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Comment on Long-Acting Lanreotide Inducing Clinical and Biochemical Remission of Acromegaly Caused by Disseminated GHRH Secreting Carcinoid

Janusz Krassowski, Wojciech Zgliczyski, Wojciech Jeske and Stefan Zgliczyski

Department of Endocrinology Medical Center of Postgraduate Education Warsaw, Poland

In the September 1998 issue of JCEM, Drange and Melmed (1) reported on the use of long-acting somatostatin analogue, lanreotide, in ectopic GHRH syndrome due to a bronchial carcinoid. A similar case was presented by us at 1997 Meeting of Polish Endocrine Surgeons in Warsaw (2). We would like to comment briefly on lanreotide treatment in ectopic acromegaly.

A 40-yr-old man was referred to our institution for the evaluation of acromegaly and thyroid tumor. At the age of 13 the patient had undergone a left inferior lobectomy for a bronchial carcinoid. Since the age of 20, a slow, gradual development of typical acromegalic features had been noted by the patient, but he did not seek medical advice. At 37, because of hemoptysis, he was admitted to the regional hospital where the recurrence of carcinoid was diagnosed by computed tomography scan, with the large tumor infiltrating both main bronchi just below the bifurcation. The tumor was considered inoperable.

On admission the patient had typical acromegalic features with a 2-cm tumor of the left lobe of thyroid gland. The endocrine evaluation showed elevated GH and IGF-I levels: 130 µg/L and 1380 µg/L, respectively. Prolactin and -subunit levels were also elevated: 74 µg/L and 15.0 µg/L, respectively. The urinary excretion of 5-HIAA was 73.5 µmol/g creatinine per day. The pituitary hyperplasia was noted on magnetic resonance imaging scan without evidence of pituitary tumor. Multiple liver metastases were demonstrated on computer tomography scan. These findings combined with the patient’s history were highly suggestive of an ectopic GHRH secretion by the bronchial carcinoid tumor. This was confirmed by the very high GHRH level: 9.2 µg/mL (normal values < 0.1 µg/mL). GHRH was determined by Professor Klaus von Werder (Schlosspark Klinik, Berlin, Germany).

As the thyroid tumor was typical of apudoma on cytologic examination, and calcitonin levels were normal we decided to perform a total thyroidectomy. The carcinoid’s metastasis was demonstrated in the resected tumor on pathologic examination. The removal of the thyroid tumor resulted in the fall in GHRH level to 6.1 µg/L.

At this point the diagnosis of the cetopic GHRH syndrome seemed certain. We started with lanreotide (Somatuline, Ipsen Beaufour, France) 30 mg im, every 2 weeks. After 20 weeks GHRH levels dropped to 3.5 µg/L, while the GH level fell to 14 µg/L. GH was estimated before every injection of lanreotide. We observed a gradual fall in GH levels during lanreotide therapy: 99 µg/L at 2 weeks, 80 µg/L at 4 weeks, 35 µg/L at 10 weeks, and 14 µg/L at 20 weeks of the therapy. The lanreotide therapy resulted in a marked and sustained clinical improvement. The patient reported a dramatic fall in perspiration and an increased sense of well-being. On magnetic resonance imaging scan, the volume of the pituitary decreased by one third at the end of 20-week treatment. No side-effects of lanreotide therapy were observed.

It is worth noting that the effect of lanreotide on GH was more pronounced than that on GHRH. In our patient GH levels decreased 8-fold during lanreotide therapy, while GHRH levels decreased only 2-fold. This may suggest a direct effect on pituitary that corroborates the recent reports on the beneficial effect of lanreotide therapy as the preparation for the neurosurgery for pituitary tumors (3).

We conclude that long-acting somatostatin analogues are the drugs of choice in the ectopic GHRH syndrome, and the evaluation of GH levels is more reliable in defining the results of the treatment than GHRH determination.

Footnotes

Address correspondence to: Janusz Krassowski, Department of Endocrinology, Medical Center of Postgraduate Education, Szpital Bielanski, ul. Ceglowska 80, Warszawa, Poland 01–809.

Received December 30, 1998.

References

1. Drange MR, Melmed S. 1998 Long-acting lanreotide induces clinical and biochemical remission of acromegaly caused by disseminated growth hormone- releasing hormone-secreting carcinoid. J Clin Endocrinol Metab. 83:3104–3109.[Abstract/Free Full Text]
2. Krassowski J, Zgliczyski W, von Werder K, Jeske W, Zgliczyski S. 1997. Acromegaly caused by the ectopic GHRH secretion by the bronchial carcinoid. Endokrynol Pol. 48[Suppl 4]:143.
3. Zgliczyski W, Zgliczyski S, Jeske W, et al. 1997 The somatostatin analog (SR-Lanreotide) pretreatment improves the surgical outcome in acromegalic patients harbouring pituitary tumors with somatostatin receptors. J Endocrinol Invest. 20[Suppl]:45–47.

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