Hyperglycaemic hyperosmolar nonketotic state as a cause of low gonadotrophin levels in postmenopausal diabetic women: a role for severe hypernatraemia.

Hypogonadotrophic hypogonadism is associated with uncontrolled diabetes mellitus. Hyperglycaemia is a unique metabolic abnormality of the hyperglycaemic hyperosmolar nonketotic state (HHNKS) and, as glucose availability regulates gonadotrophin release, we investigated whether gonadotrophin release is inhibited in diabetic women with HHNKS, and whether hyperglycaemia, hypernatraemia or both inhibit in vitro gonadotrophin-releasing hormone (GnRH) expression in GT1-7 neurones. Three groups of postmenopausal women were studied: nine diabetics with HHNKS, nine hospitalised ill nondiabetics and 15 healthy women. In addition, the effects of glucose (5.55, 33.3, 66.6 mmol/l) and sodium chloride (150 and 170 mmol/l) on GnRH expression were investigated using GT1-7 neurones. Postmenopausal diabetics with HHNKS showed a decrease in serum levels of luteinising hormone (diabetic HHNKS 2.2 +/- 0.9 IU/l versus ill nondiabetic 21.0 +/- 2.3 IU/l and healthy controls 20.9 +/- 2.8 IU/l, P < 0.01), follicle-stimulating hormone (diabetic HHNKS 8.2 +/- 2.1 IU/l versus ill nondiabetic 50.4 +/- 9.1 IU/l and controls 60.2 +/- 6.9 IU/l, P < 0.01) and free 3,5,3'-triiodothyronine (diabetic HHNKS 1.48 +/- 0.57 pmol/l versus ill nondiabetic 4.28 +/- 0.26 pmol/l and controls 3.88 +/- 0.11 pmol/l, P < 0.01). The plasma cortisol level was higher in both diabetic (985 +/- 130 nmol/l) and ill nondiabetic (726 +/- 52 nmol/l) women than in healthy women (512 +/- 47 nmol/l), but no differences were observed in plasma oestradiol, thyroid-stimulating hormone or free thyroxine. In vitro GT1-7 neurones expressed three-fold less GnRH at 170 mmol/l than at 150 mmol/l NaCl, whereas changing glucose concentrations in the culture medium did not affect GnRH expression. In conclusion, postmenopausal diabetic women with HHNKS show decreased serum gonadotrophin levels, and severe hypernatraemia may participate in the hypogonadotropism observed in HHNKS.

Etiología y patogenia de la acromegalia / Etiology and pathogenesis of acromegaly

La acromegalia es una enfermedad producida por la hipersecreción crónica e inapropiada de la hormona del crecimiento (GH) que se inicia después del cierre de los cartílagos de crecimiento. La función hipofisaria normal está sometida a un estrecho control hipotalámico y de retroalimentación negativa que comprende la propia GH, el factor de crecimiento similar a la insulina tipo I y las hormonas hipotalámicas: la hormona liberadora de GH, que potencia la secreción de GH y su transcripción génica, y la somatostatina, que inhibe su secreción y tiene escaso efecto en su síntesis. El papel de la nueva hormona ghrelina está aún por dilucidar. La acromegalia está causada en el 98% de los casos por un tumor secretor de GH localizado en la hipófisis, mientras que las causas extrahipofisarias son muy raras. La patogenia de estos tumores hipofisarios sigue siendo en gran parte desconocida y en su origen se han incluido tanto un defecto primario de la célula somatotropa hipofisaria como alteraciones en el control hipotalámico de la secreción de GH. A pesar de que se han descrito defectos moleculares asociados a estos adenomas, la base molecular de la tumorogenia hipofisaria está por definir (AU)

Acromegaly is a disease due to an inadequate and chronical hypersecretion of growth hormone initiated after epiphyseal fusion. Normal pituitary function is subjected to a strict hypothalamic control and negative feedback including GH, IGF-I and hypothalamic hormones: GH-RH improves GH secretion and its gene transcription while somatostatin inhibits its secretion and has a limited effect on its synthesis. The role of the new hormone, ghrelin, is yet to be clarified. In 98% of cases acromegaly is due to a GH- secreting tumour located in the pituitary gland. Extrapituitary causes are very uncommon. The pathogenesis of these pituitary tumours is, in its majority, unknown, involving in its origin a primary defect of pituitary somatotroph cell and also disturbances in the hypothalamic control of GH secretion. Despite the fact that molecular defects associated with these adenomas have been described, the molecular basis of pituitary tumorigenesis remains to be elucidated (AU)

Can treatment with somatostatin analogs replace neurosurgery?

There is an ongoing controversy on first-line treatment in acromegaly. Although transsphenoidal surgery has always traditionally been considered the first option, the evolution of new medical treatments is now challenging the clinical paradigm. In fact, somatostatin analogs are highly effective, convenient, avoid the growth of tumors or even shrink them, and also have the advantage of preserving normal pituitary function. On the other hand, when successful, neurosurgery has the advantage of eliminating long-term medical treatment and is less expensive. This manuscript discusses the pros and cons of both treatments.

[Superior vena cava syndrome and insular thyroid carcinoma: the stent as a palliative therapeutic alternative]. / Síndrome de vena cava superior y carcinoma insular de tiroides: el stent como alternativa terapéutica paliativa.

The superior vena cava syndrome (SVCS) is a uncommon complication of thyroid cancers. It is produced as consequence of the mediastinal spread of the tumor or by intravascular invasion with thrombosis. We describe a case of insular thyroid carcinoma with an SVCS solved by putting an intravenous stent. The patient was a 73 year old male that consulted for aphonia and presence of a tumor in the right side of the neck of two months of evolution. The PAAF of thyroid suggested the diagnosis of "follicular tumor". A total thyroidectomy was performed on the patient and the sample histological study revealed the existence of a insular carcinoma. An ablative dosis of 131I was administered to him. One year after the patient developed the SVCS. A TAC detected a tumoral relapse consistent with clinical syntoms, and was confirmed by a high level of Tg (with TgAntibodies -). As the patient showed a slight response to radiotherapy (52Gy), a thoracic phlebography was realized demostrating an extense upper vena cava obstruction. After having accomplished an angioplasty, a long stent (20 mm wide) was put into the upper vena cava that was followed by a fast clinical and radiological improvement. A new phlebography practiced three month later showed a rapid venous flux through the stent, and near total disapperance of collateral circulation on thorax wall and mediastinum.

Síndrome de vena cava superior y carcinoma insular de tiroides: el stent como alternativa terapéutica paliativa / Superior vena cava syndrome and insular thyroid carcinoma: the stent as a palliative therapeutic alternative

El síndrome de vena cava superior (SVCS) es una complicación rara del cáncer de tiroides, que se produce como consecuencia de la invasión mediastínica por el tumor o por la invasión intravascular del mismo con trombosis. Creemos describir el primer caso de carcinoma insular de tiroides (variante tumoral indiferenciada del ca. folicular) con SVCS resuelto mediante la colocación de un stent venoso, que deviene así una alternativa eficaz y menos agresiva que la quirúrgica. Se trata de un varón de 73 años que ingresa por un cuadro de disfonía y tumoración laterocervical derecha de dos meses de evolución; la PAAF de tiroides sugirió neoplasia folicular realizándose tiroidectomía total revelando el examen histológico un carcinoma insular de tiroides y administrándose una dosis ablativa de 100 mCi de I131. Al año desarrolla un SVCS, observándose en la TAC recidiva tumoral, con elevación de las cifras de tiroglobulina (Tg) previamente normales. Descartada la indicación quirúrgica se administra radioterapia (52Gy) con despreciable respuesta clínica y agravamiento del cuadro a los pocos meses. Ante la imposibilidad de cirugía y radioterapia, se realizó por vía venosa braquial una flebografía torácico-mediastínica demostrándose obstrución venosa a nivel de la vena cava superior. Se realizó angioplastia y colocación de un stent desde vena innominada hasta vena cava superior; asistiéndose inmediatamente a una franca mejoría clínica. La flebografía de control a los tres meses mostró la permeabilidad del stent con flujo venoso rápido y desaparición de la circulación colateral cérvico-mediastínica (AU)

The superior vena cava syndrome (SVCS) is a uncommon complication of thyroid cancers. It is produced as consequence of the mediastinal spread of the tumor or by intravascular invasion with thrombosis. We describe a case of insular thyroid carcinoma with an SVCS solved by putting an intravenous stent. The patient was a 73 year old male that consulted by aphonia and presence of a tumor in the right side of the neck of two months of evolution. The PAAF of thyroid suggested the diagnostic of “follicular tumor”. A total thyroidectomy was performed on the patient and the sample histological study revealed the existence of a insular carcinoma. An ablative dosis of131I was adminestered to him. One year after the patient developed the SVCS. A TAC detected a tumoral relapses consistent with clinical syntoms, and was confirmed by a high level of Tg (with TgAntibodies -). As the patient showed a light response to radiotherapy (52Gy), a thoracic flebografy was realized demostrating an extense uper cave venous obstruction. After having accomplished an angioplastia a long stent (20 mm wide) was putt into the uper cave vein that was followed by a fast clinical and radiological improvement. A new flebgraphy practiced three month later showed a rapid venous flux throuhgt the stent, and near totall disappereance of collateral circulation on thorax wall and mediastine (AU)

[Bacteremia and endocarditis caused by Streptococcus bovis in patients with alcoholic hepatopathy without evidence of colonic pathology]. / Bacteriemia y endocarditis por Streptococcus bovis en pacientes con hepatopatía alcohólica sin evidencia de patología colónica.

The association of Streptococcus bovis bacteremia and endocarditis with colonic pathology, mainly neoplastic, is well known. Its relationship with liver disease without evidence of gastrointestinal disease has been rarely described. To analyze the association between S. bovis infection and liver disease, positive blood cultures for this microorganism in hospitalized patients in the Internal Medicine and Gastroenterology Departments from December 1993 until October 1995, have been reviewed. Three cases of S. bovis infection (one bacteremia, two endocarditis) were found. Alcoholic liver disease was diagnosed in all three patients, with associated hepatitis C virus in one of them. Colonic pathology was excluded by colonoscopy and/or barium enema. Other gastrointestinal disorders were excluded by means of gastroscopy, barium gastrointestinal study and abdominal ultrasonography. Antibiotic therapy was based in betalactamics, with associated aminoglycoside in two cases. One patient needed aortic and mitral valve replacement and another one needed orthotopic liver transplantation. No new gastrointestinal pathology emerged in the follow-up (5-23 months). Cases of S. bovis bacteremia and endocarditis should be screened not also for colonic pathology, but also for liver disease, particularly in alcoholics.