Endoscopic sphincterotomy in a 6-month-old infant with choledocholithiasis and double gallbladder.
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to S Mendoza.
Explore the source record for details and available documents.
In 21 postmenopausal women, ages 45 to 55 years, we assessed the effects of 3 months of cyclic estrogen-progestin therapy on lipoprotein[a] (Lp[a]), lipids, lipoproteins, apolipoproteins, blood pressure, and insulin/glucose relationships. After a pretherapy baseline study, conjugated estrogens (0.625 mg for 21 days) and medroxyprogesterone acetate (5 mg last 10 days) were given to the women cyclically for 3 months, and then the study was repeated. During hormone replacement therapy, mean plasma Lp[a] fell 25% (from 20 to 15 mg/dl) (p = 0.0001), apolipoprotein B fell 14% (p = 0.01), and triglyceride fell 15% (p = 0.01), while high-density lipoprotein cholesterol (HDLC) rose 26% (p = 0.0001) and apolipoprotein A1 rose 25% (p = 0.003). The area under the insulin curve after oral glucose tolerance fell 33% (p = 0.0001), while the ratio of insulin area to glucose area fell 22% (p = 0.006). Mean systolic and diastolic blood pressure fell, respectively, 6% and 10% (p = 0.0001 for both). We speculate that the potential cardioprotective effect of estrogen-progestin therapy in postmenopausal women may be mediated through lowering Lp(a) as well as raising HDLC and apolipoprotein A1, lowering apolipoprotein B and blood pressure, and decreasing insulin resistance.
Explore the source record for details and available documents.
The toxigenic properties of Bordetella bronchiseptica strains associated with clinical atrophic rhinitis were compared using three biological assays: the guinea pig skin test, the mouse spleen atrophy and the suckling mice mortality assay. Forty one sick pigs were cultured and, in 20 of them B. bronchiseptica strains were isolated. Eighteen of the strains were toxigenic by at least one test. However, positivity did not always coincide amongst assays. This discrepancy raises the possibility of either differences in sensitivity between assays or the existence of more than one toxin.
In 98 children from 98 kindreds, 49 with and 49 without parental premature myocardial infarction (age < or = 45 y), our specific aim was to determine whether, and to what degree, lipoprotein(a) [Lp(a)] and other atherogenic lipids and lipoproteins might be overexpressed in children from premature infarction kindreds. Median Lp(a) (270 mg/L) in case boys was nearly twice that in control boys (140 mg/L) (p < or = 0.001). In a logistic regression model including age, Quetelet index (relative ponderosity), Lp(a), apo A1, apo B, triglyceride, and pubertal status, the 24 case boys had higher Lp(a) (p = 0.03), higher triglyceride (p = 0.036), and marginally lower apo A1 (p = 0.06) than the 26 control boys. Median Lp(a) in case girls (200 mg/L) was much higher than in control girls (150 mg/L) (p < or = 0.01). In a logistic regression model including age, Quetelet index, Lp(a), apo A1, apo B, triglyceride, and menarchal status, Lp(a) was higher (p = 0.02), apo B was marginally higher (p = 0.07), and apo A1 was lower (p = 0.008) in 25 case girls than in 23 control girls. Reflecting familial clustering of major lipid-lipoprotein risk factors for coronary heart disease, children from kindreds with premature parental myocardial infarction were distinguished from children from control kindreds by high Lp(a) and also had higher apo B and triglyceride and lower apo A1 levels.
394 patients with endoscopically diagnosed duodenal ulcer were randomly allocated to treatment with ranitidine 150 bid o ranitidine 300 mg bid in a prospective double-blind multicenter trial conducted in seven LatinoAmerican countries. Endoscopy at 4 weeks showed complete ulcer healing en 171 of 196 patients (87.2%) treated with ranitidine 150 mg bid and 178 of 198 (89.9%) treated with ranitidine 300 mg bid. Both treatment regimens were equally effective at rapidly reducing the incidence of ulcer-related symptoms. It is possible that higher dosage regimen of ranitidine would be useful in patients with more severe duodenal ulcer disease.
Dideoxyinosine (DDI) has been recently approved for the treatment of AIDS. In anticipation of its use in HIV-infected women during pregnancy, the transfer and metabolism of DDI by the perfused human placenta have been investigated. Transfer characteristics are those of simple diffusion: clearance is the same as that for L-glucose (transfer index of 0.98 +/- 0.09), it is equivalent in both directions across the placenta, and the transfer rate is proportional to the transplacental gradient over a very broad range (1 to 500 microM). Because of extensive placental metabolism, only about one-half of the cleared DDI (51 +/- 21%) is transferred intact to the fetal circulation. No dideoxyadenine triphosphate, the antiviral product of DDI, could be detected in the placenta following perfusion. Comparison of the pharmacological information on DDI and zidovudine (ZDV) indicates that treatment of HIV-infected women during pregnancy with DDI will expose the fetus to much less drug than if ZDV were used. DDI may therefore be less effective than ZDV in the treatment of the infected fetus. However, the uninfected fetus of an HIV-infected woman will gain by reduced exposure to a drug that is known to be toxic.
Explore the source record for details and available documents.
Hypericin, a polycyclic aromatic dianthroquinone, is a natural plant product with antiviral properties. We report here the development of a methodology for the extraction and quantitation of hypericin from plasma and biological fluids and the adaptation of a sensitive and selective method for detection of the compound by high-performance liquid chromatography. The methodology offers a rapid and specific means of monitoring drug blood levels in clinical and pharmacokinetic studies. The chromatographic procedure utilizes the substantial retentive properties of hypericin on reverse-phase media and detection by the strong visible absorbance maximum at 590 nm. Verification by the fluorescence spectral properties of hypericin in organic media can also be utilized. The assay is linear over a 3 log concentration range and hypericin is consistently recovered from murine, simian, and human plasma. The methodology was applied to assess the pharmacokinetic properties of hypericin in mice receiving a single bolus injection of 350 micrograms. A distribution half-life of 2.0 h and an elimination half-life of 38.5 h were calculated. We also discuss the limitations of direct analysis of hypericin by absorbance or fluorescence measurements.
We have evaluated the correlation between vasoactive intestinal polypeptide (VIP) plasma concentration and severity of gastroesophageal reflux in patients with Barrett's esophagus and the possible differences in the VIP values of these patients compared with healthy volunteers. We also evaluated the relation between VIP plasma concentration and lower esophageal sphincter (LES) pressure in 24 patients with Barrett's esophagus. The mean VIP plasma concentration in 14 patients with severe gastroesophageal reflux was 25.6 +/- 0.75 pg/ml, significantly higher than the mean value observed in 10 patients with moderate reflux (18.9 +/- 0.67 pg/ml) (p less than 0.01). The mean LES resting pressure was significantly lower in the group of patients with severe gastroesophageal reflux than that observed in patients with moderate reflux (3 +/- 0.64 and 10.3 +/- 0.69 mm Hg, respectively; p less than 0.01). The mean VIP plasma concentration in 11 healthy volunteers (20.6 +/- 0.65 pg/ml) was significantly lower than the mean value observed in the subgroup of patients with severe gastroesophageal reflux (p less than 0.01). VIP values in patients with moderate reflux were not significantly different from those observed in our volunteers. There was a significant correlation between LES pressure and VIP plasma level (r = -0.9253; p less than 0.01). In conclusion, it is possible that the decreased LES resting pressure observed in patients with Barrett's esophagus and severe gastroesophageal reflux may be due to impairment of the VIPergic innervation, resulting in an increased local VIP release with possible overflow to peripheral plasma.
The authors studied the effect of mitomycin C (MMC) and bromodeoxyuridine (BrdU) on the induction of chromosome aberrations on lymphocytes of four patients with Fanconi anemia (FA) and of one normal subject. A control culture and six experiments were designed to test the possible synergic effect of MMC and BrdU. Their results revealed no evidence of MMC-BrdU synergism on the induction of chromosome aberrations in FA lymphocytes. However, chromosomes showed more damage when FA cells were harvested 24 h after MMC stress than when cells were harvested shortly after treatment. This can be explained by a DNA repair defect or by a toxic effect of oxygenation of cells during the procedure.
Vasoactive intestinal polypeptide (VIP) has been postulated as a neuropeptide with inhibitory neurotransmitter activity in nonadrenergic noncholinergic pathways. Transcutaneous electric nerve stimulation (TENS) relaxes the lower esophageal sphincter in patients with achalasia. Such response is accompanied by a 30% increase in VIP concentrations in the systemic circulation. Since the sphincter of Oddi (SO) receives a very dense VIP nerve supply, we evaluate the effect of TENS on SO motor activity and on VIP plasma concentrations in patients with biliary dyskinesia and in healthy volunteers. TENS was performed with a pocket stimulator for 45 min. SO pressure and VIP levels were obtained before and after 45 min of TENS. In patients with SO dyskinesia, TENS produced a significant decrease in SO pressure from 80.1 +/- 11.9 mm Hg to 58.3 +/- 9.7 mm Hg p less than 0.01); this was accompanied by a significant increase in VIP plasma levels from 21.1 +/- 0.5 pg/ml to 32.6 +/- 1.5 pg/ml (p less than 0.01). In healthy volunteers, TENS did not produce significant changes in SO pressure. However, a significant increase in VIP plasma values was observed (p less than 0.01). No significant changes in amplitude, duration and frequency of SO phasic contractions were observed in either of the two groups evaluated. We conclude that, in patients with SO dyskinesia, TENS decreases SO basal pressure, possibly by a direct action of the released VIP in the systemic circulation. In healthy volunteers, TENS increases VIP plasma values without significant effect on SO basal pressure. These findings suggest that the response to TENS may be mediated by VIP. It is also possible that the alterations seen in patients with biliary dyskinesia may be due to impairment of the VIP nerve supply at the level of the SO.
In this study we describe in detail the characteristics of sphincter of Oddi motor function in a large group of healthy subjects. Studies were obtained in 50 healthy volunteers. The findings showed a sphincter of Oddi segment that had a basal pressure of 14.8 +/- 6.3 mm Hg (X +/- SD). Phasic contractions were superimposed on the basal pressure. They had an amplitude of 119.7 +/- 32 mm Hg, a duration of 4.7 +/- 1 sec, and a frequency of 5.7 +/- 1.2 contractions/min. In 40 subjects the propagation sequence of phasic contractions could be evaluated and were simultaneous in 53%, antegrade in 35%, and retrograde in 11% of the waves. In 20 subjects, pressure measurements done at the common bile duct sphincter waves. In 20 subjects, pressure measurements done at the common bile duct sphincter were similar to those obtained at the pancreatic duct sphincter. In 10 subjects, pressure values obtained at the common bile duct sphincter within a week were similar. Our study should help to establish standards for normal manometric values of the sphincter of Oddi and emphasizes the importance of having a healthy volunteer group from which to obtain the normal values of sphincter of Oddi motor function.
The transfer of zidovudine (AZT) across human placenta was studied using an in vitro perfusion system with independent maternal and fetal circulations. AZT is transferred toward the fetus more rapidly than L-glucose (transfer index 1.5), a water-soluble molecule smaller than AZT (267 vs. 180 Da) that passively diffuses across the placenta. The transfer rate is proportional to the concentration in the maternal perfusate over a range of 0.03-300 microM. Transfer rate in the reverse direction, toward the maternal perfusate, also exceeds that of L-glucose and fails to show saturability. These observations are consistent with simple diffusion. The partition of AZT and glucose between perfusion buffer and octanol is 1.04 and 0.013, respectively, indicating that AZT is more lipophilic and providing a reasonable explanation for the more rapid transfer. AZT is extensively metabolized by the placenta to more polar and as yet unidentified metabolites that are not released into the perfusate. The possibility that the placental accumulation of such metabolite(s) may exert an antiviral action and may also affect placental function must be considered.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
The effect of nifedipine on sphincter of Oddi (SO) motor activity was determined by endoscopic manometry. Sphincter of Oddi pressures and motor function were compared in 21 healthy volunteers and in 9 patients with SO dyskinesia. The effects of sublingual doses of 10 or 20 mg of nifedipine were compared with placebo. Neither placebo nor 10 mg of nifedipine produced any effect on SO motor activity. In healthy volunteers 20 mg of nifedipine produced a moderate but significant decrease in basal SO pressure from 12.0 to 6.7 mmHg as well as in the amplitude, duration, and frequency of phasic contractions. In patients with SO dyskinesia 20 mg of nifedipine also resulted in a significant but more profound decrease of the basal SO pressure from 47.1 to 17.3 mmHg as well as in a decrease of amplitude, duration, and frequency of the phasic contractions. Neither placebo nor 10 or 20 mg of nifedipine has any effect on the sequence of phasic contractions. In summary, nifedipine may have a possible therapeutic role in the treatment of SO dyskinesia.