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Note:  This is information which came from the Cleveland Clinic's website, however this informative page was removed from the internet.   Although the information regarding Carcinoid Syndrome and Systemic Mastocytosis are somewhat antiquated and new research has given more understanding to both diseases, the information contained within this article is still valid and worth reading and perhaps passing on to your doctors for their aide.  However, in regards to the information on mastocytosis as to it's diagnostic procedures and forms, there is more recent research on this forum which is of better use for doctors.






Other Diseases Causing Episodic Flushing:

Cheung et al20 have described a family with monoamine oxidase deficiency causing episodes of flushing affecting the face and chest precipitated by emotion or certain foods, followed by diarrhea, headaches, and sometimes palpitations. Blood serotonin levels in this family were elevated secondary to decreased activity of monoamine oxidase. Sertraline hydrochloride controlled the symptoms by depleting platelet serotonin.
Flushing is rare in patients with pheochromocytoma. If flushing occurs at all, it is seen after a paroxysm of hypertension, tachycardia, palpitations, chest pain, severe throbbing headaches, and excessive perspiration. Pallor is typically present during the attack, and mild flushing may occur after the attack as a rebound vasodilation of the facial cutaneous blood vessels.5 Facial flushing and headache can happen along with sweating of the face, neck, and upper trunk in patients with spinal cord lesions above T-6. This may occur as an exaggerated response to bowel or bladder distention.1 Other causes are certain pancreatic tumors, insulinoma, and POEMS (polyneuropathy, organomegaly, endocrinopathy, monoclonal proteinemia, and skin changes). Transient flushing of the face, chest, or arms has been noted after neurological deterioration secondary to rapid rise in intracranial pressure.21


ROSACEA
Persistent flushing  from whatever cause may eventually lead to rosacea. The lesions of rosacea that initially occur in the central convex areas of the face consist of papules and pustules against a background of erythema, telangiectasia, edema, and eventual permanent induration or thickening of affected skin.2 Patients with severe flushing due to mastocytosis can develop rosacea in less than a year after the onset of flushing episodes.5


]EVALUATION OF THE PATIENT WITH A FLUSHING DISORDER
It is important to consider the clinical characteristics of the flushing before embarking on expensive laboratory evaluation.5 The physician should consider four clinical characteristics in the initial evaluation of a patient with flushing: 1) provocative and palliative factors, 2) morphology, 3) associated features, and 4) temporal characteristics.2

Provocative or palliative factors: Certain agents that trigger the flush suggest an underlying systemic disease as the cause for the flushing, eg, mastocytosis and carcinoid syndrome.

Morphology: Is there a basic feature that comes and goes? Is the redness patchy or confluent? What is the color of the flush? Is there cyanosis? Is the flushing preceded or followed by pallor?2 The morphology of the flushing may suggest not only the cause of the flushing but also, in the case of carcinoids, the anatomic origin of the disorder.5

Associated features: These may include respiratory symptoms, gastrointestinal symptoms, headache, urticaria, facial edema, hypertension, hypotension, palpitations, or sweating.

Temporal characteristics: These are the frequency of the flushing and the timing of the specific features during each flushing reaction.

Important information can be obtained from a 2-week diary in which the patient records qualitative and quantitative aspects of the flushing event and lists exposure to all exogenous agents.2 When the diagnosis remains obscure after evaluation of the 2-week diary, the patient is given an exclusion diet listing foods high in histamine, foods and drugs that affect urinary 5-HIAA tests, and foods and beverages that cause flushing. If the flushing reactions completely disappear, restoring the excluded items individually can identify the causative agent. If the flushing reactions continue unchanged, then further metabolic work up may be undertaken.5
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REFERENCES
1.      Greaves MW. Flushing and flushing syndromes, rosacea and perioral dermatitis. In: Champion RH, et al, eds. Rook/Wilkinson/Ebling textbook of dermatology, 6th ed., volume 3. Oxford, UK: Blackwell Scientific, 1998:2099-2104.

2.      Cutaneous manifestations of disorders of the cardiovascular and pulmonary systems. In: Freedberg IM, et al, eds. Fitzpatrick's dermatology in general medicine, 5th ed., volume 2. New York:McGraw-Hill, 1999:2064.

3.      Wilkin J. Flushing and blushing. In: Moschella SL, Hurley HJ, eds. Dermatology, 3rd ed., volume 2. Philadelphia: W.B. Saunders, 1992:2080-2083.

4.      Dawood MY. Menopause. In: Copeland LJ, ed. Textbook of gynecology, 2nd ed. Philadelphia: W.B. Saunders, 2000.

5.      Fitzpatrick TB, Eisen AZ, et al. Dermatology in general medicine, 4th ed. New York: McGraw Hill, 1993.

6.      Vercellini P, Vendola N, Colombo A, Passadore C, Trespidi L, Crosignani PG. Veralipride for hot flushes during gonadotropin-releasing hormone agonist treatment. Gynecol Obstet Invest. 1992;34:102-104.

7.      Fink HA, MacDonald R, Rutks IR, et al. Sildenafil for male erectile dysfunction: a systemic review and meta-analysis [review]. Arch Intern Med. 2002:162:1349-1360.

8.      DeSio J, Kahn CH, Warfield CA. Facial flushing and/or generalized erythema after epidural steroid injection. Anesth Analg. 1995;80:617-619.

9.      Vinik AI. Neuroendocrine tumors of carcinoid variety. In: DeGroot LJ (Editor), Endocrinology, 3rd ed., volume 3. Philadelphia: W.B. Saunders Co, 2803-2812. 1995

10.      Wilson JD, ed. Williams textbook of endocrinology, 9th ed. Philadelphia: W.B. Saunders, 1998.

11.      O'Toole D, Ducreux M, Bommelaer G, et al. Treatment of carcinoid syndrome: a prospective crossover evaluation of lanreotide versus octreotide in terms of efficacy, patient acceptability, and tolerance. Cancer. 2000;88:770-776.

12.      Larsen PR, ed. Williams Textbook of Endocrinology, 10th ed. Philadelphia: W.B. Saunders, 2003.

13.      Rubin J, Ajani J, Schirmer W, et al. Octreotide acetate long-acting formulation versus open-label subcutaneous octreotide acetate in malignant carcinoid syndrome. J Clin Oncol. 1999;17:600-606.

14.      Greaves MW. Mastocytoses. In: Champion RH, et al, eds. Rook/Wilkinson/Ebling textbook of dermatology, 6th ed., volume 3. Oxford, UK: Blackwell Scientific, 1998:2337-2346.

15.      Corbett M, Abernethy DA. Harlequin syndrome. J Neurol Neurosurg Psychiatry. 1999;66:544.

16.      Dizon MV, Fischer G, Jopp-McKay A, Treadwell PW, Paller AS. Localized facial flushing in infancy. Auriculotemporal nerve (Frey) syndrome [review]. Arch Dermatol. 1997;133:1143-1145.

17.      Drummond PD, Boyce GM, Lance JW. Postherpetic gustatory flushing and sweating. Ann Neurol. 1987;21:559-563.

18.      Shakir KM, Jasser MZ, Yoshihashi AK, et al. Pseudocarcinoid syndrome associated with hypogonadism and response to testosterone therapy. Mayo Clinic Proc. 1996;71:1145-1149.

19.      Smith JA Jr. Management of hot flushes due to endocrine therapy for prostate carcinoma [review]. Oncology (Huntingt). 1996;10:1319-1322; discussion 1324.

20.      Cheung NW, Earl J. Monoamine oxidase deficiency: a cause of flushing and attention-deficit/hyperactivity disorder? Arch Intern Med. 2001;161:2503-2504.

21.      Hornig GW, et al. Flushing in relation to a possible rise in intracranial pressure: documentation of an unusual clinical sign. Report of five cases. J Neurosurgery. 2000;92:1040-1044