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PubMed2004

Laserinterferometric assessment of pilocarpine-induced movement of an accommodating intraocular lens: a randomized trial.

PURPOSE: To measure the axial movement of an accommodating intraocular lens (IOL) induced by ciliary muscle contraction after application of pilocarpine. DESIGN: Randomized, controlled, patient- and examiner-masked trial with intrapatient comparison. PARTICIPANTS AND CONTROLS: One hundred ten eyes of 55 patients with age-related bilateral cataract. METHODS: This study was divided into 3 parts. In the first, the accommodating IOL (1CU) was compared with a 3-piece open-loop acrylic IOL that served as the control. In the second, to assess the effect of capsule fibrosis on the potential accommodating performance of the accommodating IOL, extensive polishing of the anterior capsule with a slit cannula was compared with standard surgery. In the third, the effect of a posterior capsulorhexis was compared with that of standard surgery. Anterior chamber depth (ACD) was assessed with partial coherence interferometry, measured before and after topical application of pilocarpine 2%, and near visual acuity (VA) was evaluated 3 months after surgery. MAIN OUTCOME MEASURE: Pilocarpine-induced change in ACD. RESULTS: The accommodating IOL showed a forward movement under pilocarpine with a median amplitude of movement of -314 microm (95% confidence interval [CI]: -148 to -592), compared with the backward movement of 63 microm (95% CI: 161 to -41) for the open-loop control IOL (P = 0.001). Capsule polishing and a posterior capsulorhexis had no effect on IOL movement with the accommodating IOL. The median near VA with distance correction was 20/60. CONCLUSION: Pilocarpine induced a small but significant forward movement of the accommodating IOL. However, the amount of movement was calculated to result in a refractive change of <0.5 diopters (D) in most patients, reaching 1 D or slightly more in only single cases, with a large variability of movement. Neither polishing of the capsule bag nor a posterior capsulorhexis could enhance the accommodative ability.

Accommodation, Ocular↗
PubMed2004

Pilocarpine-induced status epilepticus in rats: lipid peroxidation level, nitrite formation, GABAergic and glutamatergic receptor alterations in the hippocampus, striatum and frontal cortex.

The aim of the study was to investigate the lipid peroxidation levels, nitrite formation, GABAergic and glutamatergic receptor densities in the hippocampus, frontal cortex and striatum of Wistar rats after seizures and status epilepticus (SE) induced by pilocarpine. The control group was treated with 0.9% saline and sacrificed 1 h after the treatment. One group of rats was administered with pilocarpine (400 mg/kg sc) and sacrificed 1 h after treatment. The result shows that pilocarpine administration and the resulting SE produced a significant increase of lipid peroxidation level in the hippocampus (46%), striatum (25%) and frontal cortex (21%). In nitrite formation, increases of 49%, 49% and 75% in hippocampus, striatum and frontal cortex, respectively, was observed. Pilocarpine treatment induced down-regulation of GABAergic receptors in the hippocampus (38%), striatum (15%) and frontal cortex (11%). However, with regard to glutamatergic receptor densities, increases in the hippocampus (11%), striatum (17%) and frontal cortex (14%) was observed during the observation period. These results show a direct evidence of lipid peroxidation and nitrite formation during seizure activity that could be responsible for the GABAergic and glutamatergic receptor concentration changes during the establishment of SE induced by pilocarpine.

Animals↗
PubMed2005

Antioxidant effect of nimodipine in young rats after pilocarpine-induced seizures.

Nimodipine (ND) is a centrally active calcium antagonist that blocks the voltage-dependent L-type channels. Its antiepileptic properties have been proved in various animal models, including pilocarpine-induced seizures in adult rats. In order to investigate protective effects of the ND (10 (ND10) and 30 mg/kg (ND30), i.p.), young male rats (21-day-old) received ND injections before pilocarpine administration (400 mg/kg, s.c., pilocarpine group (P400)). The pretreatment with ND10 and ND30 prolonged the latencies of seizures and death on this seizure model. ND pretreatment in two doses decreased the levels of lipid peroxidation when compared to pilocarpine group. The P400 administration increased the striatal catalase activity. However, the administration of ND, in dose of 30 mg/kg, 30 min before pilocarpine, preserved catalase activity in normal levels. On the other hand, no change was detected in the animals treated with the dose of 10 mg/kg. Our results confirm the neuroprotective effect of ND on the seizures in young rats, suggesting that this drug acts positively on lipid peroxidation. Our observations shows that nimodipine cannot induces these effects via blockade of Ca(2+)-channel.

Animals↗
PubMed2001

The effect of pilocarpine on salivary constituents in patients with chronic graft-versus-host disease.

Chronic graft-versus-host disease (cGVHD) is a complex clinical entity with various target organs, including the salivary glands. Oral pilocarpine (Salagen(R)), 30 mg/day, can ameliorate cGVHD-induced xerostomia and improve the flow rate from the major salivary glands. The purpose here was to evaluate the effect of this drug at 30 mg/day on salivary biochemical and immunological composition in cGVHD patients. Significantly higher concentrations of salivary sodium (Na), magnesium (Mg), total protein, albumin, epidermal growth factor (EGF) and total IgG, accompanied by a concomitant increase in total IgA which did not reach significance, were observed in cGVHD patients in comparison with controls, in both resting and stimulated conditions (p < 0.05), while salivary potassium, calcium and phosphate were not altered. Two weeks of oral pilocarpine, at 30 mg/day, resulted in normalization of the altered salivary biochemical and immunological composition in the cGVHD patients. Oral pilocarpine was able to reduce and normalise the elevated Na, Mg, total protein, albumin, EGF, IgG and IgA concentrations in both resting and stimulated conditions. The ability of oral pilocarpine to normalise and reverse the salivary biochemical and immunological alterations induced by cGVHD parallels its known stimulatory effect on salivary flow rates. As the biochemical and immunological composition of saliva provides its protective antimicrobial characteristics, the ability of pilocarpine to abrogate cGVHD salivary gland abnormalities may be of clinical significance.

Administration, Oral↗
PubMed2003

Neuronal and glial pathological changes during epileptogenesis in the mouse pilocarpine model.

The rodent pilocarpine model of epilepsy exhibits hippocampal sclerosis and spontaneous seizures and thus resembles human temporal lobe epilepsy. Use of the many available mouse mutants to study this epilepsy model would benefit from a detailed neuropathology study. To identify new features of epileptogenesis, we characterized glial and neuronal pathologies after pilocarpine-induced status epilepticus (SE) in CF1 and C57BL/6 mice focusing on the hippocampus. All CF1 mice showed spontaneous seizures by 17-27 days after SE. By 6 h there was virtually complete loss of hilar neurons, but the extent of pyramidal cell death varied considerably among mice. In the mossy fiber pathway, neuropeptide Y (NPY) was persistently upregulated beginning 1 day after SE; NPY immunoreactivity in the supragranular layer after 31 days indicated mossy fiber sprouting. beta2 microglobulin-positive activated microglia, normally absent in brains without SE, became abundant over 3-31 days in regions of neuronal loss, including the hippocampus and the amygdala. Astrogliosis developed after 10 days in damaged areas. Amyloid precursor protein immunoreactivity in the thalamus at 10 days suggested delayed axonal degeneration. The mortality after pilocarpine injection was very high in C57BL/6 mice from Jackson Laboratories but not those from Charles River, suggesting that mutant mice in the C57BL/6(JAX) strain will be difficult to study in the pilocarpine model, although their neuropathology was similar to CF1 mice. Major neuropathological changes not previously studied in the rodent pilocarpine model include widespread microglial activation, delayed thalamic axonal death, and persistent NPY upregulation in mossy fibers, together revealing extensive and persistent glial as well as neuronal pathology.

Amyloid beta-Protein Precursor↗
PubMed1985

Effect of pilocarpine in treatment of intraocular pressure elevation following neodymium: YAG laser posterior capsulotomy.

A prospective study was conducted in 30 eyes of 30 patients to determine if pilocarpine would prevent increased intraocular pressure following Q-switched neodymium (Nd):YAG laser posterior capsulotomy. Fifteen eyes were given pilocarpine 4%, immediately following laser therapy and every hour until bedtime. Fifteen eyes served as untreated controls. Our results show that without prophylactic therapy, 10 of 15 eyes (67%) had a post-laser intraocular pressure (IOP) elevation of greater than 10 mmHg, while only one of 15 (6.6%) of the pilocarpine-treated eyes had a rise of that magnitude. The facility of outflow was reduced by 42% in the untreated eyes in contrast to an increase of 3% in those eyes treated with pilocarpine. Thus, pilocarpine 4% is effective in reducing the incidence and magnitude of elevated IOP following Nd:YAG posterior capsulotomy.

Cataract Extraction↗
PubMed2000

Lithium plus pilocarpine induced status epilepticus--biochemical changes.

The aim of the study was to investigate the changes in biochemical mechanisms facilitating cellular damages in the lithium plus pilocarpine treatment and the resulting status epilepticus. The whole brain free fatty acid (FFA) level as well as the activities of superoxide dismutase (SOD), glutathione peroxidase (GPX), glutamate dehydrogenase, aspartate-aminotransferase (AST), alanine-aminotransferase, gamma-glutamoyl transferase, alkaline phosphatase (ALP), lactate dehydrogenase (LDH) and creatine kinase in the frontal cortex, cerebellum, hippocampus and pons-medulla region of Hannover-Wistar rats were determined. The control group was intact with no previous experimental history. LiCl (125 mg/kg i.p.) was injected 20 h prior to pilocarpine (30 mg/kg i.p.) and the treated rats were sacrificed 1 or 2 1/2 h after pilocarpine administration. The results show that lithium plus pilocarpine administration and the resulting status epilepticus produced the significant increase of the brain FFA content. Decreased GPX activities were detected in the frontal cortex, cerebellum and hippocampus of the treated rats without the accompanying decrease of SOD activity. Increased AST and LDH activities were observed in the frontal cortex, increased soluble ALP activities in the frontal cortex and pons-medulla region whereas the increased activity of membrane bound ALP was detected in the hippocampus of the rats with status epilepticus. Activities of the other analysed enzymes did not change in the examined brain regions. The presented data indicate clear regional differences of biochemical changes caused by lithium plus pilocarpine treatment and the resulting status epilepticus, frontal cortex being the most affected site.

Animals↗
PubMedDate not supplied

Effects of age on pilocarpine-induced c-fos expression in rat hippocampus and cortex.

The effect of age on pilocarpine-induced expression of the immediate-early gene c-fos was examined in the hippocampus and cortex of Long-Evans rats. Rats were treated with either pilocarpine (25 mg/kg) or saline, and sacrificed 90 min. following injection. The level of c-fos mRNA and Fos-like protein expression was determined using in situ hybridization histochemistry, and immunocytochemistry, respectively. In saline-treated animals, comparable levels of c-fos mRNA and Fos-like protein were observed in the hippocampus and cortical regions of young (6 month) and aged (24-26 months) rats. The expression of Fos-like protein following pilocarpine treatment was increased, however, in frontal, retrosplenial, and cingulate cortex of aged compared to young rats. In frontal and retrosplenial cortex, the changes in Fos-like protein were accompanied by changes in c-fos mRNA expression. In contrast, no age difference was detected in the hippocampus or parietal cortex of pilocarpine-treated rats. These regionally-specific age differences in response to pilocarpine administration suggest that mechanisms localized to those areas play an important role in determining the response to cholinergic stimulation mediated through post-synaptic muscarinic receptors.

Aging↗
PubMed2000

Blockade of pilocarpine-induced cerebellar phosphoinositide hydrolysis with metabotropic glutamate antagonists: evidence for an indirect control of granule cell glutamate release by muscarinic agonists.

The ability in vivo of the muscarinic agonist, pilocarpine, to increase phosphoinositol (PI) hydrolysis in lithium pretreated rats was investigated by measuring the accumulation of [(3)H]inositol phosphates (IP). As expected, 20 mg/kg s.c. pilocarpine, a muscarinic agonist, increased PI hydrolysis in the striatum, frontal cortex and hippocampus. Somewhat surprisingly, an increase in IP was also found in the cerebellar homogenates. In all four tissues the pilocarpine-induced effect could be completely inhibited by pretreatment with the muscarinic antagonist scopolamine (1.2 mg/kg i. p.). It was also found that the cerebellar but not the hippocampal pilocarpine-induced rise in PI hydrolysis could be blocked by the metabotropic glutamate (mGlu) receptor antagonist, LY341495 (100 nmol, i.c.v.). The same dose of LY341495 was found to also block both the cerebellar and hippocampal increase in IP formed by stimulation with the group I mGlu receptor agonist 3, 5-dihydroxyphenylglycine (1 micromol, i.c.v.). Given this data and the current information on the distribution of muscarinic and mGlu receptors in the cerebellum, it is suggested that these results may be a reflection of pilocarpine acting at M(2) receptors to indirectly increase glutamate release from parallel fibers by inhibition of gamma-aminobutyric acid-releasing Golgi cells.

Amino Acids↗
PubMed2000

Lipid peroxidation in hippocampus early and late after status epilepticus induced by pilocarpine or kainic acid in Wistar rats.

Oxidative stress has been implicated in a variety of acute and chronic neurologic conditions, including epilepsy. Both the kainic acid and pilocarpine are useful models of temporal lobe epilepsy in rodents. As an index of lipid peroxidation the level thiobarbituric acid reactive substances (TBARS) was measured after the status epileticus induced by pilocarpine or kainic acid. In hippocampus there was a slight enhancement in the TBARS levels measured 12-14 h after the end of status epileticus induced by pilocarpine and kainic acid. The TBARS levels in pilocarpine treated animals was significantly decreased late after status epileticus and in kainic acid model the TBARS returned to basal levels. These results indicating a putative role of reactive oxygen species in kainic acid and pilocarpine induced epilepsy.

Animals↗
PubMed2000

Prolonged effect of liposomes encapsulating pilocarpine HCl in normal and glaucomatous rabbits.

The possibility of using liposomes as an ophthalmic drug delivery carrier for the lipophilic drug, pilocarpine HCl, was investigated on the eyes of normal and glaucomatous pigmented rabbits. The intraocular pressure (IOP) of rabbits was measured, using a Shi&emptyv;tz tonometer, as a function of time after topical administration with free drug, neutral and negatively charged multilamellar vesicles (MLVs) encapsulating pilocarpine HCl. The results showed that administration with neutral MLVs displayed the most prolonged effect with respect to negatively charged MLVs and free drug. The efficiency of MLVs encapsulating pilocarpine HCl, measured using spectrophotometric technique, was found to be 96% in our modified preparations. The storage stability of MLVs encapsulating pilocarpine HCl was investigated by measuring phase transition and size distribution using light scattering technique. The results show that liposomes encapsulating pilocarpine HCl have kept their integrity and physicochemical properties for at least 15 months, which makes them suitable for commercial use.

1,2-Dipalmitoylphosphatidylcholine↗
PubMed2001

Expression of metabotropic glutamate receptor 1alpha in the hippocampus of rat pilocarpine model of status epilepticus.

The expression of metabotropic glutamate receptor 1alpha was studied in the rat hippocampus after pilocarpine-induced status epilepticus by Western blot and immunocytochemistry at both light and electron microscopic levels. At 1 day after pilocarpine-induced status epilepticus, there was marked decrease in metabotropic glutamate receptor 1alpha immunoreactivity at the border between stratum oriens and alveus in CA1 and CA3, and in the hilus of dentate gyrus. Between 3 and 31 days after pilocarpine-induced status epilepticus, metabotropic glutamate receptor 1alpha-immunoreactive dendrites and cell bodies in the border between stratum oriens and alveus gradually reappeared. Upregulation of metabotropic glutamate receptor 1alpha, however, was observed in the stratum oriens of CA1 at day 1, but returned to baseline by day 7. By electron microscopy, the metabotropic glutamate receptor 1alpha-immunoreactive product was demonstrated only in the post-synaptic elements in the border between the stratum oriens and alveus of CA1 and the hilus of the dentate gyrus in both control and experimental rats. At 1 day after pilocarpine-induced status epilepticus, metabotropic glutamate receptor 1alpha-immunoreactive degenerating neurons were identified in the border between stratum oriens and alveus of CA1 and the hilus of the dentate gyrus. At 7 and 31 days, many degenerating axons were also found. Present results suggest that excitoneurotoxicity mediated through post-synaptic metabotropic glutamate receptor 1alpha may be involved in degeneration and death of interneurons in the hilus of dentate gyrus, and the border between stratum oriens and alveus of CA1 in the early stage after pilocarpine-induced status epilepticus.

Animals↗
PubMed1996

Pilot study of controlled-release pilocarpine in normal subjects.

OBJECTIVES: Current systemic treatments with sialogogues for patients with xerostomia are limited because of minimal efficacy, short duration of activity, or problems with side effects. The purpose of this pilot study was an initial assessment of safety, efficacy, duration of action, multiple dose tolerance, and side effects of a controlled-release formulation of pilocarpine hydrochloride. STUDY DESIGN: Eight healthy hospitalized subjects were given 15 mg of a controlled-release pilocarpine formulation every 12 hours for three doses. Saliva and blood samples were collected at assigned intervals. Repeated measures analysis and paired t tests were used for statistical analyses. RESULTS: A significant (p < 0.05) increase in both parotid and whole saliva output followed all three doses beginning within 1 hour of dosing and lasting over 10 hours. Mean plasma pilocarpine concentration reached a maximum of 8.2 ng/ml at approximately 1 hour after the first dose, 11.5 ng/ml after the third dose, and declined to near baseline (0.06 ng/ml) 24 hours after the final dose. None of the participants showed evidence of adverse effects including complaints of sweating or gastrointestinal discomfort. CONCLUSIONS: A controlled-release formulation of pilocarpine may overcome the therapeutic weaknesses of current pilocarpine preparations by prolonging salivary secretion and reducing undesirable side effects.

Adult↗
PubMed1998

Radiation-induced hyposalivation and its treatment with oral pilocarpine.

OBJECTIVE: The aim of this study was to determine the effects of radiation on the secretion of saliva from mucous salivary glands in comparison with serous salivary glands. STUDY DESIGN: The minor salivary glands of the palate were used as an example of mucous glands, while the parotid glands were used as an example of a serous secretion organ. Serial flow rate measurements of the parotid and palatal glands were taken over a period of approximately 9 months in 13 patients who suffered from malignancies of the head and neck region. Twelve patients consented to take part in a second study in which salivary flow was stimulated by oral pilocarpine before and at the conclusion of radiotherapy and 7 months later. Complaints and symptoms were recorded at each time of measurement. RESULTS: After radiotherapy, the secretory performance of the parotid glands dropped off rapidly and irreversibly. Salivary secretion from the palatal glands was not totally diminished as a result of radiation. Clinical complaints and histologic findings indicate a serious alteration of the tissues irradiated; however, residual secretion from the remaining parenchyma of the mucous glands still remains. Pilocarpine produced a clinically significant increase of salivary flow from the palatal glands before and 7 months after radiation. Secretory performance of the parotid glands could not be sufficiently increased by stimulation with pilocarpine after radiotherapy. Clinical side effects and risks for the treatment of symptomatic postradiation xerostomia with pilocarpine were minimal. CONCLUSIONS: These findings emphasize the greater resistance and recoverability of the mucous secreting minor palatal glands in comparison with the serous secreting parotid glands. They also indicate the significant postradiation ability of the mucous secreting glands to be stimulated by pilocarpine.

Carcinoma, Squamous Cell↗
PubMed2002

Attenuating effects of melatonin on pilocarpine-induced seizures in rats.

Daily melatonin (10-50 mg/kg, i.p.) treatment at 08.30 h or 17.00 h for 1 week of female rats (2-months-old) increased the latency to the appearance of the first convulsion in the pilocarpine-induced seizure model. Other behavior parameters remained unaltered. The anticonvulsant effect of melatonin seemed to be more intense at the light-dark transition. Moreover, the effect of repeated melatonin treatment was also age-related, since it showed a lower threshold in 2-month-old than in 21-day-old rats, and the acute treatment was not efficient. [3H]N-methylscopolamine binding was unaltered in the hippocampus and striatum of adult rats after the association of melatonin and pilocarpine. While muscarinic binding was unaltered in adult rats, it increased in the hippocampus of young rats in the presence of melatonin (50 mg/kg) and pilocarpine, and did not change in the striatum. Melatonin partially recovered [3H]GABA binding in the hippocampus in the presence of pilocarpine-induced seizures, and intensified pilocarpine effects in the striatum of adult rats.

Age Factors↗
PubMed2001

Moxonidine reduces pilocarpine-induced salivation in rats.

Cholinergic agonists activate salivation and the alpha2-adrenergic and imidazoline receptor agonists induce opposite effects. In the present study, we investigated the effects of intracerebroventricular (i.c.v.) or intraperitoneal (i.p.) injection of moxonidine (an alpha2-adrenergic and imidazoline receptor agonist) on the salivation induced by the cholinergic agonist pilocarpine. Male Holtzman rats with stainless steel cannula implanted into the lateral ventricle (LV) were used. In rats anesthetized with tribromoethanol (200 mg kg(-1), saliva was collected using pre-weighed small cotton balls inserted in the animal's mouth. The treatment with moxonidine (5, 10 and 20 nmol in 1 microl) injected i.c.v. reduced the salivation induced by pilocarpine (1 mg kg(-1)) injected i.p. (48 +/- 5, 17 +/- 2 and 15 +/- 2 mg min(-1) vs. control, 73 +/- 7 mg min(-1)). The same doses of moxonidine injected i.c.v. also reduced the salivary secretion induced by pilocarpine (500 nmol in 1 microl) injected i.c.v. (44 +/- 1, 14 +/- 2 and 20 +/- 3 mg min(-1) vs. control, 51 +/- 2 mg min(-1)). Injection of moxonidine (20 nmol in 0.1 ml) i.p. produced no change on i.p. pilocarpine-induced salivation (58 +/- 4 mg min(-1) vs. control, 50 +/- 4 mg min(-1)). The results show that central, but not peripheral, injection of moxonidine inhibits pilocarpine-induced salivation, suggesting that central mechanisms activated by alpha2-adrenergic/imidazoline agonists inhibit cholinergic-induced salivation in rats.

Animals↗
PubMed1993

The effect of topical pilocarpine on pulsatile ocular blood flow.

Ocular blood flow is considered an important factor in determining the extent of visual damage occurring in primary open angle glaucoma (POAG). The effect of topical pilocarpine, a parasympathomimetic vasodilator, on the pulsatile ocular blood flow (POBF) in POAG subjects was studied. A pneumotonometer linked to the Langham Ocular Blood Flow System recorded the intraocular pressure (IOP) pulse from which POBF was calculated. Measurements were taken from 18 POAG subjects treated with both G pilocarpine and G timolol, 2 weeks after withdrawing G pilocarpine and again 1 week after reinstituting full treatment. Recordings from 20 POAG patients treated with only G timolol were taken as control values. There was no significant difference in the IOP or POBF between the controls and POAG patients on dual therapy. Furthermore when G pilocarpine was temporarily withdrawn there was no significant change in POBF despite a significant rise in IOP. The results imply that aqueous pilocarpine has no direct effect on the pulsatile component of ocular blood.

Administration, Topical↗
PubMed1999

Pilocarpine hydrochloride relieves xerostomia in chronic graft-versus-host disease: a sialometrical study.

Bone marrow transplantation is considered to be the treatment of choice for various hematological and solid malignancies, as well as for bone marrow failure syndromes and some genetic diseases. Unfortunately, a great number of patients who receive allogeneic BMT suffer from graft-versus-host disease (GVHD) following the procedure. Xerostomia is considered to be one of the most annoying complications of chronic GVHD (cGVHD), and the rapidly growing number of BMT patients with prolonged survival renders GVHD-related xerostomia a major clinical problem. As pilocarpine hydrochloride has been shown to relieve xerostomia in other disease categories, we administered pilocarpine hydrochloride 30 mg/day to six cGVHD patients and measured their whole saliva, parotid and submandibular-sublingual flow rates in both resting and stimulated conditions. Mean values of flow rates of whole saliva in resting conditions at 2 weeks, 2 months and 6 months following administration of pilocarpine hydrochloride 30 mg/day were 0.71 +/- 0.12 ml/min, 0.59 +/- 0.07 ml/min and 0.56 +/- 0.11 ml/min, respectively. In stimulated conditions, mean values were 1.7 +/- 0.3 ml/min, 1.0 +/- 0.17 ml/min and 0.94 +/- 0.21 ml/min, respectively. The mean values of whole saliva flow rates under both conditions represented an increase of 224-284% and 134-247%, respectively (P < 0.01). The pattern and magnitude of parotid and submandibular-sublingual flow rate increases following pilocarpine hydrochloride administration were similar. Patients were followed for 6 months and demonstrated increased levels of secretion, with some reduction after the initial peak values. The medication was discontinued at 2 months and reinstated after 2 weeks in three patients. This resulted in rapid flow rate reduction followed by another profound increase. Contrary to the sialometrical analysis, the subjective scoring showed no fluctuations during the study period. We discuss these results in the context of the clinical experience of xerostomic patients in whom even a minute increase in secretion may be significant. Our results demonstrate that objective and subjective relief from xerostomia in cGVHD patients can be achieved with the routine oral administration of pilocarpine hydrochloride.

Adolescent↗