Erectile dysfunction is associated with risk factors for cardiovascular disease.

True. Erectile dysfunction is associated with risk factors for cardiovascular disease including lipid abnormalities, HT, smoking, DM, obesity and lack of physical activity. This may be related to the fact that endothelial dysfunction and atherosclerosis are systemic disorders. Risk factors for cardiovascular disease affect vascular supplies to corpora cavernosa of the penis as well as arteries of other parts of the body. However, there is little data to support that controlling these factors would readily reverse erectile dysfunction after it has been diagnosed. As a matter of fact, sometimes treatment of these risk factors may aggravate erectile dysfunction. For example, thiazide diuretics and beta blockers for HT may exacerbate erectile dysfunction.

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Phosphodiesterase-5 inhibitors are contraindicated in patients taking nitrates.

True. Phosphodiesterase-5 (PDE5) inhibitors are contraindicated in patients taking organic nitrates, which are nitric oxide (NO) donors. NO stimulates guanylate cyclase to catalyze the formation of cGMP which relaxes smooth muscle cells of vasculatures. PDE5 breaks down cGMP. Thus a PDE5 inhibitor plus an NO donor would cause accumulation of cGMP that causes marked vasodilation and hypotension. Nitrates should not be given for at least 24 hours after the use of sildenafil (Viagra) or vardenafil (Levitra) and at least 48 hours after the use of tadalafil (Cialis).

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Phosphodiesterase-5 inhibitors are contraindicated in patients taking anti-hypertensive drugs.

False. Interactions of PDE-5 inhibitors with anti-hypertensive drugs in men with HT have not been associated with an increased incidence of adverse events. Vasodilator effects of the major classes of anti-hypertensive agents have mechanisms of action that do not involve the nitric oxide-cGMP pathway. Nonetheless, PDE-5 inhibitors should still be used with caution in patients taking multiple anti-hypertensive drugs.

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Long term use of phosphodiesterase-5 inhibitors in patients with coronary heart disease is associated with more myocardial infarction and deaths.

False. Data from prospective clinical trials, retrospective metanalyses and epidemiologic studies have shown no evidence that administration of a PDE-5 inhibitor in accord with published guidelines (including absence of nitrate therapy) would increase morbidity and mortality in men with co-existing erectile dysfunction and stable ischemic heart disease.

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Cardiac assessment is mandatory before starting phosphodiesterase-5 inhibitors for erectile dysfunction.

True. Patients who wish to start PDE-5 inhibitors therapy should receive a cardiac assessment beforehand, particularly for hypertension, congestive heart failure and ischemic heart disease. Interactions between nitrate and PDE-5 inhibitors should be clearly informed. Although firm data are lacking, pre-therapy treadmill tests to assess for the presence of stress-induced ischemia in patients with overt and covert coronary artery disease can guide the patient and physician to the risk of cardiac ischemia during sexual intercourse. If the patient can achieve 5 to 6 METS on a treadmill stress test without demonstrating ischemia, the risk of ischemia during coitus with a familiar partner, in familiar settings, without the added stress of a heavy meal or alcohol ingestion, is probably low. However, the physical and emotional stresses of sexual intercourse can be excessive in some people, particularly those who have not performed this activity in some time and who are not in good condition. These stresses themselves may produce acute ischemia or precipitate myocardial infarction. Such patients should be advised to use common sense and to moderate their physical exertion and their emotional expectations as they start PDE-5 inhibitors.

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References:
1. Feldman et al. Impotence and its medical and psychosocial correlates: results of the Massachusetts Male Aging Study. J Urol 151 (1994), 54-61.
2. ACC/AHA Expert Consensus Document. Use of Sildenail in patients with cardiovascular disease. Circulation 1999;99:168-177.

What is the clinical diagnosis?

The clinical diagnosis is macular amyloidosis (MA). It is more common in women and affects areas subject to friction including upper back, neck, shin, thigh and buttock. Pruritus may not be present and patients usually seek medical advice because of the cosmetic appearance. Typically there is macular lesions consisting of hyperpigmentation with a reticulated or rippled pattern. MA is more common among Asians, Middle Easterners, and South Americans.

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What are the clinical differential diagnoses?

Clinical differential diagnoses include post-inflammatory hyperpigmentation, poikiloderma, eythema dyschromium perstans and prurigo pigmentosa.

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What is the underlying mechanism of this dermatosis?

It is due to abnormal extracellular tissue deposition of a protein, amyloid. Amyloid comes from degenerated keratin from apoptotic keratinocytes. It was suggested that trauma such as constant friction and rubbing could induce the condition. However, no precipitating traumatic history was noted in most cases.

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How would you confirm the diagnosis?

The diagnosis is usually made on clinical grounds and could be confirmed by a skin biopsy. The amyloid deposit can be demonstrated by Congo red stain, which under polarizing light gives apple-green birefringence.

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What are the treatments?

Relief of pruritus is important as scratching will aggravate pigmentation and also cause skin textural changes. Sedating antihistamines may be used. Topical or intralesional steroid is beneficial in improving the lesions and relief of itch. In recalcitrant cases, phototherapy, laser vaporization, dermabrasion, electrodessiccation and curettage may also be tried.

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