ACTA ENDOCRINOLOGICA (BUC)

We present the case of a 29 years young man with acromegaly caused by a plurihormonal pituitary adenoma expressing GH, PRL, FSH and TSH within the tumoral cells. Immunoassays showed a high serum level of GH and PRL, and a serum level within normal ranges for FSH, TSH and LH. Tumoral immunohistochemistry (avidin biotin technique) was positive for GH, PRL and TSH. The presence and colocalisation of GH and FSH was shown by immunelectronmicroscopy with double immunogold techniques. The gold particles (sizes 10 nm for GH and 15 nm for FSH) were colocalised within the same translucent secretory granules of some tumor cells, ultrastructurally similar to gonadotroph cells, aside from other tumor somatotroph cells with dense secretory granules and only 10 nm antiserum GH gold particles. High cerebrospinal fluid (CSF) levels of FSH and a high ratio of CSF/serum FSH concentrations, above 1, were the first indicators that revealed, before pituitary surgery, that FSH is secreted from the pituitary tumor. TSH was a “mute” hormone, without biochemical or clinical expression outside the tumor. This pituitary adenoma showed a good response to surgery and to conventional high voltage conformational radiotherapy with the usual dose of 50 Gy. Bromocriptine and Octreotide, but not the gonadotropin releasing hormone agonist (Triptorelin), produced additional beneficial effects. It is tempting to suggest a somatogonadotroph cell as precursor of this pituitary tumor.

Introduction. In the community, hypoglycemic coma is commonly caused by therapies for diabetes mellitus, or excessive alcohol consumption. Little information is available on the causes and outcome of hypoglycemic coma in non-diabetic patients. Patients and Methods. We retrospectively surveyed adult patients admitted to a regional emergency hospital with hypoglycemic coma in a 18-years period, identifying 80 admissions of 79 patients. 72 cases (91.14%) presented hypoglycemic coma induced by anti-diabetic medications in attempted suicide. The others had hypoglycemic coma induced by deliberate selfpoisoning with other drugs influencing glucose metabolism, sometimes associated with excessive consumption of alcohol. Results. A history of psychiatric illness was present in 15 patients (19%), and 2 cases (2.53%) had chronic alcoholism. Neurological manifestations of hypoglycemia were the principal reason for admission, observed in all patients, and 15 patients (19%) had precipitated convulsions. Although some patients received treatment for hypoglycemia before admission, hypoglycemia recurred in 12 cases (15.19%) in hospital. Morbidity included ventricular arrhythmias (8.86%), non-cardiogenic acute pulmonary edema (1.26%), and transient neurological disturbances, in 2 elderly patients. Two cases died following admission, but death was not the direct result of hypoglycemia. Therapeutic measures consisted in antidote therapy, toxin removal, and supportive therapy. Conclusion. Though drug-induced hypoglycemic coma is rarely encountered in medical practice (2.44% in our study), management of these patients represents a challenging task in every practitioner.

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Sarcoidosis, a disease of an unknown etiology, is characterized by the presence of noncaseating granulomas that are most often found in the intrathoracic lymph nodes, lung and in other organs. Hashimoto' thyroiditis is one of the most common organ-specific autoimmune diseases. Although several reports describe the coincidence of sarcoidosis and Hashimoto's thyroiditis, the understanding of the relationship between these two disorders is limited. A 50 year old woman was admitted for cervico-thoracic goiter having a long history of nodular goiter for about 25 years and being suspect of pulmonary sarcoidosis. A chest radiograph and CT scan showed plunging intrathoracic goiter, lymphadenopathy with a pulmonary interstitial infiltrating process. A tracheo-bronchial lung biopsy revealed non-caseating granulomatous lesions consisting of epithelioid cells, confirming sarcoidosis. Angiotensin converting enzyme was high, therefore the patient was diagnosed as having sarcoidosis. The thyroid gland showed signs of goiter, tenderness and nodularity, without latero-cervical adenopathy. Thyroid function tests were normal and thyroid antibodies were positive. For cervico - thoracic goiter, total thyroidectomy with cervical lymph-adenomectomy was practiced. The histopathological exam demonstrated thyroid sarcoidosis, lymph nodes involvement and chronic thyroiditis.

Introduction. Neuroendocrine renal carcinoma represents less than 1% of all primary neoplasia of the kidney. Most frequently poorly differentiated carcinoma is diagnosed in advanced stages and they have an aggressive evolution and limited survival rate. Neuroendocrine carcinomas that arise from the renal pelvis are frequently associated with squamous cell carcinoma or adenocarcinoma. Material and method. We present the case of a female patient, known for 3 years before with an undefined retroperitoneal lymph node metastasis, being diagnosed at present with a left large cell neuroendocrine renal carcinoma, who initially had lymph node metastasis. Results. Until now, 118 cases of primary neuroendocrine renal carcinomas have been reported. A limited number of poorly differentiated neuroendocrine carcinomas have been reported. Discussion. Due to the clinical and biological findings, the aggressive evolution with early metastasis of lung and bone, the patient is included in the group of poorly differentiated carcinomas. In these cases, multimodal treatment is a gold standard. After surgical treatment and palliative chemotherapy with platinum salts, we obtained a partial remission of the disease and the control of symptoms. Conclusions. Regarding large cell neuroendocrine carcinoma, the surgical treatment remains the treatment of choice. Chemotherapy can determine limited results, improve the quality of life and enhance the overall survival rate.

Background. Advances in imaging techniques have led to increasing discovery of\r\nadrenal and pituitary &#8220;incidentalomas&#8221;, tumors with normal endocrine function and no\r\ncompression mass effects. We evaluated the age at diagnosis (AD) in patients with benign\r\nnon-functioning adrenal incidentalomas, as compared to pituitary non-functioning tumors,\r\nin a series of patients from a national center of endocrinology. Methods. From 2,123\r\nconsecutive patients with adrenal and pituitary tumors hospitalized between 1977 - 2009,\r\n2,069 patients were analysed. The study groups included: group A - 137 patients with\r\nadrenal incidentalomas (AI), group B - 534 patients with pituitary incidentalomas (PI).\r\nControl groups included 1,398 patients: group C1 147 patients with adrenal carcinomas or\r\nbenign hormone-secreting adrenal tumors, and group C2, 1,251 patients with pituitary\r\nsecreting adenomas or large non-functioning pituitary macroadenomas (NFA). Imaging was\r\ndone by computed tomography and/or magnetic resonance after 1981 and by skull X-ray or\r\npneumoencephalography before 1981. Results. Mean age AD is more advanced in patients\r\nwith AI (53 ? 11.9 years, range 21 - 78 yr) than in patients with PI (36.8 ? 13.1 years, range\r\n10 - 81 yr), p < 0.01. AD was higher in AI than in patients with secreting adrenal tumors,\r\nbut similar in patients with adrenal malignancy. There is an age-related increase in the\r\nproportion of AI among patients with adrenal tumors, and of NFA, but not of PI, among\r\npatients with pituitary tumors. In patients aged over 65 years, 74% of patients with adrenal\r\ntumors have AI, while only 18% of patients with pituitary tumors have PI and 42% have\r\nNFA. AD in NFA (49.3 ? 13.1 yr, range 12 - 79 yr) was more advanced than in PI (p < 0.01).\r\nAD does not correlate with tumor size. Tumor growth occurred in 24% of AI (follow-up 3.0\r\n? 2.8 yr) and only in 0.7% of PI, p<0.01 (follow-up 3.1 ? 2.5 yr).\r\nConclusions. Adrenal non-functioning benign tumors show a clear association with ageing,\r\nin contrast with pituitary incidentalomas. It seems unlikely that most pituitary incidentalomas in\r\nyoung patients become large NFA, whose development seems to be also age-related. It is tempting\r\nto suggest that pituitary tumorigenesis starts earlier than adrenal tumorigenesis.

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accepted. Such an intrinsec system of the pineal gland was revealed by Rumanian scientists, which found a high renin like biological activity in the rat pineal, after nephrectomy, and also de novo production of isorenin by the monolayer cultured pineal cells; angiotensin I (A I) - immunoreactivity -was also found in the rat pineal at much higher concentration than in the brain structures. In this paper we add morphological evidences regarding components of the RAS in the bovine pineal gland. Bovine pineals were processed by immunohistochemistry for angiotensinogen, angiotensins I and II, as well as for renin. Frozen pineals were processed by "in situ" hybridization for angiotensinogen and renin mRNAs. Angiotensin converting enzyme(ACE), aminopeptidase A and angiotensin III (AIII) were not investigated. Our data showed that a number of pinealocytes stains for angiotensins (AI and AII), but the renin staining was negative. No nerve fibres were stained with AI or AII. The angiotensins-positive cells were dispersed in the pineal parenchyma, without a particular distribution in relation to the blood vessels. The angiotensinogen immunohistochemistry showed sparse positive cells. The "in situ" hybridization data showed the signal for angiotensinogen mRNA located over pinealocytes, while the renin mRNA was absent. The local synthesis of angiotensinogen in the bovine pineal cells, as a substrate for generation of AI and AII are supported by our data. However, at least the first enzyme involved in this cascade is different from the typical renin. The presence of an angiotensin system without renin in the pineal gland is an additional argument to the evidence that angiotensin II and related peptides can be formed by renin- and ACE- independent protease pathways.