Additionally, individuals in professions that require constant use of the voice, such as singers, teachers, and radio hosts, may be at an increased risk for developing the disease.Because the disease is heavily linked to smoking, there is no established way to screen for Reinkes edema. Similarly, the only way to prevent Reinkes edema is to avoid smoking. By adopting a non-smoking lifestyle after being diagnosed with Reinkes edema, it is possible to stop the diseases progression, although it is not possible to reverse it. Therefore, it is critical to maintain a non-smoking lifestyle even after surgery, because the fluid can re-emerge. In fact, in many cases surgeons will not perform surgery without the guarantee that the individual will stop smoking. Mechanism
The vocal cords consist of five layers of cells:

Squamous epithelium
Superficial lamina propria (Reinkes space)
Intermediate lamina propria
Deep lamina propria
Vocalis muscleIn order for humans to produce sound for speech, the vocal folds must readily vibrate. The two layers of the vocal cords that vibrate are the Reinkes space and the overlying epithelium. In fact, these layers move freely over the more rigid intermediate and deep lamina proprias. Accumulation of fluid within the Reinkes space alters the elasticity of the vocal cord, making it less stiff and more gelatinous. This slows the vocal cord vibration, which results in a deepened and hoarse voice. Because men normally have a lower voice than women, the change is more noticeable in women.Edema usually occurs on both vocal cords. This is known as bilateral Reinkes edema.
Most often, the parents of an individual with an autosomal recessive disorder are carriers of one copy of the altered gene but do not show signs and symptoms of the disorder. Diagnosis
Tangier disease results in familial high-density lipoprotein deficiency. High-density lipoproteins are created when a protein in the bloodstream, Apolipoprotein A1 (apoA1), combines with cholesterol and phospholipids. The cholesterol and phospholipids used to form HDL originate from inside cells but are transported out of the cell into the blood via the ABCA1 transporter. People with Tangier disease have defective ABCA1 transporters resulting in a greatly reduced ability to transport cholesterol out of their cells, which leads to an accumulation of cholesterol and phospholipids in many body tissues, which can cause them to increase in size. Reduced blood levels of high-density lipoproteins is sometimes described as hypoalphalipoproteinemia.People affected by this condition also have slightly elevated amounts of fat in the blood (mild hypertriglyceridemia) and disturbances in nerve function (neuropathy). The tonsils are visibly affected by this disorder; they frequently appear orange or yellow and are extremely enlarged. Affected people often develop premature atherosclerosis, which is characterized by fatty deposits and scar-like tissue lining the arteries. Other signs of this condition may include an enlarged spleen (splenomegaly), an enlarged liver (hepatomegaly), clouding of the cornea, and early-onset cardiovascular disease. Treatment
There are drugs that can increase serum HDL such as niacin or gemfibrozil.