Short-term treatment outcome of pulpotomies in primary molars using mineral trioxide aggregate and Biodentine: a randomized clinical trial.

INTRODUCTION: An ideal pulpotomy agent for primary molars has been sought for many years. Recently, new materials that allow regeneration of residual pulp tissue have been developed. In this study, we compared the preliminary clinical results obtained using Biodentine and mineral trioxide aggregate (MTA) as pulp-dressing agents in pulpotomies of primary molars. METHODS: A randomized clinical study was performed in children aged 4-9 years with at least one primary tooth with decay or caries requiring pulp treatment. A total of 90 primary molars requiring pulpotomy were randomly allocated to the MTA or Biodentine group, and 84 pulpotomies were performed. Clinical and radiographic evaluations were undertaken 6 and 12 months after treatment. All teeth were restored with a reinforced zinc oxide-eugenol base and stainless steel crowns. Statistical analysis using Fisher's exact test was performed to determine the significant differences between the groups. RESULTS: A total of four clinical failures were observed; all involved gingival inflammation. The clinical success rate in the MTA Group after 12 months was 92 % (36/39), whereas the Biodentine Group obtained 97 % (38/39) (p = 0.346). All radiographic failures were observed at the 12-month follow-up evaluation. One molar from MTA Group showed internal resorption obtaining a radiographic success rate of 97 % (38/39). Two molars from the Biodentine Group showed radiographic failure (1 internal resorption and 1 periradicular radiolucency) obtaining a radiographic success rate of 95 % (37/39). CONCLUSIONS: Biodentine showed similar clinical results as MTA with comparable success rates when used for pulpotomies of primary molars. However, longer follow-up studies are required to confirm our findings. CLINICAL RELEVANCE: This article demonstrates the effectiveness of Biodentine as a primary teeth pulpotomy material, performing similar results as MTA at 12-months evaluation.

Buffy coat transfusions in early type I diabetes.

Fresh whole-blood buffy coats from American Red Cross volunteers were used to treat early type I diabetes. Attempts were made to adapt to human diabetic patients a protocol successfully used in prediabetic BB rats. Twenty-two type I diabetic patients (duration of disease less than 4 wk) were randomized to treatment or control groups; the treatment patients were given one buffy coat (approximately 0.6 X 10(9) T-lymphocytes) weekly for 5 wk. Plasma C-peptide (stimulated and unstimulated), insulin dose, and hemoglobin A1c were measured before and periodically after the treatment for 24 wk. The control group underwent the same studies. Although there were no significant differences for the parameters studied between the two groups, 2 of 12 patients in the treatment group underwent three complete (normal glycemia without insulin) temporary remissions. One of these patients was given a second course of transfusions after relapse from the first remission and developed a second complete remission that lasted 2 mo. No control patient had remissions during the 24-wk study. Although the future of adoptive immunotherapy in the treatment or prevention of diabetes is not known, several probable limitations of the current protocol, as discussed here, can explain the differences in results between this trial and the rodent studies.

Massive thyroxine intoxication: evaluation of plasma extraction.

Six patients were admitted after erroneous massive intake of levothyroxine (70-1200 mg over an interval of 2-12 days). All patients developed classical symptoms of thyrotoxicosis within 3 days of the first dose; five patients presented grade II-III coma and one became stuporous (days 7-10). Two patients developed left ventricular failure and three had arrhythmias (days 8-11). Total thyroid hormone levels in serum on admission ranged 935-7728 nmol/l for T4 (TT4) and 23-399 nmol/l for T3 (TT3). All patients received treatment with hydrocortisone and Propranolol. Propylthiouracil was also given in 3 cases. Extractive techniques (charcoal haemoperfusion and/or plasmapheresis) were initiated 8-14 days after the first dose of L-T4. The plasma disappearance rate (K) of TT4 with plasmapheresis was 30 times higher, on average, than under standard medical treatment (M). Also, K of TT4 under haemoperfusion was about five times higher than K under M. K changes for TT3 were higher under haemoperfusion than under plasmapheresis. Furthermore, extractive procedures shortened the average half life of TT4, (from 106.5 +/- 44.6 to 59.7 +/- 20.2 h, p less than 0.05).

Activated T-lymphocytes in newly diagnosed type I diabetic patients: relationship to residual beta cell function.

The relationship between T-lymphocyte activation and residual beta-cell function was studied in 19 newly diagnosed Type I (insulin dependent) diabetic patients, aged 6-43 years, 7-10 days after beginning insulin therapy and once normoglycemia had been achieved. Residual beta-cell function was studied by measurement of plasma C-peptide concentration 6 minutes after intravenous glucagon administration. T-lymphocyte activation markers, HLA-DR/CD3 and interleukin-2 receptor (Tac) expression, were measured in peripheral blood mononuclear cells by dual- or single-colour flow cytometry. Six patients showed increased percentages of activated T lymphocytes (increased HLA-DR positivity in four patients, and an excess of Tac-positive cells in two). The mean percentage of activated T lymphocytes was higher in patients with stimulated C-peptide levels below 300 pmol/l (8.32 +/- 1.32%) than in those with plasma stimulated C-peptide above 300 pmol/l (3.93 +/- 0.49%), P less than 0.01, or controls (3.48 +/- 0.60%), P less than 0.01. Furthermore, the six patients with increased percentages of activated T lymphocytes were in the low stimulated C-peptide group. A negative correlation was found between the percentage of activated T lymphocytes and glucagon-stimulated C-peptide (r = -0.5877, P less than 0.01). We conclude that increased T-lymphocyte activation is associated with a higher impairment of beta-cell function at the onset of Type I diabetes mellitus.

Circulating immunoreactive somatostatin in man. Effect of age, pregnancy, growth hormone deficiency and achlorhydria.

Plasma immunoreactive somatostatin (IRS) levels were measured fasting at 09.00 h in groups of adult individuals and children of different ages, as well as in pregnant women, in patients with pernicious anaemia documented to be achlorhydric, and in children with growth hormone deficiency. There was a gradual rise in the mean level of IRS from the third decade (mean 35.8 +/- 3.8 pg/ml), which reached significance at the seventh (61.1 +/- 8.4 pg/ml), eighth (66.7 +/- 5 pg/ml) and ninth decade (82.6 +/- 13.8 pg/ml). No change was observed in the second 28.3 +/- 3.8 pg/ml) and third (31.1 +/- 3.2 pg/ml) trimester of pregnancy when compared with matched, non-pregnant controls (29.7 +/- 2.2 pg/ml); however, the children aged under 2 years (69.6 +/- 11.2 pg/ml) had significantly higher values than the eldest group (12 to 16 years old) (46.3 +/- 7.2 pg/ml) (P less than 0.05). In achlorhydric patients, basal (27.2 +/- 3.7 pg/ml; P less than 0.01) and postprandial IRS (42.8 +/- 7.7 pg/ml; P less than 0.001) was significantly lower than in a matched, normal control group (basal 59.4 +/- 7.2; postprandial 132.1 +/- 26.3 pg/ml). Growth hormone deficiency was not associated with any differences in circulating IRS, basally or after insulin hypoglycaemia, when compared with values in normal children.(ABSTRACT TRUNCATED AT 250 WORDS)

Circulating immunoreactive somatostatin in gastrointestinal diseases. Decrease after vagotomy and enhancement in active ulcerative colitis, irritable bowel syndrome, and duodenal ulcer.

The main source of circulating immunoreactive somatostatin (IRS) seems to be the gastrointestinal tract. We therefore investigated plasma IRS in patients with various gastrointestinal diseases. Mean basal IRS oscillated between 46 and 73 pg/ml. A postprandial rise was observed in all patients and age-matched controls. However, the increment was significantly higher in patients with duodenal ulcer (159 +/- 20 pg/ml), active ulcerative colitis (176 +/- 17 pg/ml), and irritable bowel syndrome (194.4 +/- 20.4 pg/ml). Patients with duodenal ulcers who underwent vagotomy showed a decreased postprandial increment (107 +/- 10 pg/ml) when compared with active duodenal ulcer patients. No difference was demonstrable between controls and individuals with gastric ulcer, and patients with inactive ulcerative colitis. These results suggest that vagal innervation plays a role in postprandial IRS stimulation, whereas gastric hyperacidity, acute lesions of the colonic mucosa, and hypermotility of the gastrointestinal tract are associated with an exaggerated postprandial IRS response. Since somatostatin is known to influence many gastrointestinal functions, these variations in circulating IRS concentrations may be of pathophysiologic importance.

Plasma immunoreactive somatostatin is elevated in diabetic ketoacidosis and correlates with plasma non-esterified fatty acid concentration.

In experimental diabetes and after the administration of beta-hydroxybutyrate and non-esterified fatty acids (NEFA), an increase in circulating immunoreactive somatostatin (IRS) has been described. Both ketones and NEFA are raised in diabetic ketoacidosis. Therefore, we decided to investigate 10 patients in diabetic ketoacidosis by measuring, on admission and throughout the initial 24 hours of therapy, circulating levels of IRS, beta-hydroxybutyrate, acetoacetate, triglycerides, blood glucose, pH and NEFA. Fluids and insulin were administered IV following a previously established protocol. Nine patients showed abnormally high levels of circulating IRS. When compared with a group of controlled insulin-dependent diabetic patients, basal IRS was high (111 +/- 15 vs 28 +/- 3 pmol/l), and remained elevated for at least 24 h despite clear improvement of metabolic status. On admission we also found elevated levels of NEFA (1.04 +/- 0.2 mmol/l), triglycerides (4.7 +/- 1.1 mmol/l), beta-hydroxybutyrate (22.1 +/- 4mmol/l), and acetoacetate (4.8 +/- 1.1 mmol/l). A significant correlation was found initially between IRS and NEFA (p less than 0.01). We conclude that circulating IRS is high in most cases of diabetic ketoacidosis. The mechanism behind this hypersomatostatinaemia could be related to the abnormalities of lipid metabolism which occur in diabetic ketoacidosis.