[Fatal fulminant Epstein-Barr virus hepatitis]. / Hépatite fulminante fatale à Epstein-Barr virus.

Infectious mononucleosis is a common and benign disease. Although hepatic cytolysis is common during infectious mononucleosis, fulminant hepatitis is rare. We report an observation of a fatal fulminant hepatitis complicating a primary EBV infection in a 15 year-old male.

Effects of a combined antithrombin III and protein C supplementation in porcine acute endotoxic shock.

Antithrombin III (ATIII) and protein C (PC) are major inhibitors of the coagulation cascade and might regulate the cytokine network. We tested the possibility that a combined supplementation using these two inhibitors might have synergistic effects on sepsis-induced disseminated intravascular coagulation and shock. Hemodynamics, coagulation parameters, tumor necrosis factor (TNF) alpha, and interleukin 6 levels were measured in pigs submitted to a bolus infusion of Escherichia coli endotoxin (lipopolysaccharide). Four groups were studied: control lipopolysaccharide, ATIII (100 IU/kg), PC (50 IU/kg), and ATIII-PC (same doses). The endotoxin infusion resulted in a typical hypokinetic shock with disseminated intravascular coagulation in all animals. Compared with the control group, a significant improvement in mean arterial pressure and systemic vascular resistance was observed in the PC and ATIII-PC groups. The increase in lactate levels was almost completely blunted in the PC group. A significant lesser increase in TNFalpha levels was observed in the ATIII-PC group. No effects were seen on interleukin 6 levels. Coagulation and fibrinolysis parameters were not improved by ATIII and/or PC, except for a lesser decrease in prothrombin time in the ATIII-PC group. We conclude that in this acute endotoxic model, a combined supplementation using PC and ATIII concentrates has favorable effects on hemodynamic parameters and TNFalpha levels, independently from the anticoagulant actions of these inhibitors.

Double-blind, placebo-controlled trial of antithrombin III concentrates in septic shock with disseminated intravascular coagulation.

BACKGROUND: Septic shock is frequently complicated by a syndrome of disseminated intravascular coagulation (DIC). Numerous uncontrolled clinical studies have reported that antithrombin III (ATIII) substitution might prevent DIC and death in septic shock. METHODS: We conducted a randomized double-blind placebo-controlled trial in patients with a documented septic shock and DIC. The patients received either a placebo or ATIII (90 to 120 IU/kg in loading dose, then 90 to 120 IU/kg/d during 4 days). Administration of fresh frozen plasma, platelets, and fibrinogen concentrates was restricted to patients with hemorrhages and severe decreases in prothrombin time, platelet count, and fibrinogen levels. RESULTS: Thirty-five patients entered the study (18 placebo, 17 ATIII). Both groups were well balanced for all demographic, hemodynamic, and biologic data. Three patients were excluded before the treatment allocation code was broken. In the ATIII group, ATIII levels were rapidly corrected and remained over normal levels until day 10; sequential protein C and protein S levels were not modified. The duration of DIC was significantly reduced: in the ATIII group, 64 percent of patients were cured of DIC at day 2, and 71 percent were cured at the end of treatment vs in the placebo group, 11 percent (p < 0.01) and 33 percent (p < 0.05), respectively. In the 32 included patients, the mortality in ICU was reduced by 44 percent in the ATIII group (p = 0.22, NS). Care loads and transfusion requirements were not different. No side effect was observed. CONCLUSIONS: Mortality was reduced by 44 percent in this trial, but the difference did not reach the statistical significance. Circulating protein C and protein S levels were not modified by ATIII supplementation. High doses of ATIII concentrates significantly improved sepsis-induced DIC during septic shock. The trend toward improved survival suggests further randomized studies.

Septic shock, multiple organ failure, and disseminated intravascular coagulation. Compared patterns of antithrombin III, protein C, and protein S deficiencies.

STUDY OBJECTIVE: Our aim was to document the following in patients with septic shock and disseminated intravascular coagulation (DIC): (1) the influence of DIC in the mortality rate and the occurrence of organ failure; (2) the comparative prognostic value of initial antithrombin III (ATIII), protein C (PC), and protein S (PS) levels; and (3) the compared pattern of sequential ATIII, PC, and PS levels according to clinical outcome. DESIGN: Demographic data, criteria of severity, mortality in ICU, frequency of organ failure, hemodynamic and oxygenation parameters, and laboratory findings were compared in patients with septic shock according to the occurrence of DIC. Initial and sequential levels of ATIII (activity), PC (antigen and activity), PS (total and free), and C4b binding protein (C4bBP) were compared according to the outcome in patients with DIC. PATIENTS: Sixty patients with septic shock were studied. Forty-four entered the group DIC+; 16 entered the group DIC-. RESULTS: Simplified acute physiologic score (SAPS), frequency of acquired organ failure, blood lactate, and transaminase values were significantly higher in the group DIC+. The mortality rate reached 77 percent in group DIC+ vs 32 percent in DIC- (p less than 0.001). In patients with DIC, a fatal outcome was associated with higher bilirubin and transaminase levels, lower PaO2/FIo2 ratio, Vo2, Do2 and O2 extraction. In the group DIC+, all patients but two had severe deficiencies in ATIII and PC levels. Significant correlations were found between initial ATIII and PC levels, PC and free PS levels, and free PS and C4bBP levels. Initial ATIII levels had the best prognostic value for prediction of subsequent death. Serial measurements were consistent with a prolonged ATIII and PC deficiency with significantly different levels between survivors and nonsurvivors. CONCLUSIONS: DIC is a strong predictor of death and multiple organ failure in patients with septic shock. Sequential ATIII, PC, and PS measurements were consistent with prolonged consumption or inhibition that might account for a sustained procoagulant state and inhibition of fibrinolysis. The initial ATIII level was the best laboratory predictor of death in these patients.

Compared evolution of plasma fibronectin and angiotensin-converting enzyme levels in septic ARDS.

Serum angiotensin converting enzyme (serum ACE) levels and plasma fibronectin levels were measured daily in 46 septic patients during a ten day period. Thirty-eight patients developed ARDS; 28 survived (group 1), ten died (group 2), eight patients had no features of ARDS and survived (group 3). Sequential measurements of ACE and fibronectin levels were compared and plotted against indexes of respiratory impairment: PaO2 max Qs/Qt, static compliance and VD/VA ratio. These indexes were taken as criteria of weaning from controlled ventilation. During ARDS (groups 1 and 2), serum ACE levels decreased and were closely correlated with the severity of lung injury. Persistently decreased levels after eight days were consistent with continuing injury or lack of endothelial repair. On the other hand, plasma fibronectin levels increased throughout the study in survivors (group 1 and 3) and decreased in the group with fatal ARDS only (group 2). These results indicate that serum ACE levels might be a good index of endothelial injury and repair during ARDS and fibronectin a better index for evolution of sepsis and vital prognosis.

Angiotensin-converting enzyme in human adult respiratory distress syndrome.

Angiotensin-converting enzyme (ACE) levels, complement activation, and intravascular coagulation were studied in 36 patients with adult respiratory distress syndrome (ARDS) (17 aseptic, 19 septic), in order to investigate the possible interrelations among ACE, immunologic data, and hematologic findings. The severity of respiratory impairment was assessed with measurements of mechanical and gas exchange functional qualities of the lung. Serial measurements of ACE could be done in 14 patients during an eight-day period. During the first 24 hours, ACE levels were always normal (38 percent) or decreased (62 percent). No difference could be found between patients with septic and aseptic ARDS. Complement activation occurred in 78 percent (28/36) and used, in most cases, the classic pathway with presence of circulating immune complexes. Criteria for intravascular coagulation were present in 58 percent (21/36). No relation between coagulation, complement, and ACE could be found except for the patients with a greater respiratory impairment, who had complement activation, intravascular coagulation, and significantly lower ACE levels. In all patients together, ACE levels had no diagnostic value for aseptic cause of ARDS and a poor prognostic value. Only intravascular coagulation was linked with a higher significant mortality and a greater functional impairment. Serial measurements showed a diphasic evolution of ACE levels, with a maximum decrease between the 72nd and 96th hours and a further normalization (seventh day). The persistence of low levels seemed to be associated with evolutive sepsis or secondary aggravation and fibrosis.

Structural aspects of fish skin collagen which forms ordered arrays via liquid crystalline states.

The ability of acid-soluble type I collagen extracts from Soleidae flat fish to form ordered arrays in condensed phases has been compared with data for calf skin collagen. Liquid crystalline assemblies in vitro are optimized by preliminary treatment of the molecular population with ultrasounds. This treatment requires the stability of the fish collagen triple helicity to be controlled by X-ray diffraction and differential scanning calorimetry and the effect of sonication to be evaluated by viscosity measurements and gel electrophoresis. The collagen solution in concentrations of at least 40 mg ml(-1) showed in polarized light microscopy birefringent patterns typical of precholesteric phases indicating long-range order within the fluid collagen phase. Ultrastructural data, obtained after stabilization of the liquid crystalline collagen into a gelated matrix, showed that neutralized acid-soluble fish collagen forms cross-striated fibrils, typical of type I collagen, following sine wave-like undulations in precholesteric domains. These ordered geometries, approximating in vivo situations, give interesting mechanical properties to the material.

Myasthenia gravis and steroid-induced myopathy of the respiratory muscles.

OBJECTIVE: We report a case of corticosteroid-induced myopathy with involvement of respiratory muscles observed in a myasthenic patient. PATIENT: A 37-years-old woman, under corticosteroid treatment for two years for typical myasthenia gravis was admitted to ICU for acute myasthenic respiratory failure. Weaning from mechanical ventilation remained impossible despite 4 plasma exchanges and azathioprine. The patient exhibited a progressive 12 kg weight loss with muscular weakness and atrophy. MEASUREMENTS AND RESULTS: Peripheral and diaphragmatic electromyography as well as histological study were consistent with a steroid-induced myopathy. Discontinuation of corticosteroid treatment was followed by a rapid weight gain with general improvement and allowed weaning from mechanical ventilation with a complete recovery. CONCLUSION: This case provides evidence that corticosteroid-induced myopathy may be observed in myasthenia gravis and may involve the respiratory muscles as well as the peripheral musculature.

Intravenous nitroglycerin in acute respiratory failure of patients with chronic obstructive lung disease, secondary pulmonary hypertension and cor pulmonale.

We have studied the hemodynamic effects of an intravenous single dose of nitroglycerin in 13 patients with secondary pulmonary hypertension and Cor Pulmonale, during the acute course of respiratory failure and under assisted ventilation. We observed a significant decrease in systolic, diastolic and mean pulmonary arterial pressures, and in pulmonary resistance and systolic right ventricular work index, without any change in right or left pre-loads. The systolic arterial pressure decreased slightly, without any change in cardiac index or diastolic pressure. The arterial and mixed venous oxygen contents, and the pulmonary shunting ( Qs/Qt) were unchanged. These results suggest that nitroglycerin may be a useful therapy in patients in the acute stages of pulmonary hypertension resulting from chronic lung disease and under assisted ventilation. In addition, the lack of change in cardiac index, intrapulmonary shunting and oxygen content suggests that this decrease in pulmonary resistance is not linked with any deleterious effect in oxygen transfer.

Autonomic dysfunction in the Guillain-Barré syndrome. Hemodynamic and neurobiochemical studies.

In 12 patients suffering from the Guillain-Barré syndrome, with autonomic dysfunction, a hemodynamic study was performed and biological counts of neurotransmitter metabolites were repeatedly taken in the urine, the plasma and the lumber cerebrospinal fluid. In the course of the Guillain-Barré syndrome with autonomic dysfunction the changes in hemodynamic indices suggest a state of sympathetic hyperactivity. There is an increase in cerebrospinal neurotransmitter metabolite levels with an increase in central cathecholaminergic and serotoninergic activity. The findings point to an interference of central structures in the sympathetic hyperactivity observed.

Coagulation inhibitor substitution during sepsis.

This review presents the rationale for and main results of coagulation inhibitor substitution during experimental and human sepsis. Activation of the contact system induces activation of the classical complement pathway with generation of anaphylatoxins, of the kinins pathway and of fibrinolysis. Physiologic inhibition depends on the C1-inhibitor (C1-Inh.). Septic patients exhibit a relative deficiency of biologically active C1-Inh. Substitution with concentrations of C1-Inh has been safely performed and preliminary results are consistent with a possible beneficial effect on hypotension and vasopressor requirement in septic shock. The extrinsic pathway is the main initial coagulation process involved in sepsis-induced DIC. Endothelial and monocyte generation of tissue factor (TF) is activated by bacterial products and endotoxin. Activation of TF is counteracted by a specific tissue factor pathway inhibitor (TFPI). The potential for TFPI substitution to inhibit the activation of the coagulation cascade in sepsis requires further study. Thrombin generation is inhibited by antithrombin III (AT III) and the protein C-protein S system. During sepsis, AT III is consumed and degraded by elastase. Animal studies have shown that DIC and death were prevented by high doses of AT III concentrates. Although a significant reduction in the duration of biological symptoms of DIC has been reported in most human studies, the usefulness of AT III substitution in human sepsis is still debated. None of the studies was able to document a statistically significant reduction in mortality. Protein C is activated by thrombomodulin and, with its cofactor protein S, inhibits factors Va and VIIIa. The free level of protein S depends on the level of the C4b binding protein (C4bBP), an acute-phase complement regulatory protein. During sepsis, protein C activity is significantly reduced, either by acute consumption or by thrombomodulin down-regulation, and increased levels of plasma C4bBP inhibit protein S. Infusion of activated protein C and protein S substitution both protect animals from the lethal effects of bacteria. Combining these different coagulation inhibitors should be carefully studied before its use in septic patients is recommended.

Cefepime-induced neurotoxicity: an underestimated complication of antibiotherapy in patients with acute renal failure.

OBJECTIVES: To describe five new cases of life-threatening cefepime-induced neurotoxicity observed in a 2-year period. SETTING: A university intensive care unit. PATIENTS: Five patients recently treated with cefepime, admitted for seizures and coma. All suffered from acute renal failure, induced by sepsis and combined aminoside therapy, or by cefepime itself in one case. INTERVENTIONS: All patients underwent hemodialysis, which led to complete neurological improvement in four of them. One patient remained comatose and subsequently died. MEASUREMENTS: Blood and CSF cefepime levels were measured by high performance liquid chromatography before and after hemodialysis. CONCLUSION: The frequency of cefepime-induced neurotoxicity is probably underestimated. Monitoring of renal function and close neurological survey in treated patients should allow an early diagnosis of this complication. Urgent hemodialysis seems the best therapeutic method to obtain a rapid neurological improvement.

Effects of dental plaque antiseptic decontamination on bacterial colonization and nosocomial infections in critically ill patients.

OBJECTIVES: To document in intensive care unit (ICU) patients the effect of dental plaque antiseptic decontamination on the occurrence of plaque colonization by aerobic nosocomial pathogens and nosocomial infections. DESIGN: Single-blind randomized comparative study. SETTING: A 16-bed adult intensive care unit in a university hospital. PATIENTS: Patients consecutively admitted in the ICU with a medical condition suggesting an ICU stay of 5 days and requiring mechanical ventilation. INTERVENTIONS: After randomization, the treated group received dental plaque decontamination with 0.2% chlorhexidine gel, three times a day during the ICU stay. The control group received standard oral care. SPECIFIC MEASUREMENTS: Dental status was assessed by the Caries-Absent-Occluded index; the amount of dental plaque was assessed by a semi-quantitative plaque index. Bacterial sampling of dental plaque, nasal and tracheal aspirate, blood, and urine cultures were done on days 0, 5, 10, and every week. MAIN RESULTS: Sixty patients were included; 30 in the treated group and 30 in the control one (mean age: 51 +/- 16 years; mean Simplified Acute Physiological Score II: 35 +/- 14 points). On admission, no significant differences were found between both groups for all clinical and dental data. Compared with the control group, the nosocomial infection rate and the incidence densities related to risk exposition were significantly lower in the treated group (18 vs 33% days in the ICU and 10.7 vs 32.3% days of mechanical ventilation; P < 0.05). These results were consistent with a significant preventive effect of the antiseptic decontamination (Odds Ratio: 0.27; 95% CI: 0.09; 0.80) with a 53% relative risk reduction. There was a trend to a reduction of mortality, length of stay, and duration of mechanical ventilation. CONCLUSIONS: An antiseptic decontamination of dental plaque with a 0.2% chlorhexidine gel decreases dental bacterial colonization, and may reduce the incidence of nosocomial infections in ICU patients submitted to mechanical ventilation.

Multicentric study of monitoring alarms in the adult intensive care unit (ICU): a descriptive analysis.

OBJECTIVES: To assess the relevance of current monitoring alarms as a warning system in the adult ICU. DESIGN: Prospective, observational study. SETTINGS: Two university hospital, and three general hospital, ICUs. PATIENTS: Hundred thirty-one patients, ventilated at admission, from different shifts (morning, evening, night) combined with different stages of stay, early (0-3 days), intermediate (4-6 days) and late (> 6 days). INTERVENTIONS: Experienced nurses were asked to record the patient's characteristics and, for each alarm event, the reason, type and consequence. MEASUREMENTS AND MAIN RESULTS: The mean age of the patients included was 59.8 +/- 16.4 and SAPS1 was 15.9 +/- 7.4. We recorded 1971 h of care. The shift distribution was 78 mornings, 85 evenings and 83 nights; the stage distribution was 88 early, 78 intermediate and 80 late. There were 3188 alarms, an average of one alarm every 37 min: 23.7% were due to staff manipulation, 17.5% to technical problems and 58.8% to the patients. Alarms originated from ventilators (37.8%), cardiovascular monitors (32.7%), pulse oximeters (14.9%) and capnography (13.5%). Of the alarms, 25.8% had a consequence such as sensor repositioning, suction, modification of the therapy (drug or ventilation). Only 5.9% of the alarms led to a physician's being called. The positive predictive value of an alarm was 27% and its negative predictive value was 99%. The sensitivity was 97% and the specificity 58%. CONCLUSIONS: The study confirms that the level of monitoring in ICUs generates a great number of false-positive alarms.

Meningococcemia and purpura fulminans in adults: acute deficiencies of proteins C and S and early treatment with antithrombin III concentrates.

It has been recently suggested that an acquired deficiency of proteins C and S could contribute to the pathogenesis of meningococcemic purpura fulminans (PF) in children. Our study was designed to measure the levels of antithrombin III (AT III), protein C, and protein S during adult PF and to determine the effects of an early infusion of high doses of AT III concentrates on clinical and biological alterations of PF. We studied five consecutive adult patients with meningococcemia (type B) and PF. The levels of AT III, protein C (antigen and activity), and protein S (total and free) were measured at admission and 24 h and 1 month later. The treatment included in each case: amoxycillin, dobutamine and high doses of AT III concentrates. All patients survived and were discharged without any sequelae. At admission, biological data were consistent with severely depressed protein C and protein S levels and moderately decreased AT III levels, without any discrepancy between protein C antigen and activity. After 24 h, AT III and protein S levels were within normal ranges, whereas protein C levels were still depressed. These data are consistent with the theory of a particular imbalance in the anticoagulant systems during meningococcemic PF, contrasting with the usual findings observed during septic disseminated intravascular coagulation. The possibility must be considered that high doses of one anticoagulant (AT III concentrates) could compensate for the acute decrease in the other (protein C system).

Increased initial flow rate reduces inspiratory work of breathing during pressure support ventilation in patients with exacerbation of chronic obstructive pulmonary disease.

OBJECTIVE: To investigate whether the level of initial flow rate alters the work of breathing in chronic obstructive pulmonary disease (COPD) patients ventilated in pressure support ventilation (PSV). DESIGN: Prospective study. SETTINGS: Medical ICU in University hospital. PATIENTS: Eleven intubated COPD patients. METHODS: We modulated the initial flow rate in order to achieve seven different sequences. In each sequence, the plateau pressure was reached within a predetermined time: 0.1, 0.25, 0.50, 0.75, 1, 1.25 or 1.50 s. The more rapidly the pressure plateau was achieved, the higher was the initial flow rate. In each patient, the pressure support level was an invariable parameter. The order of the seven sequences for each patient was determined randomly. MEASUREMENTS AND RESULTS: Ten minutes after application of each initial flow rate, we measured the following parameters: inspiratory work of breathing, electromyogram (EMG) of the diaphragm (EMGdi), breathing pattern, and intrinsic positive end-expiratory pressure (PEEPi). Comparison between the means for each sequence and each variable measured was performed by two-way analysis of variance with internal comparisons between sequences by Duncan's test. The reduction of the initial flow rate induced a progressive increase in the values of the work of breathing, EMGdi, and mouth occlusion pressure (P 0.1). In contrast, the reduction of the initial flow rate did not induce any significant change in tidal volume, respiratory frequency or PEEPi. CONCLUSIONS: As the objective of PSV is to reduce the work of breathing, it seems logical to use the highest initial flow rate to induce the lowest possible work of breathing in COPD ventilated patients.

ATP-sensitive K+ channel blockade impairs O2 extraction during progressive ischemia in pig hindlimb.

Tissues maintain O2 consumption (VO2) when blood flow and O2 delivery (DO2) are decreased by better matching of blood flow to meet local cellular O2 demand, a process that increases extraction of available O2. This study tested the hypothesis that ATP-sensitive K+ channels play a significant role in the response of pig hindlimb to ischemia. We pump perfused the vascularly isolated but innervated right hindlimb of 14 anesthetized pigs with normoxic blood while measuring hindlimb DO2, VO2, perfusion pressure, and cytochrome aa3 redox state. In one-half of the pigs, the pump-perfused hindlimb was also infused with 10 micrograms.min-1.kg-1 of glibenclamide, a potent blocker of ATP-sensitive K+ channels. Control animals were infused with 5% glucose solution alone. Blood flow was then progressively reduced in both groups in 10 steps at 10-min intervals. Glibenclamide had no effect on any preischemic hindlimb or systemic measurements. Hindlimb VO2 and cytochrome aa3 redox state began to decrease at a significantly higher DO2 in glibenclamide-treated compared with control pigs. At this critical DO2, the O2 extraction ratio (VO2/DO2) was 53 +/- 4% in the glibenclamide group and 73 +/- 5% in the control group (P < 0.05). Hindlimb vascular resistance increased significantly with ischemia in the glibenclamide group but did not change in the control group. We conclude that ATP-sensitive K+ channels may be importantly involved in the vascular recruitment response that tried to meet tissue O2 needs as blood flow was progressively reduced in the pig hindlimb.

Inhibition in vivo of both infective Leishmania major and L. mexicana amazonensis mediated by a single monoclonal antibody.

Monoclonal antibodies raised against a strain of Leishmania infantum isolated in Greece were produced and tested for their protective effect in an in vivo system (in BALB/C mice). A single monoclonal antibody, IgG2b isotype, can prevent the development of two Leishmania strains in vivo: one of L. major and one of L. mexicana amazonensis. This antibody-mediated protection may be dependent on complement.

Application of an in vivo culture system for rapid demonstration of anti-Leishmania activity of monoclonal antibodies.

In mice, infection with Leishmania by the subcutaneous route becomes evident after about 2 months. This delay impedes the selection of monoclonal antibodies able to interfere with the infectiousness of the parasite. Using an in vivo culture system--intraperitoneal injection of TG 180 sarcoma cells along with promastigotes or amastigotes--it was possible to define within 15 to 20 days a monoclonal antibody preventing the development of Leishmania. Pretreatment of promastigotes and amastigotes of several Leishmania species with a monoclonal antibody raised against Leishmania infantum prevented infection equally in either system. These cross-reactions may be of importance in designing new approaches of immunotherapy.

In vivo application of intestinal pH measurement using 2',7'-bis(carboxyethyl)-5,6-carboxyfluorescein (BCECF) fluorescence imaging.

Measurement of gastrointestinal intramucosal pH (pHim) has been recognized as an important factor in the detection of hypoxia-induced dysfunctions. However, current pH measurement techniques are limited in terms of time and spatial resolutions. A major advance in accurate pH measurement was the development of the ratiometric fluorescent indicator dye, 2',7'-bis(carboxyethyl)-5,6-carboxyfluorescein (BCECF). This study aimed to set up and validate a fluorescence imaging technique to measure in vivo the intramucosal pH (pHim) of the intestine. The intestine was inserted into an optical chamber placed under a microscope. Animals were injected intravenously with the pH-sensitive fluorescent dye BCECF. Fluorescence was visualized by illuminating the intestine alternately at 490 and 470 nm. The emitted fluorescence was directed to an intensified camera. The ratio of emitted fluorescence at excitation wavelengths of 490 and 470 nm was measured, corrected and converted to pHim by constructing a calibration curve. The pHim controls were performed with a pH microelectrode and were correlated with venous blood gas sampling. Results show that pHim is determined with an accuracy of +/- 0.07 pH units and a response time of 1 min. In conclusion pHim mapping of rat intestine can be obtained by fluorescence imaging using BCECF. This technology could be easily adapted for endoscopic pH measurements.