Ghrelin is a peptide thought to be involved in the regulation of appetite. Furthermore, significant effects on the release of growth hormone (GH) and ACTH were demonstrated. Contributing to the physiological relevance of this hormone, we investigated the expression of ghrelin and its receptor (GHS-R) in several normal human tissues. RNA samples (BD Biosciences) underwent one-step TaqMan Real-Time RT-PCR. Immunohistochemistry was performed on paraffin-embedded tissues using specific primary antibodies against ghrelin and its receptor. Relevant ghrelin mRNA levels were detected in all human tissues with the highest levels in stomach, pituitary, and small intestine. By immunohistochemistry, ghrelin peptide expression was detectable in reproductive and endocrine organs (ovary, anterior pituitary, adrenal gland), and organs of the gastrointestinal tract (stomach, pancreas). GHS-R1a mRNA expression was demonstrated in 10 of 24 human organs analyzed with the highest levels in pituitary, adrenal gland, and spinal cord. Expression of the receptor peptide was detected by immunohistochemistry in endocrine and reproductive organs (anterior pituitary, thyroid, pancreas, testis), parts of the CNS (cerebrum, cerebellum), and in single cells of bone marrow. Expression of both ghrelin and its receptor in endocrine and reproductive organs may indicate new endocrine or paracrine mechanisms of regulation in these tissues.
Ghrelin is a newly characterized, widely distributed peptide thought to be involved in the regulation of appetite. Significant effects on the release of growth hormone (GH) and ACTH have been demonstrated. This study compares the expression of ghrelin and its receptor (GHS-R) in various adrenal tumors and normal adrenal gland. Normal adrenal tissue was obtained after autopsy. Tissue was obtained from 13 pheochromocytomas (PHEOs), 15 cortisol-secreting adenomas (CPAs), 12 aldosterone-secreting adenomas (APAs), and 16 nonfunctional adenomas (NFAs) following laparoscopic surgery. Expression of ghrelin and GHS-R1a was investigated on RNA levels by using real-time reverse transcription polymerase chain reaction (RT-PCR) and on protein levels by using immunohistochemistry. In the seven normal adrenal glands analyzed, ghrelin mRNA levels were 12-fold lower than in stomach. Ghrelin protein expression was confirmed by immunohistochemistry. In all adrenal tumors, relevant levels of ghrelin mRNA were observed, with significantly lower expression in PHEOs and APAs than in normal adrenal gland. Ghrelin protein was detected in 0% of PHEOs, 55% of APAs, 87% of CPAs, and 54% of NFAs. GHS-R1a mRNA expression was detectable in normal adrenal gland, but the receptor protein was absent. In adrenal tumors, detectable levels of receptor mRNA were found in 38% of PHEOs, 13% of CPAs, and 25% of NFAs. GHS-R1a protein was absent in the majority of adrenal tumors. Expression of ghrelin in normal adrenal gland and adrenal tumors may indicate some unknown physiological function. The pathophysiological relevance of ghrelin expression in adrenal tumors remains to be investigated.
A case of a 70-year-old man presenting with exsudative enteropathy due to light-chain-associated amyloidosis is reported. The diagnosis of systemic mastocytosis associated with IgG/lambda plasma cell myeloma and secondary generalised amyloidosis was carried out by morphological evaluation of bone marrow biopsy. The c-kit point mutation D816Y was detected by molecular analysis. Two years before, a cystadenolymphoma of the left parotid gland had been removed. A moderate increase of loosely scattered spindle-shaped mast cells, a subpopulation of them expressing CD25, an antigen that is not expressed by normal or reactive mast cells, was shown by retrospective analysis carried out on an intraparotideal lymph node. The c-kit mutation D816Y was shown by the molecular analysis of the lymph node. In summary, the notion that systemic mastocytosis may very rarely be associated with B cell neoplasms and that neoplastic mast cell infiltrates may be obscured because of only a minimal increase of atypical mast cells, which are outnumbered by other non-neoplastic cells in the same tissue, is supported by this case. This finding was preliminarily termed "occult" mastocytosis.
The article of Haap et al. in the Experimental and Clinical Endocrinology and Diabetes 117: 289 -293 (2009) has drawn my attention. In their interesting work, the authors describe an ACTH producing microadenoma of the pituitary in coincidence with nodular ACTH cell hyperplasias of the anterior lobe, emphasizing that this combination has not been published before. Motivated from this observation, I reviewed the known older literature on this topic. Back in the 1970 ' s I worked on ACTH cell hyperplasias in combination with ACTH cell adenomas, focusing on surgical specimens of patients with Cushing ' s disease [5 -7] which had been operated with the -at that time just invented -endoscopic transnasal transsphenoidal surgery [2] .Our key observation was that at least in some cases with Cushing ' s disease the ACTH adenomas developed from ACTH cell hyperplasias. This has also been observed in [1,3,4] . Our work was supported by fi ndings from post-mortem pituitary studies that showed nodular hyperplasias in about 6 -7 % of all cases and adenomas in 8 -10 % , respectively. Moreover, we observed many pituitaries with transitions from hyperplasias in adenomas [9] . Focal hyperplasias precede adenomas, but the existence of multifocal hyperplasia that are the basis for the development of adenoma is demonstrable mainly in Cushing ' s disease with ACTH cell adenomas. However, in hyperprolactinemia Prolactin cell hypoplasia can be found also together with Prolactin cell adenomas [7,8] . References
A 53-year-old woman had noticed numerous papules on her trunk and proximal parts of the limbs. They had healed with a central scar surrounded by a reddish wall. Four months later she had to undergo laparotomy for ileus, resulting from a perforation in the region of the middle jejunum: it was excised and sutured over. At laparotomy white plaque-like lesions were noted on the serosa of both small and large intestine. Histological examination of the jejunal exudate and of a skin biopsy both demonstrated malignant atrophic papulosis (Köhlmeier-Dégos' disease). Treatment with ticlopidine, a platelet-aggregation inhibitor (250 mg twice daily), was initiated and she has now been free of extracutaneous symptoms for 6 years.
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