Children with nephrotic syndrome have greater bone area but similar volumetric bone mineral density to healthy controls.

BACKGROUND: Glucocorticoid use has been associated with an increased fracture risk and reduced bone mineral density (BMD), particularly in the trabecular compartment. However the contribution of the underlying inflammatory disease process to these outcomes is poorly understood. Childhood nephrotic syndrome (NS) typically follows a relapsing-remitting course often requiring recurrent courses of glucocorticoids, but with low systemic inflammation during remission. NS therefore represents a useful clinical model to investigate the effects of glucocorticoids on BMD and bone geometry in childhood. METHODS: Children with NS were compared to age and sex matched healthy controls. Body composition and areal BMD (whole body, lumbar spine and hip) were assessed by DXA. Peripheral quantitative computed tomography (pQCT) scans were obtained at metaphyseal (4%) and diaphyseal (66%) sites of the tibia to determine volumetric BMD and bone cross-sectional geometry. Lifetime cumulative glucocorticoid exposure was calculated from medical records. RESULTS: 29 children with NS (55% male, age 10.7±3.1years) were compared to 29 healthy controls (55% male, age 11.0±3.0years). The children with NS were of similar height SDS to controls (p=0.28), but were heavier (0.65±1.28SDS vs -0.04±0.89SDS, p=0.022) and had greater body fat percentage SDS (0.31±1.01 vs -0.52±1.10, p=0.008). Tibial trabecular and cortical vBMD were similar between the two groups but bone cross-sectional area (CSA) was significantly greater in children with NS at both the metaphysis (954±234mm(2) vs 817±197mm(2), p=0.002) and diaphysis (534.9±162.7mm(2) vs 463.2±155.5mm(2), p=0.014). Endosteal and periosteal circumferences were greater in children with NS than controls (both p<0.01), resulting in reduced cortical thickness (2.4±0.7mm vs 2.8±0.7mm, p=0.018), but similar cortical CSA (p=0.22). The differences in cortical geometry were not statistically significant when weight was included as a confounding factor. There were no associations between cumulative steroid exposure, duration of NS or number of relapses and any bone parameter. CONCLUSIONS: Tibial bone CSA is increased in children with NS. We speculate that this is a compensatory response to increased body weight. Defects in trabecular BMD were not identified in this cohort of children with NS.

Microbiological aspects of the UK National Institute for Health and Clinical Excellence (NICE) guidance on urinary tract infection in children.

The publication in August 2007 of the UK National Institute for Health and Clinical Excellence (NICE) guidance on urinary tract infection in children provided a fresh and useful review of the management of this condition. However, it has also resulted in some controversy. In particular, the advice to use urgent microscopy for rapid screening of urine in children >or=3 months but <3 years of age has presented practical problems for some laboratories in staffing this service out of hours. Further discussion between microbiologists, paediatricians and primary care doctors regarding this recommendation is required. In addition, the abandoning of routine antibiotic prophylaxis following a first-time urine infection has caused some debate. The evidence around these issues is reviewed, as well as the differences in the laboratory processing and interpretation of paediatric urines compared with urine specimens from adults. General measures to reduce the risk of recurrence are also discussed. As mentioned in the NICE guidance, microbiologists should continue to emphasize the basic principles, particularly the importance of obtaining an accurate diagnosis from a well-collected and well-transported urine specimen.

Acute renal tubular dysfunction in association with Salmonella enteritidis.

A thirteen-year-old boy presented with acute renal tubular dysfunction after an infection with salmonella enteritidis. The child recovered following treatment with ciprofloxacin for a week.

Hypertension: a cause of growth impairment.

The effects of high blood pressure on growth are not fully understood and while hypertension may be associated with failure to thrive, hypertension causing failure to thrive in children is poorly documented. We describe four children presenting with failure to thrive due to hypertension consequent to various aetiologies. Control of hypertension with appropriate therapy resulted in improved growth. The exact pathogenesis of failure to thrive in hypertensive children is not known. These cases demonstrate the importance of careful measurement of blood pressure in children with failure to thrive.

Bacterial infection in children with HIV: a prospective study from Cape Town, South Africa.

Invasive bacterial infection in children infected with the human immunodeficiency virus (HIV) is common. South African data on this problem are limited. Over 1 year we prospectively studied 108 HIV-infected children hospitalized for 136 presumed infective episodes. Blood culture was positive in 24.8% of episodes. Streptococcus pneumoniae predominated (14/30 positive blood cultures); one-third of isolates showed resistance to penicillin. Acute lower respiratory tract infection accounted for 44% of clinical diagnoses, a bacterial cause being established for 23.8% of these. Age and stage of HIV infection did not influence the likelihood of a positive culture. A high proportion of presumed infective episodes requiring hospitalization of young HIV-infected children have a bacterial cause. Blood culture appears to be a useful method of obtaining the microbiological information required to focus antibiotic therapy.

Effects of long-term high-altitude hypoxia on isolated fetal ovine coronary arteries.

OBJECTIVE: To examine the effects of long-term high-altitude hypoxia on the contractile properties of isolated fetal coronary arteries. METHODS: Maximal contractile responses (T(max)) to 90 mmol/L KCl and the thromboxane A(2) mimetic U46619 were measured in proximal (PLCx) and distal left circumflex (DLCx), left anterior descending (LAD), and right coronary arterial (RCA) rings from high-altitude and control fetuses. Paired studies were conducted with and without nitric oxide synthase (NOS) inhibitors, Nomega-nitro-L-arginine and Nomega-nitro-L-arginine ester. RESULTS: In high-altitude fetuses, 90 mmol/L KCl T(max) responses in both intact and NOS-blocked rings decreased by approximately 62% in PLCx, approximately 59% in DLCx, approximately 57% in LAD, and approximately 47% in RCA (n = 9-18/group; P <.05). High-altitude vessels also exhibited decreased sensitivity to U46619. NOS blockade potentiated T(max) to U46619 in the high-altitude RCA segments and augmented T(max) to U46619 in high-altitude RCA compared with its treated control counterpart (P <. 05). CONCLUSION: These results suggest that nitric oxide influences the pharmacologic responsiveness of the RCA to U46619. Furthermore, long-term high-altitude hypoxia significantly alters the contractile capabilities of fetal coronary arteries. These observations may partially explain the maintained redistribution of cardiac output to the fetal heart during exposure to long-term high-altitude hypoxia.

Ca(2+) sensitivity of fetal coronary arteries exposed to long-term, high-altitude hypoxia.

OBJECTIVE: To determine the contribution of decreased calcium responsiveness of fetal coronary arteries to decreased contractile responses to potassium and the thromboxane A(2) analogue U46619 in these arteries after exposure to chronic hypoxemia. METHODS: Concentration-response curves to Ca(2+) in beta-escin-permeabilized left circumflex (LCx), left anterior descending (LAD), and right coronary artery (RCA) rings from high-altitude (HA) and control (CON) fetuses were measured. In a second set of beta-escin-permeabilized coronary artery rings, the effect of U46619 on Ca(2+) sensitivity was tested. RESULTS: Maximum Ca(2+)-activated force (T(max)) was decreased in HA LCx (CON 0.091+/-0.010 versus HA 0.057+/-0.006 g/cm(2); P<.05) and HA LAD (CON 0.065+/-0.012 versus HA 0.031+/-0.007 g/cm(2); P <.05). No significant difference was observed in the RCA. There was no change in the pD(2) (-log EC(50)) values between CON and HA coronary rings. The Ca(2+) sensitizing effect of U46619 on submaximal Ca(2+)-activated force was lower only in the HA LCx (CON 0.044+/-0.010 versus HA 0.023+/-0.006 g/cm(2) at 10(-5) mol/L; P<.05). CONCLUSION: These results indicate that maximum tension development in response to Ca(2+) was decreased in the HA LCx and LAD but not the RCA; however, Ca(2+) sensitivity of the contractile apparatus was unaltered in all of them. Decreased Ca(2+) responsiveness may partially explain the decreased contractile capability of fetal LCx and LAD during long-term, high-altitude intrauterine hypoxemia.

Efficacy of a chlorine dioxide-containing mouthrinse in oral malodor.

Studies have suggested that when chlorine dioxide is contained in a mouthrinse, it neutralizes volatile sulfur compounds in mouth air. The efficacy of a chlorine dioxide-containing mouthrinse in the reduction of oral malodor was evaluated in a randomized, controlled, double-blind, parallel group study of 31 men and women. Subjects with a maximum odor pleasantness score of < or = -1 (slightly unpleasant/stale) on a 7-point ordinal scale at both screening and baseline were randomized to treatment with the chlorine dioxide-containing rinse (n = 16) or distilled water (negative control) (n = 15). Oral malodor was evaluated at baseline (prerinse) and at 2, 4, 8, 24, 48, 72, and 96 hours postrinse by both a trained, previously calibrated panel of organoleptic judges and a factory-calibrated portable sulfide monitor. The sulfide monitor measured concentrations of volatile sulfur compounds in the subjects' mouth air 3 minutes after completion of the organoleptic assessment at each time point. The correlation between the organoleptic assessments and log-transformed sulfide monitor values was evaluated. With the chlorine dioxide mouthrinse, a statistically significant improvement in odor pleasantness, reduction in odor intensity, and reduction in oral volatile sulfur compound concentrations compared to the water control were evident at 2 hours postrinse and persisted through 8 hours postrinse. The mean (+/- SD) odor pleasantness improved from -1.25 +/- 0.31 at baseline to -0.73 +/- 0.33 at 2 hours postrinse in the chlorine dioxide group compared to -1.40 +/- 0.38 at baseline to -1.31 +/- 0.67 at 2 hours in the control group (P < 0.01). Odor pleasantness reached its maximum change from baseline to 0.63 +/- 0.45 at 8 hours postrinse. The mean (+/- SD) log-transformed sulfide monitor measurement decreased from 5.40 +/- 0.29 at baseline to 5.17 +/- 0.13 at 2 hours postrinse in the chlorine dioxide group, but increased from 5.47 +/- 0.40 at baseline to 5.56 +/- 0.54 at 2 hours in the control group (P < 0.01). As measured by the sulfide monitor, the mean volatile sulfur compound concentration in the chlorine dioxide group reached its minimum level at 8 hours postrinse (change from baseline in the log-transformed Halimeter measurement of -0.35 +/- 0.31). Thus, this study demonstrates that a one-time use of a chlorine dioxide-containing mouthrinse significantly improves mouth odor pleasantness, reduces mouth odor intensity, and reduces volatile sulfur compound concentrations in mouth air for at least 8 hours after use.

A randomized, clinical evaluation of the safety and efficacy of a novel oral irrigator.

PURPOSE: To evaluate the safety and efficacy of the Braun Oral-B OxyJet (MD15) Oral Irrigator when used as an adjunct to manual brushing. MATERIALS AND METHODS: 64 subjects with mild-to-moderate gingivitis entered this randomized, parallel-group, examiner-blind 8-week study. Subjects were assigned to use either the MD15 and a manual brush, or a manual brush alone. Both groups brushed twice daily; the MD15 subjects, in addition to brushing, also used the irrigator in the evening. Subjects were scored at baseline, week 4 and week 8 at up to 168 oral sites for gingival inflammation (modified gingival index), gingival bleeding (angular bleeding index), and plaque (modified plaque index). RESULTS: No adverse events related to study treatment were reported. Use of the MD15 in conjunction with manual brushing resulted in significant (P < 0.05) decreases from baseline in the plaque index at week 8, the gingival index at week 4, and the bleeding index at weeks 4 and 8. The gingival index was also decreased from baseline at week 8, but this was not statistically significant (P = 0.069). The control group also showed significant decreases from baseline for the gingival index at week 8 and the bleeding index at weeks 4 and 8, but plaque scores were not significantly reduced. Although use of the MD15 plus brushing significantly reduced plaque levels from baseline, while brushing alone did not, the difference between the two groups did not achieve statistical significance (P = 0.065). Differences between the groups with respect to the gingival and bleeding indices were also not statistically significant. It is concluded that use of the OxyJet Oral Irrigator in conjunction with manual brushing is safe, reduces plaque and improves gingival health.

Cocaine induces apoptosis in fetal myocardial cells through a mitochondria-dependent pathway.

In the present study, we examined the direct cytotoxic effects of cocaine on fetal cardiac myocytes. Cocaine treatment of cultured fetal rat (21 days) myocardial cells (FRMCs) induced a time- and concentration-dependent increase in apoptotic cells in FRMCs. Cocaine induced surface exposure of phosphatidylserine in FRMCs at 12-h treatment and increased apoptotic cells up to 96 h. Corresponding DNA fragmentation induced by cocaine in these cells was demonstrated in situ by terminal deoxynucleotidyl transferase biotin-dUTP nick end labeling assay and by electrophoresis of labeled DNA fragments, showing the characteristic apoptotic ladders. The pD(2) and maximum increase of cocaine-induced apoptosis in FRMCs were 4.3 and 3.2-fold, respectively. Both caspase-9 and caspase-3 inhibitors (Z-LEHD-FMK and Ac-DEVD-CHO, respectively) blocked cocaine-induced apoptosis. In addition, cyclosporin A inhibited cocaine-induced apoptosis in a concentration-dependent manner with an IC(50) value of 0.1 microM. The maximum of 86% inhibition was obtained with 3 microM cyclosporin A. Cocaine induced the release of cytochrome c from the mitochondria and increased its levels in the cytosol by 3.1-fold. In accordance, the level of cytochrome c in the mitochondria fraction decreased by approximately 60%. Cocaine-induced translocation of cytochrome c was inhibited by cyclosporin A. The results indicate that cocaine has a direct cytotoxic effect on fetal cardiomyocytes by inducing apoptosis in the cells. Furthermore, the release of cytochrome c from the mitochondria and its subsequent activation of caspase-9 and caspase-3 play a key role in cocaine-induced apoptosis.

Quantitative electron microscopic study of the hypoxic fetal sheep heart.

In order to determine the effects of chronic, high-altitude hypoxia on the ovine fetal heart, we exposed pregnant ewes to 3,820 m beginning at 30 days gestation. We previously showed that following approximately 110 days of hypoxia the fetal heart showed significant reduction in cardiac output (76% of control) and contractility, and elevated levels of citrate synthase and lactate dehydrogenase. To investigate ultrastructural influences on these observed physiologic changes at altitude, we hypothesized that the volume densities of myofibrils and mitochondria, and glycogen content would be reduced in the ovine fetal heart and that this may contribute to contraction and cardiac output deficits in hypoxia. Mitochondria and myofibril volume density were determined by standard point-counting techniques and glycogen content was determined by biochemical analysis. The glycogen content from the hypoxic right ventricle (4.8 +/- 0.3%) was significantly lower than in control right ventricle (6.8 +/- 0.5%) and both left ventricles (hypoxia, 7.2 +/- 0.5; control, 7.8 +/- 0. 4%). Total mitochondrial volume density was also significantly reduced following hypoxia (15.5 +/- 0.7%) compared to controls (16.9 +/- 0.4%). As is common in the ovine fetal heart, the myofibril volume density of the right ventricle from both groups was significantly higher than the left ventricle (RV, 58.6 +/- 1.6; LV 54.3 +/- 0.9%). However, it was not different between control and high altitude. In support of our hypothesis, we may speculate that deficits in the quantity of myocyte glycogen and mitochondria contribute to the observed reduction in cardiac output and contractility, despite the upregulation of citrate synthase and lactate dehydrogenase. In contrast, myofibril volume density was unchanged.

Effects of long-term, high-altitude hypoxia on the capillarity of the ovine fetal heart.

To determine the effect of chronic hypoxia on myocardial capillarity, we exposed pregnant ewes to an altitude of 3,820 m from day 30 to day 139 of gestation and compared the fetus to low-altitude (approximately 300 m) controls. We hypothesized that capillarity would increase in the hypoxic myocardium to optimize oxygen and metabolite flux to hypoxic tissues. Fetal hearts were fixed by retrograde aortic perfusion and processed for microscopy and stereological evaluation. Fiber cross-sectional area and capillary density were measured and standardized to sarcomere length. Capillary volume density and capillary diameter were measured, capillary-to-fiber ratio and capillary length density were calculated, and the capillary anisotropy coefficient was obtained from a table of known values. Capillary-to-fiber ratio, capillary volume density, and the capillary anisotropy coefficient were not different between hypoxia and control groups. Capillary diameter was significantly larger in the right compared with the left ventricle of hypoxic but not control hearts; fiber cross-sectional area tended to be larger in the right ventricle of both groups, but this was not significant. As a result of larger fiber size, capillary density and capillary length density were significantly smaller in the right ventricle of hypoxic but not control fetal hearts. Contrary to our hypothesis, the ovine fetus does not show morphological adaptation in the myocardium after approximately 109 days of high-altitude hypoxic stress.

Fetal myocardial responses to long-term hypoxemia.

In fetal sheep subjected to high altitude hypoxemia for 110 days beginning on day 30 of gestation, cardiac output was decreased 24% compared to normoxic control fetuses. This decrease was due to a 33% reduction in right ventricular output, with only a 14% reduction in left ventricular output. There were no changes in preload or heart rate, but approximately 7% of the reduction in cardiac output could be explained by an increase in arterial blood pressure (afterload). In papillary muscle isolated from long-term hypoxemic fetal hearts, maximum developed tension in response to increasing concentrations of calcium was reduced in both the right and left ventricles, but sensitivity to calcium was increased in both. This finding suggests alterations in the calcium pathway for excitation-contraction coupling in the hypoxemic fetal hearts may be responsible for the reduction in contractility. The mechanism for the decrease in contractility could not be explained by changes in sarcolemmal L-type calcium channel number or sarcoplasmic reticulum calcium release channel number. In addition, there were no changes in the calcium-induced calcium release mechanism involving the sarcoplasmic reticulum, which could explain the reduced contractility. We speculate that the decreased calcium response may be due to other factors, such as the amount of calcium stored in the sarcoplasmic reticulum, myofilament calcium sensitivity, or cellular content of myofilaments.

Oxygen dose-response curve of cardiac papillary muscle from fetal and nonpregnant adult sheep exposed to long-term, high-altitude hypoxemia.

OBJECTIVE: We tested the hypothesis that hearts of fetal and nonpregnant adult sheep exposed to long-term hypoxemia would be able to sustain higher contractile function during exposure to acute hypoxia than hearts from normoxic animals. METHODS: Pregnant and nonpregnant sheep were exposed to high altitude (3820 m) for 100 days. Right and left ventricular papillary muscle strips were obtained from fetuses and nonpregnant adults, mounted in an isolated bath system, stimulated electrically and subjected to acute hypoxia in a dose response manner. Measurements were made of maximum tension production (Tmax), maximum rate of tension development (+dT/dtmax), maximum rate of relaxation (-dT/dtmax), time to peak tension, and duration of contraction. Results were compared to papillary muscle from a normoxic group of animals. RESULTS: Baseline values (95% O2 + 5% CO2 bubbled in the bath) of Tmax and +/- dt/dtmax for each ventricle were greater in adults than fetuses in both normoxic and long-term hypoxemic groups. During hypoxia (at 40 and 20% O2) Tmax and +/- dT/dtmax, were all maintained at significantly higher values in papillary muscle from long-term hypoxemic fetuses than in papillary muscle from normoxic fetuses. Duration of contraction and time to peak tension did not differ between the normoxic and hypoxemic groups. In both ventricles of the long-term hypoxemic adult, Tmax and +/- dT/dtmax, as well as duration and time to peak tension, were significantly higher than in normoxic adults, but only at the lowest level of hypoxia (20% O2). CONCLUSIONS: Contrary to the original hypothesis, heart muscle from both fetal and adult sheep that had been exposed to long-term hypoxemia could maintain contractile function better during acute hypoxia. The responsible mechanisms are not clearly understood.

Activator calcium and myocardial contractility in fetal sheep exposed to long-term high-altitude hypoxia.

We studied myocardial contractility in fetal sheep from ewes exposed to approximately 112 days of hypoxia at high altitude (3,820 m). We measured the inotropic response to extracellular Ca2+ concentration ([Ca2+]o, 0.2-10 mM) and ryanodine (10(-10) to 10(-4) M) in isometrically contracting papillary muscles and quantified dihydropyridine (DHPR) and ryanodine (RyR) receptors. In hypoxic fetuses, curves describing the force-[Ca2+]o relationship were shifted left, and the top plateaus were decreased by approximately 35% in both left and right ventricles. In normoxic and hypoxic fetuses, ryanodine (10(-4) M) reduced maximum active tension (Tmax) to approximately 25-40% of baseline values, indicating that the sarcoplasmic reticulum was the chief source of activator Ca2+ and that Ca2+ influx alone was not sufficient to activate a contraction of normal amplitude. Hypoxia resulted in a lower Tmax in the right ventricle and a lower maximum rate of rise in the left ventricle after treatment with ryanodine. DHPR number did not change, but RyR number and the RyR/DHPR in both ventricles were higher in hypoxic fetuses. We conclude that hypoxia decreases contractility, possibly by reducing the availability of activator Ca2+. Further studies are needed to directly measure the Ca2+ current and intracellular Ca2+ transient and to examine myofilament protein and adenosinetriphosphatase activity.

Cardiac beta-adrenergic receptor function in fetal sheep exposed to long-term high-altitude hypoxemia.

In this study, we hypothesized that a reduction in beta-adrenergic receptor number or a decrease in functional coupling of the receptor to the adenylate cyclase system may be responsible for the blunted inotropic response to isoproterenol observed in fetal sheep exposed to high altitude (3,820 m) from 30 to 138-142 days gestation. We measured the contractile response to increasing doses of isoproterenol and forskolin in papillary muscles from both ventricles, estimated beta-adrenergic receptor density (Bmax) and ligand affinity (Kd) using [125I]iodocyanopindolol, and measured adenosine 3',5'-cyclic monophosphate (cAMP) levels before and after maximally stimulating doses of isoproterenol and forskolin. Left ventricular wet weight was unchanged, but right ventricular weight was 20% lower than controls. At the highest concentration of isoproterenol (10 microM), maximum active tension was 32 and 20% lower than controls in hypoxemic left and right ventricles, respectively. The contractile response to forskolin was severely attenuated in both hypoxemic ventricles. Bmax was unchanged in the left ventricle, but increased by 55% in the hypoxemic right ventricle. Kd was not different from controls in either ventricle. Basal cAMP levels were not different from controls, but isoproterenol-stimulated and forskolin-stimulated cAMP levels were 1.4- to 2-fold higher than controls in both hypoxemic ventricles. The results suggest mechanisms downstream from cAMP in the beta-adrenergic receptor pathway are responsible for the attenuated contractile responses to isoproterenol.

Abdominal aortic aneurysms in children.

Abdominal aortic aneurysms are rare in children. Causes include mycotic aneurysms, vasculitides (eg, Takayasu's arteritis), connective tissue diseases (eg, Marfan's syndrome, Ehlers-Danlos syndrome, and tuberous sclerosis) and traumatic false aneurysms. Four cases are described. Case 1 was a 12-year-old boy who presented with an acute unheralded rupture of the subdiaphragmatic aorta accompanied by lower limb paralysis and ischemia. Attempted repair failed because of extensive friability of the large arteries. Histological evaluation confirmed cystic medial necrosis despite Marfanoid phenotype. Cases 2 and 3 were boys aged 12 and 11 with Takayasu's arteritis who presented with hypertensive encephalopathy and heart failure. Although both had involvement of the origins of the renal arteries, one aneurysm was predominantly suprarenal and the other infrarenal. Currently both children are being managed successfully with antihypertensive therapy. Case 4 was a 5-year-old girl who presented with hypertension and a pulsatile abdominal mass after treatment of infective endocarditis 18 months previously. Arteriography and three-dimensional computed tomography confirmed an aneurysm (6 x 5 x 4 cm) arising from the aorta and involving the right renal artery. Aneurysmectomy, removal of a small ischemic right kidney, and Gore-Tex grafting resulted in cure of the hypertension and uneventful recovery. The present series confirms that rupture is a fatal complication, renovascular complications are common, and medical control of hypertension is an essential part of management. Management strategies need to be highly individualized, and may be successful without surgical intervention. Close clinical and ultrasound follow-up of those managed nonoperatively is essential.

Measurement of blood flow with radiolabeled microspheres in reflected mucogingival flaps in cats.

To quantify and compare blood flow in maxillary mucogingival flaps, a total of 16 cats (32 mucogingival specimens) were divided into two groups. In group I the blood flow in attached or reflected maxillary tissues were measured. In Group II the effects on blood flow were measured in reflected tissues after the injection of the following solutions: (1) saline solution; (2) 2% lidocaine plain; (3) 2% lidocaine with 1:50,000 epinephrine; (4) no injection. After an injection of 153 Gadolinium microspheres into the left ventricle of the heart, the tissues were harvested and placed in a gamma counter. Group I had a mean blood flow value of 34.4 ml/min/100 gm of tissue for the unreflected samples and 152.3 ml/min/100 gm of reflected tissue. The levels of blood flow in tissue samples in group II results were: no injection (control), 41.2 ml/min/100 gm; saline solution, 46.8 ml/min/110 gm; 2% lidocaine with 1:50,000 epinephrine, 60.6 ml/min/100 gm; and 2% lidocaine plain, 90.2 ml/min/100 gm. On the basis of these results it appears that reflection of gingival tissue and injection of 2% lidocaine plain induces increased blood flow 90 minutes postoperatively.

Pearson's syndrome presenting with Fanconi syndrome.

A case of Pearson's marrow-pancreas syndrome is presented. The dominant clinical feature was a generalized disorder of proximal tubule function with severe renal magnesium wasting. Renal and muscle biopsies were performed and showed bizarre giant mitochondria.