A Spanish adaptation of the Quality in Psychiatric Care-Inpatient (QPC-IP) instrument: Psychometric properties and factor structure.

BACKGROUND AND AIM: Western countries share an interest in evaluating and improving quality of care in the healthcare field. The aim was to develop and examine the psychometric properties and factor structure of the Spanish version of the Quality in Psychiatric Care-Inpatient (QPC-IP) instrument. METHODS: A psychometric study was conducted, translating the QPC-IPS instrument into Spanish, revision of the instrument by a panel of experts, and assessing its psychometric properties. 150 psychiatric inpatients completed the QPC-IP. Test-retest reliability was assessed by re-administering the questionnaire to 75 of these patients. RESULTS: After conducting pilot testing and a cognitive interview with 30 inpatients, it was determined that the QPC-IPS was adequate and could be self-administered. A Cronbach's alpha of 0.94 was obtained for the full instrument and values of 0.52-0.89 for the various dimensions of the questionnaire. Test re test reliability: The Intraclass Correlation Coefficient for the full questionnaire was 0.69, while for the individual dimensions values between 0.62 and 0.74 were obtained, indicating acceptable temporal stability. Convergent validity was analysed using 10-point numerical satisfaction scale, giving a positive correlation (0.49). Confirmatory factor analysis revealed six factors consistent with the original scale. The Spanish version yielded adequate results in terms of validity and reliability. CONCLUSION: Our findings provide evidence of the convergent validity, reliability, temporal stability and construct validity of the Spanish QPC-IP for measuring patient quality in psychiatric care in Spanish hospitals. Hospital administrators can use this tool to assess and identify areas for improvement to enhance quality in psychiatric care.

A Spanish adaptation of the Quality in Psychiatric Care - Inpatient Staff (QPC-IPS) instrument: Psychometric properties and factor structure.

BACKGROUND: Western countries share an interest in evaluating quality of care in the healthcare field. In spite of this, there is a lack of intercultural comparison of the perceptions of professionals. One reason for this may be the lack of standardized instruments. The objective of this study was to investigate the psychometric properties and dimensions of the Spanish version of the Quality in Psychiatric Care-Inpatients Staff (QPC-IPS) instrument. METHODS: After translation and revision of the instrument by a panel of experts, a questionnaire was obtained in Spanish that was administered to a pilot sample. A total of 163 professionals participated in the study. RESULTS: After conducting pilot testing and a cognitive interview with 30 professionals, it was determined that the QPC-IPS was adequate and could be self-administered. Confirmatory factor analysis confirmed six factors that explained 60.9% of the variation. In terms of internal consistency, a Cronbach's alpha of 0.92 was obtained for the full instrument. For test re-test reliability, the intraclass correlation coefficient for the overall questionnaire was 0.91. Convergent validity was analyzed using the NTP394 satisfaction instrument, yielding a positive correlation (0.58). CONCLUSIONS: The results demonstrated that the psychometric properties in terms of internal consistency, temporal stability (test-retest), content validity, and construct validity (confirmatory factor analysis) were adequate. These results confirm that the structure of the Spanish version is similar to the original Swedish version of the QPC-IP.

Donor-derived Strongyloides stercoralis hyperinfection syndrome after simultaneous kidney/pancreas transplantation.

Most cases of strongyloidiasis associated with solid organ transplantation have been due to the reactivation of a latent infection in the recipient as a result of the immunosuppressive therapy; however, donor-derived infections are becoming increasingly frequent. The case of a patient who nearly died of a Strongyloides stercoralis hyperinfection after receiving simultaneous kidney/pancreas transplants is described herein. No specific parasitological tests were performed pre-transplantation, despite the fact that both the recipient and the donor originated from endemic areas. Serological analysis of the donor's serum performed retrospectively revealed the origin of the infection, which if it had been done beforehand would have prevented the serious complications. Current practice guidelines need to be updated to incorporate immunological and molecular techniques for the rapid screening of Strongyloides prior to transplantation, and empirical treatment with ivermectin should be applied systematically when there is the slightest risk of infection in the donor or recipient.

Hipoglucemia por hiperinsulinemia endógena en el adulto / Hypoglycemia due to endogenous hyperinsulinism in an adult

Introducción: La nesidioblastosis es una causa conocida de hipoglucemia en recién nacidos. Sin embargo, en adultos permanece poco entendida, creando un dilema tanto diagnóstico como terapéutico. Exponemos el caso de un paciente varón de 63 años que presenta hipoglucemia hiperinsulinémica en el que no se identificó la existencia de insulinoma antes ni durante la cirugía, practicándosele una pancreatectomía subtotal. La histología mostró la existencia de una nesidioblastosis. Conclusión: Identificamos un paciente con hipoglucemia hiperinsulinémica grave ocasionada por una proliferación difusa de los islotes pancreáticos, por lo que pensamos que esta entidad debe ser tenida en consideración ante un paciente que se intervenga con el diagnóstico de insulinoma no identificado previamente. En estos casos debe considerarse la realización de una pancreatectomía subtotal, a pesar de que el tratamiento óptimo está por determinar

Introduction: Nesidioblastosis is a well-known cause of hypoglycemia in neonates. However, it is poorly understood in adults, creating both diagnostic and therapeutic dilemmas. Case report: A 63-year-old man presented with hyperinsulinemic hypoglycemia. An insulinoma was not identified prior to or during surgery, and subtotal pancreatectomy was performed. Histological examination revealed the presence of nesidioblastosis. Conclusion: We identified a patient with severe hyperinsulinemic hypoglycemia due to diffuse islet cell disease. This etiology should always be considered in patients with a preoperative presumptive diagnosis of insulinoma. In these cases, partial pancreatectomy is indicated, although the optimal treatment remains to be determined

Plasma lipids and blood fluidity in patients with polygenic hypercholesterolaemia treated with fluvastatin.

The clinical benefit brought about by HMG-CoA reductase inhibitors (statins) may not entirely be due to their lipid-lowering effect. Further investigation is necessary in order to determine the significance of ancillary effects to the clinical benefit of statin treatment. We studied 27 polygenic hypercholesterolaemia (PHC) patients before and 3 and 6 months after fluvastatin treatment. A control group of 38 normal, sex and age matched, subjects were also studied. The following parameters were measured: haematimetry, serum lipids and general biochemistry, apo-A/B and lipoproteins, fibrinogen, blood filterability, red blood cell aggregation, blood and plasma viscosity. PHC patients showed lower blood filterability (16.00+/-0.99 vs 19.90+/-2.90 microl/s), higher plasma fibrinogen (274.8+/-41.5 vs 241.6+/-43.2 mg/dl), increased erythrocyte aggregation at low shear stress (8.10+/-1.15 vs 7.19+/-1.29) and increased plasma viscosity (1.26+/-0.06 vs 1.23+/-0.05 mPa.s). Notable lipid changes after 6 months fluvastatin treatment were not accompanied by measurable changes in the haemorheological alterations of the PHC patients.

Influence of age on clinical and immunological characteristics of newly diagnosed type 1 diabetic patients.

The aim of this study was to analyse the immunological and clinical characteristics of a group of patients at the onset of type 1 diabetes and to determine if these findings are age related. For this purpose, 68 newly diagnosed type 1 diabetes mellitus patients referred to our hospital between 1997 and 1999 were studied; 42 were adults (mean age 24+/-3.5 years) and 26 children (mean age 6.1+/-4 years). Autoantibody markers islet cell antibodies, glutamic acid decarboxylase antibodies (GADA) and tyrosine phosphatase antibodies (IA-2A), pancreatic reserve (glucagon test) and HbA1c were determined. Some clinical characteristics, such as mode of presentation and insulin requirements, were also analysed. Type 1 diabetes mellitus was found to be autoimmune in 83.8% of the patients and idiopathic in 16.2%, without significant differences between adults and children. In the whole autoimmune group, GADA was more prevalent in adults and IA-2A more frequent in children. On the other hand, adults showing autoimmune markers developed ketosis more frequently and needed higher insulin doses at diagnosis, while children did not exhibit clinically significant differences associated with the presence or absence of antibodies. In conclusion, in children the presence of autoimmune markers is not related to the mode of presentation or characteristics of type 1 diabetes. In adults, however, the autoimmune group presents with more-severe clinical disease than antibody negative patients. Age at onset seems to be an important parameter in the natural history of type 1 diabetes and must be taken into account in epidemiological or intervention studies.

Optimal insulin treatment in syngeneic islet transplantation.

Insulin-induced normoglycemia has shown to have a beneficial effect on the outcome of pancreatic islets transplanted to diabetic recipients. The aim of the study was to identify the insulin treatment that can maximize its beneficial effect on islet transplants. Six groups of streptozotocin diabetic C57Bl/6 mice were transplanted (Tx) with 100 syngeneic islets, an insufficient beta cell mass to restore normoglycemia, and were treated with insulin as follows: group 1 (n = 9): from day 10 before Tx to day 14 after Tx; group 2 (n = 11): from day 6 before Tx to Tx day; group 3 (n = 11): from Tx day to day 6 after Tx; group 4 (n = 7): from Tx day to day 14 after Tx; group 5 (n = 8): from day 10 to day 24 after Tx; group 6 (n = 18): Tx mice were not treated with insulin. Sixty days after Tx, normoglycemia was achieved in 100% of mice in groups 1, 4, and 5, in 73% of mice in group 2, and in only 45% and 33% of mice in groups 3 and 6, respectively (p < 0.01). Intraperitoneal glucose tolerance, determined only in normoglycemic mice, was similar in groups 1, 2, 4, and normal controls. In contrast, normoglycemic mice from groups 3, 5, and 6, exposed to more severe and prolonged hyperglycemia after Tx, showed higher glucose values after glucose injection, suggesting that hyperglycemia had a long-lasting deleterious effect on transplanted beta cell function. The initially transplanted beta cell mass was maintained in the grafts of normoglycemic mice, but was severely reduced in hyperglycemic mice. Transplanted beta cell mass was similar in normoglycemic groups with normal or impaired glucose tolerance, indicating that impaired glucose tolerance was not due to reduced beta cell mass. In summary, the beneficial effect of insulin-induced normoglycemia on transplanted islets was maximal when insulin treatment was maintained the initial 14 days after transplantation. Exposure to sustained hyperglycemia initially after transplantation had a long-lasting deleterious effect on transplanted islets.

Normoglycemia restores beta-cell replicative response to glucose in transplanted islets exposed to chronic hyperglycemia.

We studied the effects of chronic hyperglycemia on beta-cell replication and mass in transplanted (Tx) islets. Five groups of streptozocin-induced diabetic C57Bl/6 mice were transplanted with 100 (Tx-100) syngeneic islets, an insufficient beta-cell mass to restore normoglycemia. Groups 1 and 2 remained hyperglycemic throughout the study; after 30 days of hyperglycemia, a second transplantation of 250 islets (Tx-250) restored normoglycemia in groups 3, 4, and 5. Tx-250 was harvested on day 60 in all three groups, and transient mild hyperglycemia developed (10-12 days); thereafter, Tx-100 maintained blood glucose values in the normal range. Tx-100 was harvested 14 (group 1), 60 (groups 2 and 3), 74 (group 4), and 90 (group 5) days after transplantation. Hyperglycemia increased beta-cell replication after 14 days (group 1: 1.26 +/- 0.18%, P < 0.05) but not after 60 days (group 2: 0.59 +/- 0.13%) compared with islets exposed to normoglycemia (group 3: 0.51 +/- 0.07%) (analysis of variance [ANOVA], P < 0.0002). beta-cell replication in group 4 increased after Tx-250 harvesting (0.94 +/- 0.16%, P < 0.05). The initially Tx beta-cell mass (0.21 +/- 0.014 mg) was progressively reduced in hyperglycemic groups (group 1: 0.13 +/- 0.020 mg; group 2: 0.048 +/- 0.012 mg; P < 0.05) (ANOVA, P = 0.0001). Restoration of normoglycemia after Tx-250 did not modify beta-cell mass in Tx-100 grafts (group 3: 0.076 +/- 0.008 mg). However, after Tx-250 harvesting, beta-cell mass increased progressively (group 4: 0.11 +/- 0.018 mg; group 5: 0.14 +/- 0.026 mg, P < 0.05), although it was still reduced compared with the initially Tx beta-cell mass (P < 0.05). In summary, Tx islets exposed to severe chronic hyperglycemia showed a limited beta-cell replication and a progressive reduction in beta-cell mass. With normoglycemia, the Tx beta-cells recovered the replicative response to glucose and partially restored the initially Tx beta-cell mass, indicating that normoglycemia, even after long-term hyperglycemia, has a beneficial effect in islet transplantation.

Improved outcome of islet transplantation in insulin-treated diabetic mice: effects on beta-cell mass and function.

Insulin treatment may improve the outcome of islet transplantation. To determine the effects of insulin treatment on transplanted islets, 4 groups of streptozotocin-diabetic C57BL/6 mice were transplanted with 100 islets, an insufficient beta-cell mass to restore normoglycaemia. Groups 1 (n = 12) and 2 (n = 12), were kept normoglycaemic with insulin treatment from day 10 before transplantation to day 14 after transplantation; groups 3 (n = 12) and 4 (n = 18), were not treated with insulin. Grafts were harvested 14 (groups 1 and 3) or 60 (groups 2 and 4) days after transplantation and beta-cell mass and replication were measured. When insulin was discontinued all mice maintained normoglycaemia; in contrast, non-insulin-treated groups remained hyperglycaemic throughout the study. Fourteen days after transplantation the beta-cell mass was reduced both in group 1 (0.09 +/- 0.01 mg) and group 3 (0.14 +/- 0.02 mg) compared to the initially transplanted mass (0.22 +/- 0.02 mg, p < 0.01); beta-cell replication and area did not change in group 1, but were increased in group 3. Insulin content, expressed as a function of beta-cell mass, was maintained in group 1 grafts (12.5 +/- 2.0 micrograms/mg), but was severely reduced in group 3 (1.0 +/- 0.2 micrograms/mg) compared to non-transplanted islets (20.4 +/- 3.3 micrograms/mg). In group 2, beta-cell mass increased when insulin was discontinued; 60 days after transplantation beta-cell mass was similar to the initially transplanted mass (0.23 +/- 0.04 mg), glucose levels after an intraperitoneal glucose challenge were normal, and insulin content was preserved (19.6 +/- 2.7 micrograms/mg). In contrast, beta-cell mass was progressively reduced in group 4 (0.08 +/- 0.02 mg, p < 0.001). In summary, insulin treatment reduced the beta-cell mass needed to achieve normoglycaemia in islet transplantation. Islets transplanted to insulin-treated mice showed better beta-cell function, preserved insulin content, and were able to increase their beta-cell mass to meet an increased functional demand.

Beta-cell growth and mass are preserved in long-term syngeneic islet transplantation in streptozocin-induced diabetic Lewis rats.

We determined beta-cell replication and mass in basal and stimulated conditions in long-term transplanted islets. Three groups of streptozocin-induced diabetic Lewis rats were transplanted with 1,000 islets (500 islets under left and right kidney capsules). At 2 (Tx-2), 5 (Tx-5), or 9 (Tx-9) months after transplantation, one of the two grafts (basal) was harvested; 14 days later, the contralateral graft (stimulated) was also harvested. Normoglycemia was achieved and maintained in all transplanted rats, although the capacity to respond to a glucose challenge deteriorated slightly 9 months after transplantation. Beta-cell replication remained stable in Tx-2, Tx-5, and Tx-9 basal grafts and was similar to replication in a control group of nontransplanted rats (0.28 +/- 0.06%); replication increased in Tx-2 (0.90 +/- 0.23%, P < 0.05) and Tx-9 (0.72 +/- 0.09%, P < 0.05) stimulated grafts. Beta-cell mass in basal grafts was similar to the initially transplanted mass (1.24 +/- 0.06 mg) and increased in stimulated grafts in Tx-2 (1.91 +/- 0.38 mg, P < 0.05) and Tx-5 (1.73 +/- 0.27 mg, P = 0.01) groups, compared with basal grafts, and in Tx-2 and Tx-9 groups (1.92 +/- 0.30 mg, P < 0.05), compared with initially transplanted mass. Therefore, beta-cell replication and mass were preserved up to 9 months after syngeneic transplantation, and beta-cells maintained the capacity to respond to increased metabolic demand, suggesting that replication is not a limiting factor in the survival of transplanted islets.

Ketoacidosis at diagnosis is predictive of lower residual beta-cell function and poor metabolic control in type 1 diabetes.

To determine the factors at diagnosis predictive of changes in residual beta-cell function and metabolic control in Type 1 diabetes, 125 patients older than 7 years of age consecutively diagnosed between March 1986 and June 1991 were followed prospectively for two years. The effect of age, gender and the presence of ketoacidosis (DKA) and islet-cell antibodies (ICA) on beta-cell function, metabolic control and insulin requirements were studied by multivariate analysis of variance (repeated measurements over time) in 90 patients who completed follow-up. DKA had an independent negative effect on residual beta-cell function over time (p = 0.001). ICA-positive patients had lower residual beta-cell function at the end of follow-up (p < 0.05), but overall differences were not significant. DKA and younger age had an independent negative influence on metabolic control (p < 0.05) and insulin requirements (p < 0.001) over time. It is concluded that residual beta-cell function in Type 1 diabetic patients two years after diagnosis was independently influenced by DKA and ICA at diagnosis. Moreover, DKA and age influenced metabolic control and could thus be used to predict those patients with rapidly deteriorating metabolic control who might benefit from a more intensive therapeutic approach.