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Los prolactinomas son adenomas hipofisarios productores de prolactina, que constituyen aproximadamente el 40% de todos los adenomas hipofisarios secretores del adulto. De ellos la mayoria, el 90%, son microprolactinomas. Su tratamiento puede ser medico, quirurgico o con radioterapia, constituyendo el tratamiento medico con agonistas dopaminergicos, la primera alternativa terapeutica mas acertada. Considerando la escasez de estudios a largo plazo con los diferentes agonistas dopaminergicos empleados en el tratamiento de los prolactinomas, nuestro trabajo se ha centrado fundamentalmente en el uso de bromocriptina y en menos casos de cabergolina. Por tanto nuestra hipotesis principal es: el prolactinoma puede ser curado con este tipo de farmacos. Como hipotesis secundaria: existe una gran variabilidad individual en el tiempo necesario para considerar curada esta enfermedad.

Introduction Prolactinoma is the most frequent functioning pituitary adenoma. Most commonly occurs as microprolactinoma (less than 1 cm in size), which may be cured with medical therapy, but few long-term studies are available about optimal duration of treatment with dopamine agonists to ensure cure after drug discontinuation and its withdrawal without recurrence are do not report consistent results. Objective To establish criteria for cure of microprolactinoma with medical treatment and to analyze the potential predictors involved. Patients A retrospective study was conducted on 47 adult women with microprolactinoma followed up between 1975 and 2010; none of them had undergone prior surgery or radiotherapy, and all of them received treatment with a dopamine agonist for at least 4 years. They were divided into two groups for analysis: cured patients with at least 4 years with normal prolactin levels after drug discontinuation, and not cured patients. Results Cure was achieved in 57.4% of patients. Only age at diagnosis was a significant predictor: there were more young patients in the cured group and youngest patients needed less time to cure. Development of empty sella turcica or normal MRI was similar regarding time to cure. Conclusions Microprolactinoma may be cured with dopamine agonists, and life-long treatment is not required, although more than 10 years may be required to achieve cure, 11.6 ± 5.3 years in our experience.

In order to assess the association between empty sella (ES) and primary autoimmune hypothyroidism, and the possibility of a common pathogenesis. We retrospectively studied all patients with presumed ES diagnosed in the last 20 years, most of whom were treated by our Endocrinology Department. Subjects with a known etiology were excluded. Incomplete records or those with a doubtful diagnosis were also excluded. A total of 56 subjects were included in the study. ES was diagnosed by pituitary MRI. The measurement of free T4, TSH, and antithyroid antibodies (TPOAb and TgAb) was assayed using commercial kits. The cases of hypothyroidism obtained were compared with those in another group of similar patients, diagnosed with diabetes mellitus type 2, through χ2 test. A total of 15 (26.78%) patients of 56 with ES had autoimmune thyroid disease (subclinical or clinical hypothyroidism). Primary hypothyroidism with negative antithyroid autoantibodies was found in a further 13 patients (23.21%). The 46.42% of ES had primary hypothyroidism; this result had obtained a statistically significant difference when compared to the ratio obtained in the group of diabetes mellitus type 2 (P < 0.0029). There is an important association between ES and autoimmune thyroid disease, which reached 26.78% in our series. We suggest the possibility of a common pathogenesis for certain cases of ES and autoimmune thyroid disease, with the end point of ES in the pituitary, and atrophy in the thyroid gland.

Purpose: A new technique for stem cells intrapancreatic autotransplantation in rats. Basic Procedures: Section of a femoral diaphysis and aspirations of the bone marrow in both femoral segments were performed. A Kirschner needle was placed into the femur. Cells were isolated in Ficoll gradients and preserved at 4–68C. The second day, cells were injected, via aortic celiac trunk, into the pancreas of the same rat. Results: Femoral surgery were well tolerated. Intrapancreatic homing of the injected cells was suggested with methylene blue injection that stained the pancreas, and proved by labeled cells in pancreas sections. Cell counts after Ficoll isolation were 1 10 6 6 2 10 5 ES. Conclusions: A technique is described for stem cell autotransplantation in rats. First we obtain autologous bone marrow-derived stem cells. Second, we inject the cells in the pancreas of the donor rat. This approach can be applied to experimental diabetes and other pancreatic processes. V V C 2006 Wiley-Liss, Inc. Microsurgery 26:539–542, 2006.

We have reported, previously, some effect of allogenic hepatic cells for islet tolerance when they are injected mixed (hepatic cells and islets) in different proportions via portal vein, in diabetic Wistar rats. Now we have studied the role of allogenic hepatic cells injected sequentially 15 min before islets, comparing via the portal vein (A and B groups) and via the cava vein (C and D groups) with a control group of islets alone. The allogenic islets were always injected via portal vein, in similar conditions, while the ratio of hepatic cells/islets was 100:1 (A, C groups) or 200:1 (B, D groups). Islets and hepatic cells were obtained from several different rats. The transplanted rats were observed during 30 days and results compared among the different rat groups: porta-porta (P/P), cava-porta (C/P), and control group. Statistically, a significant interaction between type of transplant and proportion of hepatic cells was observed. Also, C plus D groups showed statistical difference with the control group (p < 0.017) and also all the groups together (p < 0.047). These results suggest that hepatic cells can induce, in some cases, islet graft prolongation in Wistar rats. Better results were obtained when hepatic cells were injected via the cava vein than via the portal vein. Because we used a liver cell suspension integrated for several kinds of cells, the study does not clarify if this effect can be related to some specific hepatic cell subpopulation. To confirm the results and to determine if the hypothetical mechanism can be attributed to a block of the immune system or to some factor secreted by hepatic cells, more studies must be performed.

El termino diabetes mellitus postrasplante (DMPT) se refiere a la aparicion de diabetes mellitus en individuos que han sido previamente sometidos a trasplante de organos, fenomeno que se ha observado a medida que las tasas de supervivencia de los receptores de trasplante se prolongan, gracias a la mejora en las tecnicas de trasplante y la introduccion de nuevos medicamentos inmunodepresores. De entrada surgen dos planteamientos: a) la posibilidad de que estos pacientes podrian haber desarrollado diabetes aunque no hubiesen sido trasplantados 1 , y b) la relacion causal con los medicamentos empleados durante y despues del trasplante. Aunque siempre influiran la predisposicion individual y la historia familiar de cada paciente, en muchos casos existe evidencia clinica y experimental de que los inmunodepresores pueden ser la causa del incremento del riesgo de padecer diabetes postrasplante 2 . El numero de pacientes que sobreviven mas de 10 anos al trasplante de organos es cada vez mayor, y el desarrollo de diabetes mellitus en ellos puede ocasionar morbimortalidad debido a complicaciones micro y macrovasculares

Feminizing adrenal tumours are very rare. We report the clinical and hormonal study of a case, a 49 years old male, since his first consultation until his death 6 years after the initial diagnosis, and a review of the other 5 Spanish patients previously published. His initial symptoms were gynecomastia and libido decrease, with increase of plasmatic and urinary oestrogen levels, plasma testosterone near low normal level and a right adrenal gland tumour that, after its removal, showed a benign histology and was classified as an adrenocortical adenoma. Three years after, initial symptoms returned, with oestrogen, glucocorticoid and androgen hypersecretion, tumour local relapse and peritoneal, liver and lung metastasis. After mitotane and aminoglutethimide therapy, hormonal concentrations fell temporary and then raised again until his death 3 years later. The main special feature of this case is the apparently benign initial adrenal tumour with only oestrogen hypersecretion, and its relapse 3 years later with secretion of several steroid hormones, generalized metastasis and no response to medical therapy.

Our patient was a 65-year-old woman previously diagnosed with Addison's disease. She presented an empty sella turcica and, at the age of 47, was discovered to have autonomous hypersecretion of adrenocorticotropic hormone (ACTH), suggesting a corticotropic adenoma secondary to Addison's disease, with a lack of response to high levels of dexamethasone. She maintained high ACTH levels despite corticosteroid treatment.The patient underwent a CRH stimulation test using an intravenous bolus (100 microg) with samples every 30 minutes for 3 hours and, the day after, an octreotide infusion (0.1 mg/200 cc saline) for 2 hours with measurements every 30 minutes for 3 hours. The following month she received subcutaneous octreotide 0.1 mg tid., and samples were taken every week.Thirty minutes after the corticotropic-releasing-hormone (CRH) stimulation test, baseline ACTH levels (1 063 pg/ml) increased to 1530, the other values lying between 1 020-862. After octreotide infusion, baseline ACTH (1 212 pg/ml) was 946-643-1 630-4 600-1 730 at 30-60-90-120-180 minutes. The following month, with octreotide treatment, serum ACTH levels were 454-768-1233-429 pg/ml each week.Octreotide acts mainly on somatostatin type 2 receptors (SSTR2) and has no effect in Cushing's syndrome, although a suppressor effect in some ACTH ectopic hypersecretions and in Nelson's syndrome has been demonstrated. It has been observed that SSTR5 appear more frequently than SSTR2 in corticotropic adenomas and corticosteroids downregulate octreotide sensitivity.Octreotide did not suppress secretion of ACTH in suspected corticotropic adenoma. Newer somatostatin analogues, acting mainly on SSTR5, may be able to control ACTH hypersecretion in cases such as this.