En fait le ratio se calcule sur des unités différentes...je sais c'est bizarre comme concept, mai c'est comme ça

Voila des infos:
In refractory cases of Sarcoidosis, the production of 1,25-dihydroxyvitamin D is essentially unregulated, and there is an extremely active hydroxylase biochemistry within the granuloma. Any 25-hydroxyvitamin D resulting from sunlight exposure or dietary supplement is vigorously converted into the active hormone within the inflammatory granuloma. This results in sarcoid patients typically having lower values of serum 25-hydroxyvitamin D than normals.
We have developed the D-Ratio:
Serum 1,25-dihydroxyvitamin D (pg/ml)
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Serum 25-hydroxyvitamin D (ng/ml)
to reflect the activity of the 25-OH-D-1-hydroxylase4 in the inflamed tissue. We use a D-Ratio of 1.25 as the normal mean, with a 0.5 standard deviation. Sarcoid patients, typically have D-Ratios above 4.0 and are thus sensitive to dietary Vitamin D and extremely sensitive to sunlight. D-Ratios less than 2.5 indicate that inflammatory production of 1,25-dihydroxyvitamin D is approaching ‘normal’, and that renal control is returning. The patient is approaching remission from the run-away inflammation of sarcoidosis.
Interpreting the Patient’s D-Ratio data
--> Tableau manquant, désolé!
All these patients present with fatigue and paresthesia, together with a sampling of other symptoms of Hypervitaminosis D. Based on data from the Danish population study5, we use a value of 25 pg/ml for the 1,25-dihydroxyvitamin D population mean, and a 9.5 Standard Deviation. Four of the patients had 1,25-dihydroxyvitamin D values in the top percentile of the population (99% of the population would have lower values).
Patient A had been on 5mg of prednisone daily for two years. Although the corticosteroid had effectively eliminated the serum ACE, it had not been so effective at reducing the extra-renal production of 1,25-dihydroxyvitamin D.
Patient B had an ACE value which was low-to-normal, regardless of ACE genotype, and a ratio of 1.29, which also indicated minimal inflammation. The symptomatic Hypervitaminosis D was due to Vitamin D supplementation within a Calcium preparation which had been prescribed for this patient’s osteoporosis.
Patients C,D and E all have high D-Ratios. Patient E had been counseled about exposure to sunlight, and, although still intermittently symptomatic with Hypervitaminosis D, had clearly managed to minimize those symptoms by reducing her 25-hydroxyvitamin D production. As a result, her 1,25-dihydroxvitamin D assay was essentially normal even though the high D-Ratio indicates significant granulomatous activity.
Bacteria induce Sarcoid Inflammation
For nearly a century, optical microscopy has allowed us to observe the non-necrotic granuloma of Sarcoidosis, but we found nothing that would induce the macrophage biochemistry to produce the excessive 1,25-dihydroxyvitamin-D levels which perpetuate the sarcoid granuloma. Recently, ‘Rickettsia Helvetica’ (gram-negative) bacteria have been found in biopsy samples from Swedish sarcoid patients8. Electron microscopy of the Rickettsia bacteria, at an 84,000 magnification, has shown that this bacteria can live and multiply within the cells of sarcoid granuloma8, one of the most inhospitable environments in the body. Whenever pathology indicates some ‘empty’ granuloma we should now assume a bacterial pathogenesis.
Therefore, as part of any treatment regimen for sarcoidosis, it is essential to ensure that all possibility of gram-negative bacteria living in the granulomatous tissue has been precluded. We have found the careful use of non-generic low-dose Minocin9 in combination with high-dose ARB therapy1 represents an appropriate intervention.