Pituitary adenomas secreting both, growth hormone and thyrotropin, are rare. Octreotide has been used in pituitary adenomas secreting growth hormone and (in fewer cases) in pituitary adenomas secreting thyrotropin. However, there is very little data on the efficacy of octreotide in patients with bihormonal pituitary adenomas. We report on a 55 years old female patient, presenting with acromegaly and hyperthyroidism due to pituitary growth hormone and thyrotropin-hypersecretion. Concomitant morbidity included diabetes mellitus type II and hypertension. A MR scan demonstrated a 5cm large pituitary tumour without compression of the optic chiasm. We initiated a therapy with octreotide (Sandostatin 30mg LAR® i.m.) in monthly intervals which resulted in a prompt biochemical and clinical control of bihormonal hypersecretion. Subsequent endoscopic, transsphenoidal pituitary surgery resulted in further improvement of the clinical status. A post-operative endocrine re-evaluation revealed a persistent resolution of bihormonal hypersecretion even without octreotide treatment. A follow-up MR scan showed tumour remnants in the left cavernous sinus. The patient refused radiotherapy and she will receive regular follow-up MR scans and endocrine re-evaluations. This is the first report on a case of preoperative endocrine control of both, growth hormone and thyrotropin hypersecretion, in a large pituitary macroadenoma by the long-acting octreotide Sandostatin LAR®. Larger studies of octreotide treatment in bi- and also plurihormonal hypersecreting pituitary adenomas are warranted to clarify efficacy and safety as well as special characteristics of octreotide treatment in this subgroup of hormone secreting pituitary tumours.

Hereditary pancreatitis is due to heterozygosity for gain-of-function mutations in the cationic trypsinogen gene which result in increased levels of active trypsin within pancreatic acinar cells and autodigestion of the pancreas. The number of disease-causing defects is generally considered to be low. To gain further insight into the molecular basis of this disorder, DNA sequence analysis of all five exons was performed in 109 unrelated patients with idiopathic chronic pancreatitis in order to determine the variability of the underlying mutations. Two German females and one German male were carriers of the most common N29I and R122H mutations (trypsinogen numbering system). In a Turkish proband, an arginine (CGT) to cysteine (TGT) substitution at amino acid position 116 was identified. Family screening demonstrated that the patient had inherited the mutation from his asymptomatic father and that he had transmitted it to both of his children, his daughter being symptomatic since the age of 3 years. In addition, a German male was found to be a heterozygote for a D100H (GAC→CAC) amino acid replacement. Our data provide evidence for genetic heterogeneity of hereditary pancreatitis. The growing number of cationic trypsinogen mutations is expected to change current mutation screening practices for this disease.