Obese patients with T2D showed significantly reduced levels of OC in comparison with patients with lower degrees of glucose tolerance derangement. Our results also suggest that OC was the only bone marker independently related to the degree of glucose metabolism derangement in these patients.

No abstract

♦ Objective Helicobacter pylori (HP) infection has frequently been found in dialysis patients. Chronic infections induce overproduction of pro-inflammatory substances. Inflammation has been associated with cachexia and anorexia. We explored the relationship between HP infection, anorexia, and malnutrition in peritoneal dialysis (PD) patients. ♦ Patients and Methods The study included 48 clinically stable PD patients divided into four groups: HP+ with anorexia (group I, n = 12); HP+ without anorexia (group II, n = 4); HP- with anorexia (group III, n = 5); and HP- without anorexia (group IV, n = 27). Infection with HP was diagnosed by breath test. Anorexia was evaluated using a personal interview and an eating motivation scale (VAS). The VAS included five questions that are answered before and after eating. The questions concern desire to eat, hunger, feeling of fullness, prospective consumption, and palatability. Biochemical markers of nutrition and inflammation were also determined. ♦ Results At baseline, group I showed lower scores for desire to eat, hunger sensation, prospective consumption, and palatability. They also showed lower lymphocyte counts, prealbumin, transferrin, serum albumin, normalized equivalent of protein–nitrogen appearance (nPNA), and residual renal function (RRF). In addition, the same group showed higher levels of C-reactive protein (CRP) and more sensation of fullness than the remaining groups. In the entire series, we found significant linear correlations between the following markers of nutrition and certain questions on the VAS: albumin with before-lunch desire to eat ( r = 0.38, p < 0.05), and prealbumin with before-lunch hunger ( r = 0.41, p < 0.05) and after-lunch hunger ( r = -0.35, p < 0.05). Negative linear correlations were found between albumin and fullness before lunch ( r = -0.45, p < 0.01), and between prealbumin and before-lunch desire to eat ( r = -0.39, p < 0.05). Negative linear correlations were also seen between CRP and albumin ( r = -0.35, p < 0.05) and between CRP and prealbumin ( r = -0.36, p < 0.05). Similarly, CRP showed a negative correlation with before-lunch desire to eat ( r = -0.38, p < 0.05) and after-lunch desire to eat ( r = -0.45, p < 0.01). After HP eradication, group I showed a significant increase in markers of nutrition and in VAS scores for almost all questions. Simultaneously, they showed a decrease in CRP level. Significant differences were also found in lymphocyte count (1105 ± 259.4 cells/mm3 vs 1330.8 ± 316 cells/mm3, p < 0.05), nPNA (0.9 ± 0.16 g/kg/day vs 1.07 ± 0.3 g/kg/day, p < 0.05), prealbumin (26.7 ± 6.5 mg/dL vs 33.9 ± 56.6 mg/dL, p < 0.01), albumin (3.48 ± 0.3 g/dL vs 3.67 ± 0.35 g/dL, p < 0.05), CRP (1.16 ± 1.14 mg/dL vs 0.88 ± 1.2 mg/dL, p < 0.054), before-lunch desire to eat (56.6 ± 6.8 vs 72.2 ± 4, p < 0.001), after-lunch desire to eat (5.4 ± 2.6 vs 12.3 ± 2, p < 0.01), hunger before lunch (55.4 ± 5.4 vs 73.1 ± 4.6, p < 0.001), hunger after lunch (5.8 ± 2.9 vs 11 ± 4, p < 0.01), fullness before lunch (36.6 ± 10.3 vs 18.7 ± 8.8, p < 0.001), consumption after lunch (5 ± 4.7 vs 17.5 ± 18, p < 0.05), and palatability (61 ± 5.3 vs 74.1 ± 4.1, p < 0.001). ♦ Conclusion Infection with HP is associated with anorexia, inflammation, and malnutrition in PD patients. Eradication of HP significantly improves this syndrome. Residual renal function seem to have a protective effect on appetite preservation. The present study supports the hypothesis of the involvement of inflammation in the pathogenesis of malnutrition in PD patients.

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The medical therapy for advanced or metastatic medullary thyroid carcinoma has not been fully established. Somatostatin analogs have been used with variable success in the therapy of a few patients with medullary thyroid carcinoma. In the present study, we evaluated the effects of somatostatin analog therapy on calcitonin (ct) and carcinoembryonic antigen in patients with advanced medullary thyroid carcinoma. Five patients (2 men and 3 women, aged 35-57 yr) with post-operative recurrent medullary thyroid carcinoma received somatostatin analog therapy for 12 weeks. All had been previously treated with total thyroidectomy and lymphadenectomy. Four of them showed positive uptake in (111)In-pentetreotide scanning. One patient was treated with sc octreotide (100 microg/8 h), 3 patients received im slow release lanreotide (30 mg/14 days), and a further one received im octreotide LAR (30 mg/28 days). Serum samples for ct and carcinoembryonic antigen were obtained at 0, 1, 2, 4, 8 and 12 weeks of therapy. Therapy was well-tolerated in general, with minimal side-effects. One patient died after the first month of therapy because of advanced disease. Another patient showed normalization of his ct and carcinoembryonic antigen concentrations at the second week of therapy, maintaining elevated values thereafter. No clinically relevant changes in serum concentrations of ct and carcinoembryonic antigen were observed in the rest of the patients. One patient with positive (111)In-pentetreotide scan, showed no uptake after somatostatin analog therapy. No significant decrease in the size of metastases was evident in the remaining patients. In conclusion, therapy with different formulations of octreotide and lanreotide does not seem to modify serum concentrations of ct and carcinoembryonic antigen in patients with recurrent medullary thyroid carcinoma.