Serum concentrations of gastrin after famotidine and omeprazole administration to dogs.

BACKGROUND: The duration of antacid-induced hypergastrinemia after cessation of administration of omeprazole and famotidine apparently has not been determined in dogs. HYPOTHESIS: That serum gastrin will return to basal concentrations by 7 days after cessation of famotidine or omeprazole administration. ANIMALS: Nine healthy, adult, male, research colony dogs. METHODS: Randomized, cross-over design. Serum gastrin was determined daily for 7 days to establish baseline concentrations. Famotidine (1.0 mg/kg q24h) or omeprazole (1.0 mg/kg q24h) was administered PO for 7 days followed by a 14-day washout. Serum concentrations of gastrin were determined daily during 7 days of administration and daily for 7 days after cessation of administration. Each drug was evaluated in 8 of the 9 dogs. RESULTS: Omeprazole caused a significant increase in serum gastrin concentration (37.2 ± 7.3 to 71.3 ± 19.0 ng/L; P = .006). Famotidine induced a transient increase in serum gastrin (37.2 ± 7.3 to 65.5 ± 38.5 ng/L; P = .02) that peaked at administration day 3 and declined thereafter. By day 7 after cessation of both drugs, there was no difference in serum gastrin concentrations compared to those before administration (famotidine P = .99; omeprazole P = .99). During or after administration, gastrin concentrations above 3 times the upper reference range were rare (12 of 224 samples). CONCLUSIONS AND CLINICAL IMPORTANCE: A 7-day withdrawal from short-term administration of famotidine or omeprazole is sufficient for serum gastrin to return to baseline concentrations. Withholding famotidine or omeprazole for longer before investigating pathologic causes of hypergastrinemia is unnecessary.

Relationships between different tooth shapes and patient's periodontal phenotype.

BACKGROUND AND OBJECTIVE: The purpose of the present study was to establish whether any correlation exists between tooth shapes and patient-related factors such as gingival and periodontal characteristics. MATERIAL AND METHODS: Clinical measurements, including the width and the height of maxillary central incisor crowns, the apico incisal height of the keratinized mucosa (KM), the buccal gingival thickness (GT), the depth of the sulcus (SD), the bone-sounding depth (BS) and the height of the interproximal maxillary central papilla (Ph), were investigated in 50 healthy individuals. These individuals were then divided into three groups based on the shape of their maxillary central incisor crowns: triangular; square; or square-tapered. The three groups were analyzed to determine any significant differences among the groups in the values obtained for clinical measurements. RESULTS: There were no significant differences among the three groups in terms of the SD (p = 0.11) or the BS (p = 0.54), whilst statistically significant differences were observed for the KM (p < 0.001), the GT (p = 0.012) and the Ph (p < 0.001). CONCLUSION: The results of this study indicate that different tooth shapes are associated with significantly different values for the extent of the KM, its bucco-lingual thickness and the height of the interproximal maxillary central papilla.

[Anderson-Fabry's disease: diagnostic problems, therapeutic relevance, and clinical experience in the treatment of the disease with enzyme replacement therapy in nephropathic patients]. / Malattia di Anderson-Fabry: problematiche diagnostiche, attualità terapeutiche ed esperienza clinica nel trattamento della malattia con terapia enzimatica sostitutiva in pazienti nefropatici.

Aim of this study was to confirm the initial results of a clinical trial on the treatment of Fabry's disease carried out in 13 Italian Nephrology Units. Fabry's disease is a rare, X-linked inherited disease, characterized by a-galactosidase (a-GAL) deficiency, a lysosomial enzymatic activity that results in the accumulation of neutral glycosphingolipids in the endothelial cells of the whole body, and causes painful crises, acroparesthesiae, angiokeratomas, corneal and lens dystrophy, and progressive damage to kidneys, heart and central nervous system, as well as potentially leading to death. The present availability of the recombinant form of a-GAL allows us to prevent or stop the long-term complications of this disease. A clinical trial, generously supported by Genzyme, was started on February 2001. In this trial 20 patients affected by Fabry's disease were periodically treated with agalsidase-beta, the commercial form of the enzyme. The initial results of the trial have indicated that the drug is capable of reducing both the number and intensity of painful crises, improving the patient's sensation of well-being, thus suggesting that this therapeutic approach might theoretically increase life expectancy in these patients.