ-DRs (155%, SDR; 125%, STZ-DR). No change was noted for NDRs. All these changes were restored toward normal after treatment with insulin. These data suggest that in diabetes the defect in the cAMP PDE-CM-INH system is demonstrated in both an environmental model, as illustrated by STZ-DRs, and a genetic model, as shown by SDRs and NDRs. The inhibitor activity, however, is not changed significantly in NDRs. We speculate that the inhibitor activity plays a role in dictating whether the genetic NDR will or will not become clinically diabetic.

3',5'-Cyclic-AMP Phosphodiesterases↗
PubMed1987

False elevation of hemoglobin A1 by hereditary persistence of fetal hemoglobin.

Measurement of glycosylated hemoglobin (HgA1) is frequently helpful in the management of patients with diabetes mellitus as it provides an index of average glucose control over the previous two to three months. The present case of a diabetic patient with a markedly increased hemoglobin A1 to 42% (normal 5.2-9.2%) with good glucose control prompted an investigation into the etiology of the increased hemoglobin A1 levels. Hemoglobin electrophoresis revealed that the patient had hereditary persistence of fetal hemoglobin. Hemoglobin F was quantitated and found to be responsible for 73% of the hemoglobin A1 determination. Hemoglobin F co-migrates with hemoglobin A1 on column chromatography and, when present in increased quantities, can falsely elevate the measured hemoglobin A1. Thus, if one utilizes the hemoglobin A1 assay to help guide management of patients with diabetes mellitus, it is important to remember that hemoglobin F can cause falsely elevated hemoglobin A1 levels.

Adult↗
PubMed1986

Treatment of sexually transmitted chlamydial infections.

Tetracycline hydrochloride, 500 mg orally four times a day for seven days, remains the treatment of choice for C trachomatis infections in men and nonpregnant women. Either erythromycin, 500 mg orally four times daily for seven days, or an equivalent dosage of another erythromycin product is an alternative treatment for patients who cannot tolerate tetracycline and for pregnant women. These two treatment regimens can be generalized to include nongonococcal urethritis and mucopurulent cervicitis. However, other treatment regimens that are effective against C trachomatis may not be effective for treating nongonococcal urethritis or mucopurulent cervicitis not caused by C trachomatis. The optimal treatment for pregnant women with C trachomatis infections and women with acute PID has not been established. Additional treatment trials with both groups of patients are needed to determine the effectiveness of antimicrobial agents in addition to those currently used, to establish the appropriate dose of each antimicrobial agent, and to clarify the appropriate duration of treatment. All individuals who are sexual partners of patients with nongonococcal urethritis, mucopurulent cervicitis, and acute PID (within the 30 days prior to onset of their symptoms or time of positive clinical evaluation findings) should be examined for sexually transmitted disease and treated promptly with a regimen effective against uncomplicated gonorrhea and chlamydial infections. Prompt treatment of sexual partners reduces the rate of treatment failure due to reinfection, reduces the transmission of infection, and reduces the frequency of occurrence of adverse sequelae of infection.

Acute Disease↗
PubMed1986

Use of dot-immunobinding and immunofluorescence assays to investigate clinically suspected cases of chancroid.

In 1984 and 1985, outbreaks of genital ulcers occurred in Florida and New York. Initial investigations for syphilis, herpes simplex, Chlamydia trachomatis, and Haemophilus ducreyi did not implicate any of these organisms as etiologic agents. From the results of dot-immunobinding assays, we found that sera from the patients had higher levels of IgM (30 [47.6%] of 63 patients) and IgG (22 [34.9%] of 63 patients) reactivities with an outer-membrane preparation from H. ducreyi strain CIP542 than with outer-membrane preparations from Haemophilus influenzae ATCC 10211 or Haemophilus parainfluenzae ATCC 7901. In contrast, sera from 35 patients in the control group did not react with any of the outer-membrane preparations (P less than .01 for both IgM and and IgG reactivity), nor did sera from eight individuals with disease caused by H. influenzae (P = .051 for IgM reactivity, P = .02 for IgG reactivity). Indirect immunofluorescence assay using a monoclonal antibody reactive with outer-membrane preparations from H. ducreyi strain CIP542 stained organisms in smears of lesion material from genital ulcers from three of six patients. These results suggested that the cause of both outbreaks of genital ulcers was H. ducreyi which was subsequently isolated in both geographic areas.

Antibodies, Bacterial↗
PubMed1981

Spontaneous diabetes mellitus in the New Zealand white rabbit: physiologic characteristics.

Spontaneous diabetes mellitus has been observed in a female New Zealand white rabbit. By inbreeding of this individual and her offspring, 39 litters comprising 157 animals have been studied and a closed colony of diabetic rabbits established. Three groups of animals can be identified. Twenty-nine (19%) have overt diabetes characterized by fasting hyperglycemia and depressed intravenous glucose stimulated serum insulin levels. This abnormality is seen between 1 and 3 yr of life. Forty-three of the animals (27%) have developed abnormal glucose disposal with normal or slight elevations in fasting serum glucose levels. Glucose stimulated insulin levels are also significantly lower in the rabbits with abnormal glucose disposal. The remaining 85 animals (54%) exhibit no apparent abnormalities of glucose metabolism. All animals with overt diabetes pass through a stage in which glucose disposal as measured by k values is less than 1.0, a value not observed in normal animals. Fasting and arginine stimulated glucagon levels were no different in 4 diabetic animals and 7 normal colony rabbits. Insulin therapy corrected the hyperglycemia in the diabetic rabbits. Insulin was withheld in 5 diabetic rabbits and serum and urinary glucose and ketones were measured for 9 days. Despite marked increases in serum and urinary glucose, only mild ketonemia was observed. The relatively late onset of diabetic symptoms, lack of obesity, severe hyperglycemia, and depressed insulin secretion without ketoacidosis make this a model with many of the characteristics of insulin responsive diabetes as seen in nonobese human adults.

Acetoacetates↗
PubMed1980

Spontaneous diabetes mellitus in the New Zealand white rabbit: preliminary morphologic characterization.

Electron microscopic studies on a closed colony of rabbits with an 18.5 per cent incidence of spontaneous onset insulin-dependent diabetes mellitus revealed that the beta-cells of the islets of Langerhans of the diabetic animals were hypergranulated. This finding contrasts with most other animal models of spontaneous diabetes mellitus which show degranulation of the beta-cells. There was no evidence of hyperplasia, insulitis, amyloid, or fibrosis of the islets by either light or electron microscopy. Correlation of our morphologic findings with physiologic data suggests a defect in insulin secretion. Rabbits with normal glucose metabolism showed a normal degree of granulation of their beta-cells. The alpha and delta cells were within normal limits in all animals. No other abnormalities associated with diabetes in humans or other animals were noted except for minimal fusion of the glomerular epithelial foot processes and mineralization of the proximal tubules and Bowman's capsules.

Animals↗
PubMed1976

Gastric emptying of hypertonic glucose in diabetes mellitus and duodenal ulcer.

Gastric emptying of hypertonic glucose liquid meals was studied in diabetes, duodenal ulcer, and hospitalized controls by means of the 10% glucose 30-minute test meal, with phenol red as nonabsorbable marker. Acid secreted into the meal was measured. Results revealed no significant difference in gastric emptying between controls and patients with duodenal ulcer and diabetes mellitus. Among diabetics, some individuals empty this meal more rapidly than normal. The results show that alterations of gastric emptying cannot account for the late peaks observed on oral glucose tolerance tests in diabetics, nor for any tendency toward reactive hypoglycemia in duodenal ulcer. They suggest that autovagotomy may occur in some diabetics.

Diabetes Mellitus↗