Cutaneous Flushing Is A Common Complaint Biology Essay

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Introduction

In normal circumstances flushing is the body's physiological response to an increase in temperature which results in increased cutaneous blood flow caused by temporary vasodilation {{59 Izikson, L., English J.C., Zirwas M. J. 2006}}. Cutaneous flushing is a common complaint that can be defined as a reddening of the skin and a feeling of warmth mainly presenting in the blush areas of the face, neck, upper chest and upper limbs and can be either episodic or constant {{59 Izikson, L., English J.C., Zirwas M. J. 2006}}. Episodic flushing is distinguished from constant erythema of the face which may be a symptom of an autoimmune connective tissue disease such as lupus erythematosus and dermatomyositis, photo dermatitis and facial contact dermatitis.

The vasodilation can be due to increased circulation of mediators such as histamine, catecholamines, neuropeptides, kinins, leukotrienes and prostaglandins {{60 Greaves, M.W., Burova, E. P. 1997}}{{61 Mohyi, D., Tabassi, K., Simon, J. 1997}}. The flushes may also be caused by neurologically mediated vasodilation, which produces sweating {{61 Mohyi, D., Tabassi, K., Simon, J. 1997}} or a relaxation of the vasoconstrictor autonomic nerve fibres {{60 Greaves, M.W., Burova, E. P. 1997}}. It is thought that the main blush areas of flushing are supplied by vasodilators rather than vasoconstrictors and that it is these that produce the episodes of flushing.

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Accurate diagnosis requires a full and complete examination of the patient taking into consideration the age, gender, occupation, stresses and worries of the patient as well as food intake and any intolerances, drug (both pharmalogical and recreational) and the duration of the episodes of each flush. The examination may also need to include laboratory, radiologic and histopathologic tests to reach a full and complete diagnosis.

The differential diagnosis of flushing is extensive and there are many benign, rare and some malignant causes that include flushing as a symptom, as well as more common causes of flushing such as rosacea, hormonal climacteric, fever and emotional flushing. Flushing as an abnormal response can indicate a more serious underlying condition such as pheochromocytoma, mastocytosis which will be explored further, as well as climacteric flushing.

Pheochromocytoma

Pheochromocytoma is a tumour that arises from the chromaffin cells of the adrenal medullary {{62 Underwood, J.C.E 2004}}. Chromaffin cells produce, store and release catecholamines: adrenaline, noradrenaline and dopamine derived from the amino acid tyrosine {{59 Izikson, L., English J.C., Zirwas M. J. 2006}}. Catecholamines can affect neurons, the cardiovascular system and also metabolic rate, temperature and operation of smooth muscle.

Although pheochromocytoma is usually benign, 8 to 10% of tumours can present as malignant {{63 Bravo, E. L., Ray, W. G. 1984}} and is characterised by the secretion of the catecholamines, which can result in hypertension and associated paroxysmal attacks. The attack can produce symptoms of flushing or pallor, hypertension and tachycardia; also common are headaches, sweating, palpitations, a sense of impending doom or apprehension, chest or abdominal pain sometimes with nausea or vomiting {{59 Izikson, L., English J.C., Zirwas M. J. 2006}}. The hypertension and attacks are very distinct symptoms of pheochromocytoma and help to diagnosis and differentiate from other conditions that produce flushing, especially if the hypertension occurs in a child or younger person {{62 Underwood, J.C.E 2004}}.

The symptoms presented during an attack can give some guidance as to what catecholamine is being over secreted. When noradrenalin is the primary hormone secreted the usual symptom is pallor and if adrenaline is being over produced flushing is the dominant symptom (need reference here!). The flushing mechanism in pheochromocytoma is thought to be the increased production of catecholamines when given exogenuously or when production has been increased by the reduction of sympathetic suppression {{59 Izikson, L., English J.C., Zirwas M. J. 2006}}. In a person's face there are predominantly more sympathetic vasodilator fibres than adrenergic vasoconstriction fibres therefore the effect of the increased catecholamine would be flushing and vasodilation {{59 Izikson, L., English J.C., Zirwas M. J. 2006}}. Other reasons why flushing would be present include a blood pressure instability and an increase in cardiac output. The pheochromocytoma may also produce other mediators that cause flushing such as calcitonin gene-related peptide and VIP (vasoactive intestinal polypeptide) and adrenomedullin {{59 Izikson, L., English J.C., Zirwas M. J. 2006}}.

Diagnosis of pheochromocytoma can be achieved with the use of tests and investigations. The first being a 24 hour urine sample to test for increased levels of catecholamines, catecholamine metabolites homovaniliac acid and vanillymandelic acid. Alternatively a test to suppress the plasma catecholamines can be used: measurements of plasma catecholamines are taken three hours before and three hours after an oral administration of 0.3mg of chonidine is given. If the plasma catecholamines have not been suppressed this would suggest a diagnosis of pheochromocytoma {{59 Izikson, L., English J.C., Zirwas M. J. 2006}}.

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A computerised tomography (CT) of the adrenal can be useful in successfully identifying intra-adrenal lesions {{61 Mohyi, D., Tabassi, K., Simon, J. 1997}} also useful if the urine sample test is negative is a abdominal aortography to identify extra adrenal pheochromocytoma within the abdomen {{61 Mohyi, D., Tabassi, K., Simon, J. 1997}}. Another biochemical test which measures the plasma levels of free metanephrines (o-methylated metabolites of catecholamines) gives a very effective measurement and means of diagnosing pheochromocytoma {{64 Pacak, K., Linehan, W. M., Eisenhofer, G., McClellan M.W., Goldstein, D. S 2001}}.

The most successful treatment for pheochromocytoma is to surgically remove the tumour but this has several complications: anesthesia and the handling of the tumour could produce an intensive outpouring of catecholamines resulting in a hypertension attack, stroke, arrhythmias or myocardial infarction {{64 Pacak, K., Linehan, W. M., Eisenhofer, G., McClellan M.W., Goldstein, D. S 2001}}. To prevent this, the patient with pheochromocytoma must undergo a treatment of alpha adrenergic blockers, beta-adrenergic blockers, catecholamine-synthesis antagonists and calcium channel blockers so that catecholamine synthesises or release is restricted {{64 Pacak, K., Linehan, W. M., Eisenhofer, G., McClellan M.W., Goldstein, D. S 2001}}.

Mastocytosis

Mastocytosis encompasses a range of symptoms due to an accumulation of mast cells as a result of an activating mutation of the tyrosine kinase receptor (Kit) in more than 90% of adult sufferers {{65 Amon, U., Hartmann, K., Horny, H-P., Nowak, A. 2010}} and from a localised overproduction of stem cell factor {{68 Worobec, A. S., Metcalfe, D. D. 2009}}. This mutation is less common in children.

Mastocytosis can be cutaneous or systemic. Cutaneous mastocytosis presents in children more often than adults, and will present with mast cell infiltration of the tissue called urticaria pigmentosa, a localised brown maculopapular skin rash caused by multiple mast cell collection {{59 Izikson, L., English J.C., Zirwas M. J. 2006}}. The majority of children affected will spontaneously diffuse the lesions thereby resolving the problem. Spontaneous diffusion is less common in adults.

A variety of symptoms can present with systemic mastocytosis which include pruritus, flushing and dyspepsia due to gastric hypersecretion. The most common symptom is flushing. Other less specific symptoms include diarrhoea, fatigue, fever, malaise and weight loss {{67 Editors Beers, M., Porter, R. S., Jones, T. V., Kaplan, J. L., Berkwits, M 2006; 59 Izikson, L., English J.C., Zirwas M. J. 2006}}. Symptoms, particularly flushing, usually occur as a result of mediator release such as histamine, leukotrienes, and inflammatory cytokines, these mediators can be triggered to release by physical touch, stroking or rubbing the skin lesions causes urticaria and erythema around the lesion (Darier's sign), exercise, alcohol, NSAIDs, opioids, insect stings or foods {{67 Editors Beers, M., Porter, R. S., Jones, T. V., Kaplan, J. L., Berkwits, M 2006}}. Systemic mastocytosis is characterised by multifocal bone marrow lesions which can also involve other organs: the skin, lymph nodes, liver, spleen and GI tract {{67 Editors Beers, M., Porter, R. S., Jones, T. V., Kaplan, J. L., Berkwits, M 2006}}.

Tests should be completed for any patient that presents with unexplained flushing, and who do not have the characteristic skin lesions of urticaria pigmentosa present, especially if the symptoms are associated with hypertension as these are similar in diagnosis for anaphylaxis, pheochromocytoma, carcinoid syndrome and Zollinger-Ellison syndrome {{59 Izikson, L., English J.C., Zirwas M. J. 2006; 67 Editors Beers, M., Porter, R. S., Jones, T. V., Kaplan, J. L., Berkwits, M 2006}}.

Plasma and urine measurements of elevated levels of mast cell mediators and their metabolites can produce an uncertain diagnosis {{69 Lippincott Williams & Wilkins 2005}}. Also tryptase, a marker of mast cell degeneration can be measured for elevated levels in systemic mastocytosis although this marker can present with normal levels in cutaneous mastocytosis. {{69 Lippincott Williams & Wilkins 2005}}. A more accurate diagnosis is biopsy of skin lesions and bone marrow which will present findings of excessive mast cells {{67 Editors Beers, M., Porter, R. S., Jones, T. V., Kaplan, J. L., Berkwits, M 2006}}.

An accurate diagnosis should be made to determine the type of mastocytosis although at present there is no cure for mastocytosis and treatment involves avoidance of agitating factors such as heat and friction. Hypotension and flushing can be resolved by the use of intravenous adrenalin and treatment with H1 receptor antagonists have a combined blockade of H1 and H2 receptors to prevent vasodilatory effects of histamine, other treatments can include topical and oral steroids, ultraviolet and laser treatments {{59 Izikson, L., English J.C., Zirwas M. J. 2006; 67 Editors Beers, M., Porter, R. S., Jones, T. V., Kaplan, J. L., Berkwits, M 2006}}.

Climacteric

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Hot flushes are the most common complaint of both perimenopausal and postmenopausal women and effects around 50 to 85 per cent of women and can last for 3 to 5 minutes or up to 10 minutes and in some cases will occur every so often or every hour {{70 Stearns, V., Ullmer, L., Lopex, J. F., Smith, Y., Isaacs, C., Hayes, D. F. 2002}}. It occurs with an episode of intense heat in the flush area around the chest, head and neck, that is followed by sweating and then chills, palpitations and anxiety {{59 Izikson, L., English J.C., Zirwas M. J. 2006}}. Hot flushes can also be caused by systemic diseases as discussed above, neurological disorders, alcohol, drugs, eating habits and food additives {{70 Stearns, V., Ullmer, L., Lopex, J. F., Smith, Y., Isaacs, C., Hayes, D. F. 2002}}.

The mechanism which causes hot flushes is still unknown but results from a disturbance of the temperature regulating mechanism resident in the hypothalamus which may be affected by hormone releasing factors, gonadotrophins and neurohumorals {{66 Sturdee, D. W. 2008}}. More recently there has been interest in serotonin (5-HT) and oestrogen 5-HT and its role in the flushing mechanism although the effectiveness of serotonin reuptake inhibitors used in the treatment of hot flushes has not been as effective as the use of oestrogen {{66 Sturdee, D. W. 2008}}. Oestrogen deficiency or fluctuations play an important role in the mechanism of flushing, as oestrogen influences capillary tone and prevents excessive dilation {{59 Izikson, L., English J.C., Zirwas M. J. 2006}}.

Confirmation of a menopausal pattern can be shown by taking a Female Hormone Profile, which tests the levels of oestrogen, progestrogen and testosterone, and can confirm if low estradiol levels and very high levels of luteinising hormone (LH) and follicle stimulating hormone (FSH) are present or not ({{71 Kumar, P., Clark M. 2005}} which are all markers of the menopausal pattern.

Until recently Hormone Replacement Therapy (HRT) was used as an effective treatment for climacteric flushing. Currently though HRT is used with caution and in reduced amounts and for the shortest amount of time, as it has been liked to increased risk of cancer (breast, endometrium and prostate), heart disease, stroke and thrombosis {{70 Stearns, V., Ullmer, L., Lopex, J. F., Smith, Y., Isaacs, C., Hayes, D. F. 2002}}. The most successful HRT contains either oestradiol or progestational agents which both reduce the number and intensity of hot flushes as well as having some good effect on the oestrogenic compounds in bone density {{70 Stearns, V., Ullmer, L., Lopex, J. F., Smith, Y., Isaacs, C., Hayes, D. F. 2002}}.