Guidelines for Writing a Case Report Abstract:

1. Please recognize that rarity is not a reason in itself for submitting a case report; but rather, there should be learning points or lessons.
2. The title of the abstract should be transparent.
3. The sections of the abstract should include: Introduction/Background; Clinical Case (to include diagnostic evaluation, treatment and follow-up); Clinical Lesson(s)/Conclusion
4. The conclusion should emphasize the learning point(s) and implications for practice.
5. Abbreviations that are familiar to endocrinologists are acceptable without explanation (e.g., PCR, GHRH, TSH).
6. For laboratory parameters, the units of measurement and normal ranges must be provided.
7. Statements about ongoing studies or pending results should be avoided. 8. References are not necessary and should be kept to a minimum.

Here is an example of an outstanding Case Report Abstract:

[OR51-4] ACTH-Independent Macronodular Adrenal Hyperplasia and Histamine-Induced Cortisol Secretion: In Vivo and In Vitro Studies.

Maarten O van Aken, Richard A Feelders, Wouter W de Herder, Alberto M Pereira, Neveen A Hamdy, Steven W Lamberts, Aart Jan van der Lely, Leo J Hofland, Johannes A Romijn. Intern Med, Sect Endocrinol, Erasmus Med Ctr, Rotterdam, Netherlands; Endocrinol and Metab, Leiden Univ Med Ctr, Leiden, Netherlands

Background: In several animal species, histamine (H) has been shown to stimulate adrenal steroid secretion. In humans, however, this has not been reported yet.

Clinical case: A 51-year women showed typical symptoms of Cushing's syndrome (CS). Initial tests were consistent with ACTH-independent CS: elevated 24hr urinary cortisol secretion (449 and 517 nmol/24hr, n<220 nmol/24hr), abnormal 1 mg dexamethason overnight test (cortisol after 1 mg dex 620 nmol/l, n<50 nmol/l), elevated midnight serum cortisol (670 nmol/l, n<220 nmol/l), ACTH-concentrations below the level of detection (< 4 ng/l). An abdominal CT-scan showed bilateral macronodular adrenal hyperplasia (diameter adrenal glands right 3 cm, left 2 cm). A screening protocol, as proposed by Lacroix et al. (1), revealed no change in cortisol secretion in response to LHRH, TRH, food, posture, metoclopramide or cisapride.

Unexpectedly, an increased 24 hr urinary N-Methyl-Histamine (N-M-H) excretion was found (2623 and 2720 µmol/mol creat, n < 200 µmol/mol creat). Bone marrow biopsy did not show mastocytosis. Evaluating a possible link between H and cortisol secretion, a single i.v. dose of H1 and H2-antagonists (clemastine 4 mg and ranitidine 300 mg) did not affect serum cortisol concentrations. The patient was treated by laparoscopic biadrenalectomy. Histological examination showed macronodular hyperplasia of the adrenal cortex. Noteworthy, 24 hr urinary N-M-H excretion fell to near normal levels (370 µmol/mol creat), suggesting previous H-excess from adrenal origin.

In vitro studies: Directly after laparoscopic removal, adrenal cortical tissue was processed to cell suspensions for further testing. H (10-7 M) increased cortisol production (131% of contr), similar to the effect of ACTH (615 pg/ml) (146% of contr). Ranitidine or clemastine completely aborted the H-stimulated cortisol production. In control experiments on hyperplastic adrenal tissue from patients with persistent Cushing's disease, H (10-6 M) increased cortisol secretion in 1 of 6 subjects (189% of contr), with unaltered cortisol secretion in the other 5 subjects. Finally, mRNA from H type 1 receptor and H type 2 receptor was detected both in adrenocortical tissue from the patient and in normal or hyperplastic adrenocortical tissue (n=8), using a semi-quantitative PCR-technique.

Conclusion: This is the first case demonstrating the possible role of histamine in ACTH-independent Cushing's syndrome with in vitro proof of histamine-induced cortisol secretion.

(1) Lacroix, A.,Ndiaye, N.,Tremblay, J.,Hamet, P. Ectopic and abnormal hormone receptors in adrenal Cushing's syndrome. Endocr. Rev. 2001;22;75-110.