Some Possible New Support, 2012

Some Thoughts about Behcet's disease (A letter sent to some indivudals interested in Behçet's disease)

I have studied DHEA since 1984. I have found that many diseases exhibit malfunctions / deficiencies in DHEA. I accidentally came across Behçet's disease in a literature search; I had not heard of this disease before this time. The article, in which I found reference to Behçet's disease, fit some of my work in other diseases. I examined Behçet's disease according to my ideas and found some interesting relationships.

This article immediately suggested to me that Behçet's disease may be due to low DHEA. When I saw the symptoms, it also suggested to me that low DHEA may be involved as I think all tissues rely on sufficient levels of DHEA for optimal function. I found no research regarding DHEA levels in Behçet's disease. Therefore, I looked for what I consider to be another marker of low DHEA, that is, high prolactin. A new report found that "Prolactinemia was significantly higher (mean=19.34 ng/mL) in BD patients vs controls (mean=9.83 ng/mL) (p=0.009)." (Eur J Ophthalmol. 2007 May-Jun;17(3):404-7). I think that when sufficient levels of DHEA are produced by the adrenals, this feeds back to reduce prolactin production. (Prolactin has been found to specifically stimulate DHEA production by the adrenal glands. It has been found, in a study of cortisol, the other major adrenal gland steroid, that “the hypothalamo-pituitary adrenal axis is partially suppressed in Behçet's disease.” (J Eur Acad Dermatol Venereol. 2006 Jul;20(6):721-5). Cortisol levels are partially normal in BD but I think DHEA may be low. A prolonged, excessive cortisol to DHEA ratio should produce damage.)

"Conclusion: During the aging process in rat arteries, the expression of eNOS is lowered, the function of oxidation resistance is weakened, and the response of the vascular smooth muscle to NO is apparently decreased. DHEA is able to ameliorate the function of NO-related signal pathways and delay the aging process of the blood vessels." Gerontology 2007; 53: 234-237

I suggest that low DHEA may be the disease-producing factor in Behçet's disease which produces its symptoms in a pattern characteristic of affected individuals according to their genome, their specific set of genes. Low DHEA may affect other individuals in a different way according to their genes. Treatment with DHEA may ameliorate / cure Behçet's disease.

New Support, Read Both of the Following

The following new research may add direct support of my explanation of increased thrombosi (deep vein thrombosis, pulmonary embolism) caused by low DHEA. As you read the following, you should know that protein C deficiency increases thromboembolism. "Conclusions: These results suggest that lower circulating levels of dehydroepiandrosterone are associated with decreased activated protein C generation and higher intima-media thickness in patients with Type 2 diabetes." (Diabetic Medicine 2012: "Correlation of circulating dehydroepiandrosterone with activated protein C generation and carotid intima-media thickness in male patients with Type 2 diabetes." Suzuki, et al.)

Acta Dermatovenerol Croat. 2011 Jun;19(2):87-90.

Activated protein C resistance and its correlation with thrombophlebitis in Behçet's disease.

Kavala M, Namdar ND, Kocatürk E, Türkoglu Z, Zindanci I.

SourceDepartment of Dermatology, Göztepe Training and Research Hospital, Istanbul, Turkey.

Abstract

Patients with Behçet's disease (BD) have been recognized to be at an increased risk of thrombosis and thrombotic complications have been reported in 12%-40% of patients. The precise pathogenetic mechanisms underlying the thrombotic tendency of BD are not known. In recent researches, it is reported that procoagulant mutations might play a role in thrombotic process in BD patients. We aimed to evaluate the frequency of activated protein C resistance (APCR) in our BD patients and to investigate the association between thrombophlebitis and APCR. The study included 116 patients with BD who fulfilled the International Study Group criteria and 70 healthy individuals as a control group. APCR levels were measured by the clotting method. APCR levels were 129.63 ± 39.70 and 152.26 ± 22.62 in BD patients and control group, respectively (P<0.01). APCR was found in 47.4% and 8.6% of BD patients and control group, respectively (P<0.01). There was no statistically significant difference regarding APCR levels between patients with thrombophlebitis and without thrombophlebitis (46.4% vs. 48.3%). We found the frequency of APCR to be increased in BD patients with or without thrombophlebitis. The lack of association between thrombophlebitis and APCR in our series of BD patients suggests that some factors like endothelial abnormalities other than thrombophilia play a major role in the pathogenesis of thrombosis in BD.