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The pathogenesis of irritable bowel syndrome (IBS) has not been clearly understood. Numerous factors, including neurotransmitters, can interfere with the functions of the digestive tract.The aim of present study was to determine the secretion and metabolism of serotonin in patients with unclassified irritable bowel syndrome (IBS-U).The study included 50 healthy subjects (Controls) and 50 patients with IBS-U, diagnosed according to Rome IV Criteria of functional gastrointestinal disorders. The severity of gastrointestinal symptoms was assessed using the Gastrointestinal Symptom Rating Scale (GSRS- IBS). The quality of sleep was estimated by Insomnia Severity Index (ISI). The serum serotonin and melatonin levels and 5-hydroxyindoleacetic acid (5-HIAA) and 6-sulfatoxymelatonin (aMT6s) concentration in urine were determined with ELISA method.Compared to control group, patients with IBS-U had a higher serum levels (201.3 ± 37.8 vs 145.4 ± 36.9 ng/ml, p0.001) and lower levels of melatonin (5.86 ± 1,16 vs9.11 ±2.43 pg/ml, p0.001). Likewise, in IBS-U patients urinary excretion of 5-HIAA was greater, while aMT6s excretion was lower. Due to the above changes cyproheptadine (6 mg daily) or melatonin (7 mg daily) was recommended to be taken. After 12 weeks of taking cyproheptadine, the IBS symptoms disappeared in 86.6% patients, and in 20.0% of those taking melatonin. Both drugs improved sleep in equal measure.Increased serotonin secretion may be the cause of abdominal complaints in unclassified irritable bowel syndrome, what should be considered in its treatment.

Background Dyspeptic syndrome is particularly common in postmenopausal women in the form of epigastric pain. The aim of the study was to assess the role of melatonin in chronic dyspepsia in this group of women, and examine the role of Helicobacter infection. Methods The study comprised 152 subjects including 30 healthy women (Group I), 60 women with asymptomatic H.pylori infection (Group II), and 64 women with H. pylori infection with chronic dyspepsia (Group III). Endoscopic examination was performed, as well as histological assessment of gastric end duodenal mucosa, urease breath test (UBT-13C), and immunoenzymatic assessment of serum 17-β-estradiol, follicle stimulating hormone and melatonin, and urinary 6-sulfatoxymelatonin. In Group III, 14-day antibacterial treatment was introduced with pantoprazole, amoxicillin and levofloxacin followed a six-month treatment with placebo in 32 women (Group IIIa), and melatonin 1 mg/morning and 3 mg/at bedtime in the other 32 women (Group IIIb). Results No significant differences were found between serum level of female hormone. Serum melatonin levels were similar between Group I (12.5 ± 2.72 pg/ml) and Group II (10.5 ± 3.73 pg/ml; p > 0,05). The level was significantly lower in Group III (5.72 ± 1.42 pg/ml; p H.pylori was obtained in 75.0% women in Group IIIa, and in 84.3% in Group IIIb (p > 0.05). After six months, dyspeptic symptoms resolved in 43.7% patients in Group IIIa and 84.3% in Group IIIb (p Conclusion Melatonin supplementation is useful in treating H. pylori-associated dyspepsia, particularly in postmenopausal women with lower levels of this hormone. Trial registration NCT04352062, date of registration: 15.04.2020.

Introduction: Postmenopausal women manifest emotional disorders associated with an increase in appetite. The aim of the study was to assess the serotonin and melatonin secretion and metabolism in postmenopausal women in relation to eating disorders. Material and methods: Sixty postmenopausal women and 30 women without hormonal disturbances were enrolled into the study and divided into three groups: group I (control) – women without menstrual disorders, group II — postmenopausal women without appetite disorders and change in body weight, and group III — postmenopausal women with increased appetite and weight gain. Serum melatonin, serotonin, urinary 6-sulfatoxymelatonin (aMT6s), and 5-hydroxyindoleacetic acid (5-HIAA) excretion were measured. Results: Serum serotonin and melatonin levels in groups II and III were lower compared to group I. Urinary 5-HIAA and aMT6s excretion was lower in overweight women. In group III the correlation between the serum level of serotonin, melatonin, and BMI was negative; a high statistical significance was found between BMI and urinary aMT6s excretion. Conclusions: Melatonin supplementation and use of drugs modulating the serotonin homeostasis together with female hormones have a beneficial effect in complex treatment of disorders of eating in postmenopausal women. (Endokrynol Pol 2016; 67 (3): 299–304)

Inflammatory bowel diseases, particularly ulcerative colitis (UC) and lymphocytic colitis (LC), affect many people. The role of melatonin in the pathogenesis of UC is precisely determined, whereas in LC it remains unknown. The aim of this study was to compare the expression of the melatonin-synthesizing enzymes tryptophan hydroxylase (TPH1), arylalkylamine-N-acetyltransferase (AANAT), and N-acetylserotonin methyltransferase (ASMT) in the colonic mucosa and urinary excretion of 6-sulfatoxymelatonin in patients with ulcerative and lymphocytic colitis. The study included 30 healthy subjects (group C), 30 patients with severe ulcerative colitis (group UC), and 30 patients with lymphocytic colitis (group LC). The diagnosis was based on endoscopic, histological, and laboratory examinations. Biopsy specimens were collected from right, transverse, and left parts of the colon. The levels of mRNA expression, TPH1, AANAT, and ASMT were estimated in the colonic mucosa with RT-PCR. The urine concentration of aMT6s was determined by the photometric method. The expression of TPH1, AANAT, and ASMT in colonic mucosa in UC and LC patients was significantly higher than in healthy subjects. Significant differences were found in the urinary aMT6s excretion: group C—13.4 ± 4.8 µg/24 h, group UC—7.8 ± 2.6 µg/24 h (p < 0.01), group LC—19.2 ± 6.1 µg/24 h (p < 0.01). Moreover, a negative correlation was found between fecal calprotectin and MT6s—in patients with UC − r = −0.888 and with LC − r = −0.658. These results indicate that patients with UC and those with LC may display high levels of melatonin-synthesizing enzymes in their colonic mucosa, which could possibly be related to increased melatonin synthesis as an adaptive antioxidant activity.

Melatonin can be synthesized by different cells in the gastrointestinal tract. The aim of this study was to evaluate the expression of melatonin-synthesizing enzymes: arylalkylamine-N-acetyltransferase(AANAT) and N-acetylserotonin methyltransferase (ASMT) in colonic mucosa and urinary 6-sulfatoxymelatonin excretion(aMT6s) in patients with lymphocytic colitis(LC) related to the number of intraepithelial lymphocytes(IEL) and enterochromaffin cells (EC). The study included 32 healthy subjects (HS group) and 36 patients with lymphocytic colitis (LC group). The diagnosis was based on histological and immunohistochemical performances using mouse monoclonal antibodies (chromogranin A –LK 2H10). EC were counted in 10 fields of each bioptate at 40x magnification. The level of mRNA expression of AANAT and ASMT was estimated in colonic mucosa with RT-PCR. The urine concentration of aMT6s was determined by photometric method. Significant differences were found in obtained results between HS and LC group: the number of IEL 14.1±3.41 vs. 32.4±5.50 per 100 surface colonocytes (p less than 0.001); the number of EC 32.2±10.1 vs. 70.4±21.2 (p less than 0.001); AANAT -1.32±0.47 vs. 2.32±0.65 (pless than 0.001; ASMT – 1.51±0.59 vs. 2.80±0.92 (p less than 0.001) aMT6s- 13.4±4.87 vs. 19.9±6.29 (p less than 0.001). Moreover, a positive correlation was found between the number of EC and ASMT (p= 0.011) and between EC and aMT6s (p less than 0.001). No correlation occurred between the number of IEL and AANAT p=0.932) and AMST (n=0.536) and aMT6s (p=9.288). These results indicate that the enterochromaffin cells in colonic mucosa are the main extrapineal source of melatonin in patients with lymphocytic colitis.

Estrogen deficiency is considered to be the main cause of increased appetite and increased weight in postmenopausal women. In this period, reduced secretion of melatonin (MEL) was also observed. The aim of the study was to evaluate the secretion of melatonin, 17-β estradiol and follicle-stimulating hormone (FSH) in relation to body mass index (BMI) in pre- and postmenopausal women. The study included 90 women divided into three equal groups: group I (control)—women without menstrual disorders, group II—postmenopausal women without change in appetite and body weight, group III—postmenopausal women experiencing increased appetite and weight gain. In each patient, serum melatonin, 17-β-estradiol, FSH and urine a 6-sulfatoxymelatonin (aMT6s) were determined. Compared to the control group, the level of melatonin and estradiol was statistically lower. The FSH level was higher than in the groups of postmenopausal women. No significant correlation was found in all groups between the level of melatonin and the levels of estradiol and FSH. A negative correlation was found between aMT6s excretion and BMI, and a positive correlation between the level of FSH and BMI, mainly in overweight women. The obtained results indicate a significant effect of melatonin deficiency on the process of weight gain in postmenopausal women and justify its use in treatment of these disorders.

Taking statins can cause increase in the level of aspartate and alanine aminotransferase. The aim of this study was to assess the usefulness of melatonin in counteracting the adverse hepatic events from statins. Methods. The research program included 60 patients (aged 47–65 years, 41 women and 19 men) with hyperlipidemia taking atorvastatin or rosuvastatin at a dose of 20–40 mg daily. The patients were randomly allocated in two groups. Group I (n=30) was recommended to take the same statin at a standardized daily dose of 20 mg together with melatonin at a dose of 2×5 mg. Group II (n=30) patients took statin with placebo at the same dose and time of the day. Follow-up laboratory tests (AST, ALT, GGT, and ALP) were evaluated after 2, 4, and 6 months of treatment. Results. In Group I the levels of all enzymes decreased after 6 months, particularly AST, 97,2±19,1 U/L versus 52,8±12,3 U/L (p<0,001); ALT, 87,4±15,6 U/L versus 49,8±14,5 U/L (p<0,001); and GGT, 84,1±14,8 U/L versus 59,6 U/L (p<0,001). Conclusion. Melatonin exerts a hepatoprotective effect in patients taking statins.

Helicobacter pylori (H. pylori) infection plays an important role in gastric carcinogenesis. This bacterium may induce cancer transformation and change the susceptibility of gastric mucosa cells to various exogenous dietary irritants. The aim of the study was to evaluate the influence of H. pylori infection on the reaction of the stomach cells to a genotoxic effect of heterocyclic amines (HCAs). These well-known mutagens are formed during cooking of protein-rich foods, primarily meat. Taking into account that persons consuming a mixed-western diet are exposed to these compound nearly an entire lifetime and more than half of human population is infected with H. pylori, it is important to assess the combined effect of H. pylori infection and HCAs in the context of DNA damage in gastric mucosa cells, which is a prerequisite to cancer transformation. We employed 2-amino-3-methylimidazo[4,5-f]quinoline (IQ), 2-amino-3,8-dimethyl-imidazo[4,5-f]quinoxaline (MeIQx) and 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP) because these substances are present in a great amount in cooked and fried meat. Using alkaline comet assay, we showed that the extent of the DNA damage induced by HCAs was significantly higher in H. pylori infected gastric mucosa cells than in non-infected counterparts. We did not observed any difference in the efficiency of repair of DNA lesions induced by HCAs in both type of cells. Vitamin C reduced the genotoxic effects of HCAs in H. pylori infected and non-infected gastric mucosa cells. Melatonin more effectively decreased DNA damage caused by HCAs in H. pylori infected gastric mucosa cells as compared with control. Our results suggest that H. pylori infection may influence the susceptibility of gastric mucosa cells to HCAs and dietary antioxidative substances, including vitamin C and melatonin may inhibit the genotoxic effects of HCAs on gastric mucosa cells and may reduce the risk of carcinogenesis caused by food borne mutagens and H. pylori infection.

Background and Aim The rhythm of melatonin secretion and its blood level changes in cirrhotic patients, but the causes of these alterations have not been sufficiently appreciated. The aim of study was to estimate the dependence between melatonin secretion and metabolism and the severity of hepatic encephalopathy. Methods The study included 75 alcoholic cirrhotic patients (A, B, C) with hepatic insufficiency and 25 healthy subjects (group K). Three groups of patients were identified, 25 patients each, with grade 1, 2, and 3 hepatic encephalopathy according to West-Haven Scale. Immunoenzymatic method was used to measure serum melatonin (at 02:00 h and 09:00 h) level and 6-sulfatoxymelatonin (6-HMS) excretion in the urine (during night and day). Results Nocturnal serum melatonin levels (pg/mL) in groups were: K—57.1 ± 11.4, A—38.5 ± 11.2, B—53.4 ± 17.9, C—79.5 ± 27.9 (P

Helicobacter pyloricolonization of gastric mucosa causes pain of unknown etiology in about 15–20% of infected subjects. The aim of the present work was to determine the level of expression of enzymes involved in the synthesis of melatonin in gastric mucosa of asymptomatic and symptomaticH. pyloriinfected patients. To diagnoseH. pyloriinfection, histological analysis and the urea breath test (UBT C13) were performed. The levels of mRNA expression of arylalkylamine-N-acetyltransferase (AA-NAT) and acetylserotonin methyltransferase (ASMT) were estimated in gastric mucosa with RT-PCR. The level of AA-NAT expression and AMST was decreased inH. pyloriinfected patients and was increased afterH. pylorieradication. We conclude that decreased expression of melatonin synthesizing enzymes, AA-NAT and ASMT, in patients with symptomaticH. pyloriinfection returns to normal level afterH. pylorieradication.

Postmenopausal women manifest emotional disorders associated with an increase in appetite. The aim of the study was to assess the serotonin and melatonin secretion and metabolism in postmenopausal women in relation to eating disorders.Sixty postmenopausal women and 30 women without hormonal disturbances were enrolled into the study and divided into three groups: group I (control) - women without menstrual disorders, group II - postmenopausal women without appetite disorders and change in body weight, and group III - postmenopausal women with increased appetite and weight gain. Serum melatonin, serotonin, urinary 6-sulfatoxymelatonin (aMT6s), and 5-hydroxyindoleacetic acid (5-HIAA) excretion were measured.Serum serotonin and melatonin levels in groups II and III were lower compared to group I. Urinary 5-HIAA and aMT6s excretion was lower in overweight women. In group III the correlation between the serum level of serotonin, melatonin, and BMI was negative; a high statistical significance was found between BMI and urinary aMT6s excretion.Melatonin supplementation and use of drugs modulating the serotonin homeostasis together with female hormones have a beneficial effect in complex treatment of disorders of eating in postmenopausal women. (Endokrynol Pol 2016; 67 (3): 299-304).

Aim of the study : We evaluated the effect of melatonin supplementation on the nutritional status of postmenopausal women. Material and methods: The study included 56 women (51-65 years) and 25 healthy women (27-36 years). The emotional state was assessed using Hamilton Depression Rating Scale (HAM-D), the quality of sleep using Insomnia Severity Index (ISI). Body mass index (BMI) and waist-hip ratio (WHR) were also calculated. The patients were divided into 3 groups: group I (control) – 25 women with normal body weight, group II – 26 postmenopausal women with normal body weight, group III – 30 postmenopausal women with high body weight. In women from group II and III, routine laboratory tests, levels of thyroid-stimulating hormone (TSH), 17-estradiol, prolactin, follicle-stimulating hormone (FSH) and the concentration of 6-hydroxymelatonin sulphate (6-HMS) in day/night urine fractions were determined. On the day of the examination, women remained on a liquid diet (1800 kcal). Next, a balanced diet of 1500 kcal and 5 mg of melatonin administration were recommended. The follow-up examinations were performed after 4, 8, 12, 16, 20 and 24 weeks. Results : The patients from groups II and III showed similar mild levels of anxiety and depression and a significant degree of sleep disorders. In group III, lower urinary 6-HMS excretion was observed at night. In both groups a negative correlation was found between urinary 6-HMS excretion and the degree of sleep disorders. After 24 weeks, a statistically significant improvement of quality of sleep was obtained. A negative correlation was detected between urinary 6-HMS excretion and BMI. Conclusion : Melatonin supplementation contributed to body weight reduction.

The liver plays a key role in the detoxification of numerous molecules which results in the formation of an excessive number of toxic reactive oxygen species. This results in oxidative damage to the hepatocytes, which when severe, compromises the function of this critical organ. A variety of antioxidants protect the liver from free radical-mediated damage, one of the best of which is melatonin. Clinical studies have confirmed the melatonin, as well as it precursor tryptophan, protect the liver from non-alcoholic liver disease and also during the surgical procedure of partial liver resection.

Melatonin (MEL) exerts beneficial effects on the gut partly by myorelaxative properties upon the smooth muscle. Its secretion decreases with age, particularly in postmenopausal women. This study was aimed at evaluating the effect of MEL on the symptoms of irritable bowel syndrome (IBS) in this group of patients.The investigations were carried out in 80 postmenopausal women, aged 48-65 years, divided into two equal groups, diagnosed according to Rome Criteria III: i.e. patients with IBS with constipation predominant (IBS-C), and patients with IBS with diarrhoea predominant (IBS-D). The control group (C) included healthy women aged 46-65 years. In all subjects, 6-sulfatoxymelatonin (6-HMS) concentration urine was measured using ELISA assay. Patients in both groups over the course of six months were given melatonin (at a dose of 3 mg fasting and 5 mg at bedtime) or a placebo (double blind trial). Disease activity was evaluated after two, four and six months, using a ten-point scale to assess the main somatic symptoms: visceral pain, abdominal bloating, etc.The amounts of 6-HMS urine excretion (μg/24 h) were: C 11.4 ± 3.0, IBS-C 10.2 ± 3.2, IBS-D 14.0 ± 6.3 (p 〈 0.05). Correlation between values of symptoms score and contrary excretion of 6-HMS: IBS-C r = -0.714, IBS-D r = 0.409. After six months in the IBS-C group, the intensity of visceral pain and abdominal bloating had decreased in 70% of patients (p 〈 0.01) and constipation in 50% of patients (p 〈 0.05). Beneficial changes in the IBS-D group were noted in 45% of patients, but this was not better compared to the placebo.Melatonin can be used as part of the treatment of IBS, particularly in patients with constipation-predominant IBS.

The rhythm of melatonin secretion and its blood level changes in cirrhotic patients, but the causes of these alterations have not been sufficiently appreciated. The aim of study was to estimate the dependence between melatonin secretion and metabolism and the severity of hepatic encephalopathy.The study included 75 alcoholic cirrhotic patients (A, B, C) with hepatic insufficiency and 25 healthy subjects (group K). Three groups of patients were identified, 25 patients each, with grade 1, 2, and 3 hepatic encephalopathy according to West-Haven Scale. Immunoenzymatic method was used to measure serum melatonin (at 02:00 h and 09:00 h) level and 6-sulfatoxymelatonin (6-HMS) excretion in the urine (during night and day).Nocturnal serum melatonin levels (pg/mL) in groups were: K-57.1 ± 11.4, A-38.5 ± 11.2, B-53.4 ± 17.9, C-79.5 ± 27.9 (P 0.01); whereas diurnal levels were: K-10.9 ± 3.5, A-33.5 ± 12.0, B-53.8 ± 23.1, C-98.5 ± 34.6 (P 0.01). Similar differences were found in the evaluation of 6-HMS excretion (μg/9 h) in urine at night: group K-23.4 ± 14.4, A-16.6 ± 5.4, B-14.3 ± 6.2 (P 0.01), C-3.3 ± 1.5 (P 0.001). Diurnal 6-HMS excretion (μg/15 h) was lower only in group C and it was respectively: K-6.9 ± 3.4, A-7.1 ± 1.7, B-7.6 ± 1.7, C-4.3 ± 2.2 (P 0.001). Serum ammonia concentrations (μg/dL) were: group K-30.4 ± 8.9, A-51.8 ± 25.4 (P 0.05), B-73.0 ± 29.8 (P 0.001), C-107.5 ± 34.8 (P 0.001). No correlation between melatonin and ammonia levels in all groups was found.The elevated melatonin blood levels both at night and day may account for some of the clinical manifestations of hepatic encephalopathy (daytime sleepiness, fatigue).

Hepatic encephalopathy is one of the symptoms of liver failure. The exact causes of encephalopathy are complex and still unclear. Apart from elevated blood ammonia levels, the role of numerous other factors is being considered.The aim of the study was to determine the serum level of serotonin and melatonin and the urinary excretion of their metabolites (5-hydroxyindoleacetic acid [5-HIAA] and 6-sulfatoxymelatonin [6-HMS]) in patients with various stages of liver cirrhosis.The study comprised 75 patients with alcohol-induced liver cirrhosis and 25 healthy subjects (control group). Based on the Child-Pugh classification, 3 groups of 25 patients each were distinguished - group A, B, and C with grade A, B, and C of liver failure, respectively. Blood samples were drawn at fasting at 9 a.m., and 24-hour urine collection was performed. Immunoenzymatic assays were used to determine serum melatonin and serotonin levels as well as urine 5-HIAA and 6-HMS concentrations.Serum serotonin levels were 159.8 ± 23.1 ng/ml in controls, 179.3 ± 21.1 ng/ml in group A (P0.05), 143.2 ± 22.8 ng/ml in group B (P0.05), and 114.5 ± 37.6 ng/ml in group C (P0.01). Serum melatonin levels were 10.6 ± 1.7 in controls, 31.2 ± 9.8 pg/ml in group A (P0.01), 49.8 ± 12.2 pg/ml in group B (P0.001), and 94.8 ± 22.6 pg/ml in group C (P0.001). Urinary 5-HIAA excretion was 5.9 ± 2.1 mg/24 h in controls, 5.9 ± 1.9 mg/24 h in group A (P0.05), 4.8 ± 1.2 mg/24 h in group B (P0.05), and 4.6 ± 1.4 mg/24 h in group C (P0.05). Urinary 6-HMS excretion was 26.6 ± 15.1 μg/24 h in controls, 23.2 ± 7.9 μg/24 h in group A (P0.05), 18.3 ± 10.6 μg/24 h in group B (P0.05), and 6.5 ± 3.6 μg/24 h in group C (P0.001).Disturbances in serotonin and melatonin homeostasis observed in patients with liver cirrhosis may be associated with advanced encopaholopathy.

Cirrhotic patients exhibit disturbed melatonin homeostasis, which may lead to sleep disturbances, but an influence on the hepatic encephalopathy has not been elucidated.Aim. In the present study, the association of melatonin levels in serum and ascitic fluid and ammonia concentration related to the intensity of hepatic encephalopathy (HE) was investigated.Material and Methods. The study included 90 alcoholic patients with hepatic encephalopathy and 30 healthy volunteers (C). Patients were divided in three groups according to 0–4 West-Haven Score: HE1(n=28), HE2(n=30), and HE3(n=32). Melatonin was measured by radioimmune assay.Results. In fasting patients with hepatic encephalopathy we noted higher melatonin serum levels [pg/mL] than in healthy subjects groups: C—11.3 ± 3.9, HE1– 34.3 ± 12.2(P<0.01), HE2—54.8 ± 23.9, and HE3—119.8 ± 96.4(P<0.001). No correlation between melatonin and ammonia levels was found. Melatonin was detected in ascetic fluid in 24 patients of group HE2and 27 patients of group HE2of hepatic encephalopathy.Conclusions. Our results suggest that high blood levels of melatonin in cirrhotic liver patients may account for some of the clinical manifestations of hepatic encephalopathy, for example, daytime sleepiness, fatigue.

AIM: To evaluate blood concentration of melatonin and urinary excretion of its metabolite, 6-sulfatoxymelatonin (6-OHMS), in functional dyspepsia (FD). METHODS: Ninety individuals were enrolled in the study: 30 in each study group: patients with postprandial distress syndrome (PDS), epigastric pain syndrome (EPS), and controls. Blood samples were drawn at 02:00 and 09:00 h and 24-h urine collection was performed. Serum melatonin and urinary 6-OHMS concentrations were measured by enzyme-linked immunosorbent assay. RESULTS: Serum melatonin concentration at night and in the morning was significantly (P < 0.001) higher in PDS patients [at 02:00 h-93.3 pg/mL, quartile range (QR): 79.8-116.2; at 09.00 h-14.3 pg/mL, QR: 7.06-19.0] than in EPS (57.2 pg/mL, QR: 42.6-73.1; 8.1 pg/mL, QR: 4.1-9.3) and control patients (57.7 pg/mL, QR: 51.2-62.5; 8.1 pg/mL, QR: 5.4-10.3). A similar relationship was observed for urinary 6-OHMS excretion. Patients with severe PDS symptoms had a higher melatonin concentration than these with moderate syndromes, whereas patients with severe EPS had a lower urinary 6-OHMS excretion than patients with moderate symptoms. CONCLUSION: Evaluation of melatonin serum concentrations and 24-h urinary 6-OHMS excretion are useful methods for differential diagnosis of various clinical forms of FD.

The main aim of the research was a characteristic of selected personality traits and coping as well as estimation of a level of melatonin in serum in patients with functional dyspepsia (FD).36 patients with FD (14 men and 24 women) at age 19-43 (mean: 31.6) were examined. The control group consisted of 30 healthy persons at age 21-23 (mean: 37.2). CO-16 and CISS questionnaires were used to diagnose selected traits of personality and coping styles. Furthermore, melatonin concentration in serum was examined at 10 p.m., 2 a.m. and at 6 a.m. with the immunoenzymatic method (ELISA).Coping style focused on problems and emotions were the most frequent ones in the examined group. Cyclothymia, tendency towards neuroticism and depression, submission and sensitivity were these that characterised patients with FD well. It was also stated that the level of melatonin was higher than in healthy subjects.There are common personality traits and coping styles in the group of patients with FD. A level of melatonin in serum is increased.

The pathogenesis of functional dyspepsia is very complicated and its etiology is still not clear. One of the supposed pathophysiological mechanisms is the deficiency of melatonin. The deficiency of melatonin leads to increase the oxide reactive form's concentration as nitric oxide metabolites and to decrease of antyoxidative enzymes activity. This last factor seems to be very important in correct digestive tract function. The aim of our study was answer the question if is the difference between NO metabolites concentraction in gastric juice in patients with functional dyspepsia and in healthy subjects and wheather the treatment with melatonin plays the role in normal digestive tract function.The study included 60 subjects between of 18 to 48 years with diagnosed functional dyspepsia (according to the Rome III Criteria). The study group was divided into two subgroups: group I--30 subjects with Epigastric Pain Syndrome-EPS and group II--30 subjects with Postprandial Disorders Syndrome-PDS. Control group comprised 25 healthy subjects (without any clinical or morphological symptoms of digestive tract disease). In each patient the gastroscopy was performed. During gastroscopy 5 ml gastric juice was collected. The juice was centrifuged for 15 min (4500 rotations). The undiluted supernatant was frozen in the temperature -70 degrees C. The concentration of nitric oxide metabolites in gastric juice was determined with spectrophotometric based on ELISA test (540 nm wavelength) using a microplates reader (Multiscan, Labsystems). In patients with functional dyspepsja the investigations were performer twice before and after 6 weeks treatment with melatonin. Melatonin was applied in dose 5 mg daily, in the evening.The concentration of nitric oxide metabolites in gastric juice in healthy subjects was 6.81 +/- 2.23 microM. In patients with functional dyspepsia was significantly higher; in patients with Epigastric Pain Syndrome--10.99 +/- 2.46 microM (p0.05), in patients with Postprandial Disorders Syndrome--9.28 +/- 2.18 microM (p0.05). After treatment with melatonin the concentration of nitric oxide metabolites in gastric juice in both groups decreased and were 8.21 +/- 1.83 microM in patients with Epigastric Pain Syndrome and 6.93 +/- 1.61 microM in patients with Postprandial Disorders Syndrome.In patients with functional dyspepsia the concentration of nitric oxide metabolites in gastric juice was significantly higher than in control group. After treatment with melatonin the concentration of nitric oxide metabolites in gastric juice in both groups decreased--in patients with Epigastric Pain Syndrome as well as in patients with Postprandial Disorders Syndrome. The treatment with melatonin seems to be suitable in combined therapy of functional dyspepsia.

It was confirmed that enterochromaffin cells (EC) in the digestive system are a source of serotonin and melatonin. Both hormones possess an important, but opposed, influence on secretory and motoric function of gut. The aim of our study was to evaluate fasting secretion of serotonin and melatonin in patients with functional dyspepsia. Material and methods. 25 healthy subjects (K, group I), 25 patients with epigastric pain syndrome (EPS, group II) and 25 patients with postprandial distress syndrome (PDS, group III), aged 18-50 years, were included in this study. Diagnosis of functional dyspepsia was established according to the Rome Criteria III. Organic diseases of gut, H. pylori infection and another disorders were excluded. Seven days before the examinations the patients were told to abstain from drugs intake and equal diet was applied. On the day of investigation the subjects remained in a red-light room at night and received standard liquid diet (Nutridrink, 4 x 200 ml, 1800 kcal). Blood samples were taken for examination at 8 am on the subsequent day and serum was frozen in -80 degrees C. The concentration of serotonin and melatonin was measured by ELSA, using antibodies from IBL (catalogue no. RE 59121, RE 54021).The mean concentration of serotonin in group I (K) was 162.9 +/- 49.1 ng/ml, in group II (EPS)--225.8 +/- 111.3 ng/ml (p0.05) and in group III (PDS)--152.7 +/- 83.2 ng/ml (p0.05). The concentration of melatonin was in group I--7.3 +/- 4.0 pg/ml, in group II 8.7 +/- 8.0 (p0.05) and in group III 14.3 +/- 10.1 (p0.01).During fasting time secretion of serotonin is higher in patients with EPS, and similarly higher secretion of melatonin in patients with PDS, compared to healthy subjects.

Melatonin is synthesized not only in the pineal gland, but also in gastrointestinal tract by enterochromaffin cells (EC) and it has a gastroprotective properties. Helicobacter pylori infection causes functional and organic changes of gastric mucosa, particularly in endocrine cells (D, G, ECL, EC).The aim of own studies was to evaluate nocturnal secretion of Melatonin in subjects with asymptomatic and symptomatic (dyspepsia, duodenal ulcer disease) H. pylori infection (Hp).116 subjects, aged 19-61 years were included in this study. Four groups were distinguished: group I (n=30) healthy subjects, Hp (-), group II (n=26)--subjects with asymptomatic infection Hp, group III (n=32) patients with ulcer-like dyspepsia, Hp (+), and group IV (n=28) patients with duodenal ulcer Hp(+). H. pylori infection was diagnosed by using urea breath test (UBT-(13)C) and rapid urease test. The concentration of melatonin in serum was measured with ELISA method, before and after eradication of H. pylori. Blood samples were taken for examination at 10:00 p.m., 2:00 a.m. and 6:00 a.m.The average melatonin concentration at night hours was found in group I--34.74 +/- 4.77 pg/ml, in group II--48.29 +/- 12.22 pg/ml (pO.005), in group III--41.56 +/- 12.31 pg/ml (p0.05) and in group IV--26.16 +/- 6.89 pg/ml p0.01). Such statistical differences were not observed in all group after eradication H. pylori.(1) Nocturnal secretion of melatonin in subjects with asymptomatic infection of H. pylori is higher than in patients with ulcer-like dyspepsia and with duodenal ulcer disease. (2) Lower nocturnal secretion of melatonin probably may play role in pathogenesis of upper digestive tract diseases.

AIM: To study an assessment of the number of enterochromaffin cells and expression of hydroxyindole-O-methyltransferase in colonic mucosa and urine excretion of 6-sulfatoxymelatonin in patients with ulcerative colitis. METHODS: The study included 30 healthy subjects (group I-C), 30 patients with ulcerative proctitis [group II-ulcerative proctitis (UP)] and 30 patients with ulcerative colitis [group III-ulcerative colitis (UC)] in acute phases of these diseases. The number of enterochromaffin cells (EC) was estimated in rectal and colonic mucosa. Bioptates were assembled from many different parts of the large intestine. Immunorective cells collected from various parts of the colon were counted according to the Eurovision DAKO (Dako A/S, Copenhagen, Denmark) System in the range of 10 fields in each bioptate at × 200 magnification. The level of mRNA expression of hydroxyindole-O-methyltransferase (HIOMT) in colonic mucosa was estimated with RT-PCR. Urine 6-sulfatoxymelatonin (6-HMS) excretion was determined immunoenzymatically using an IBL (IBL International GmbH, Hamburg, Germany) kit (RE 54031). RESULTS: The number of EC cells in healthy subjects (C) was 132.40 ± 31.26. In patients of group II (UP) and group III (UC) the number of these cells was higher - 225.40 ± 37.35 (P < 0.001) and - 225.24 ± 40.50 (P < 0.001) respectively. Similar differences were related to HIOMT expression, which was 1.04 ± 0.36 in group C, 1.56 ± 0.56 (P < 0.01) in group UP and 2.00 ± 0.35 (P < 0.001) in group UC. Twenty-four hour 6-HMS urinary excretion was as follows: C - 16.32 ± 4.95 μg/24 h, UP - 26.30 ± 7.29 μg/24 h (P < 0.01), UC - 42.30 ± 12.56 μg/24h (P < 0.001). A correlation between number of EC cells and 6-HMS excretion was noted in all groups: r = 0.766 in patients with UP, r = 0.703 with UC and r = 0.8551 in the control group; the correlation between the results is statistically significant. CONCLUSION: In the acute phases of both UP and UC, proliferation of EC cells and high expression of HIOMT and urine excretion of 6-HMS is noted. These changes may represent a beneficial response in the anti-inflammatory and defense mechanism.