Je huisarts wilde niet meewerken?
Wel die Vitamine 1,25 dat is niet eens ter sprake gekomen bij mijn laatste huisarts bezoek maar aangezien ze bij voor mij wel iets belangrijkere punten al zat te eikelen (ivm antibiotica kuren en verdere onderzoeken naar mogelijke co-infecties) heb ik niet eens de moeite genomen. Ik ben dat hele circus ondertussen wel beu wat dat betreft. En ik heb niemands goeddunken of verdere toestemming nodig om van mijn eigen centen zelf onderzoeken te laten uitvoeren.
Maar goed terugkomend op je eigen vreemde hoge Vitamine D 1,25/Calcitriol waardes heb je al zelf aangegeven dat je geen dermate hoge Vitamine D supplementatie gebruikte of een buitengewone bloodstelling aan zonlicht hebt/had wat een mogelijk oorzaak zou kunnen zijn geweest. In tegendeel zelfs wat het op eerste zicht alleen maar vreemder maakt. Echter is er misschien een verklaring voor je hoge Vitamine D 1,25/Calcitriol en gevoeligheid voor zonlicht. Ik denk dan met name aan de ziekte Sarcoïdose.
Hoge 1,25/Calcitriol waardes komen bij Sarcoïdose veelvuldig voor met name in samenspan met hypercalcemie. Lees de volgende medische publicaties maar eens:
Enhanced production rate of 1,25-dihydroxyvitamin D in sarcoidosis.
However, the mean serum 1,25-(OH)2D concentration was significantly higher in the patients with sarcoidosis (211 +/- 60 pmol/L) than in either of the other 2 groups. The mean 1,25-(OH)2D production rate was markedly elevated in the patients with sarcoidosis (12.4 +/- 5.3 mumol/day), being more than 2-fold greater than the normal mean value (5.4 +/- 1.2 mumol/day). The highest production rates were found in patients with hypercalcemia, whereas subjects with hypercalciuria had production rates comparable to those in the patients with absorptive hypercalciuria.
Biochemical indicators of disordered vitamin D and calcium homeostasis in sarcoidosis.
All seven hypercalcemic/hypercalciuric patients with sarcoidosis had a serum ACE level greater than 40 IU/L (normal less than 35 IU/L). All five patients with hypercalcemia (Ca greater than or equal to 10.5 mg/dl) had a serum 1,25-(OH)2-D concentration above the normal range (greater than 60 pg/ml), and in all 19 patients the serum calcium was positively correlated to the serum 1,25-(OH)2-D concentration (r = 0.55, p less than 0.01). The capacity of PAM to synthesize [3H]1,25-(OH)2-D3 in vitro was. with one exception, greater in cells from patients with diffuse infiltrative pulmonary disease (roentgenographic stage II or III) and positively correlated to the serum calcium concentration (r = 0.72, p less than 0.001) and serum ACE (r = 0.43, p less than 0.05).
Evidence that Increased Circulating 1α,25-Dihydroxyvitamin D is the Probable Cause for Abnormal Calcium Metabolism in Sarcoidosis
Mean plasma 1α,25-dihydroxyvitamin D[1α,25(OH)2D] was significantly increased and serum parathyroid hormone was suppressed in three patients with sarcoidosis and hypercalcemia. Prednisone lowered the mean plasma 1α,25(OH)2D to normal range and corrected the hypercalcemia. To elucidate the mechanism for the increased sensitivity to vitamin D in this disorder, the effects of orally-administered vitamin D2 were determined in seven normal subjects, four patients with sarcoidosis and normal calcium metabolism and three patients with sarcoidosis and a history of hypercalcemia who were normocalcemic when studied. Serum and urinary calcium, serum 25-hydroxyvitamin D (25-OHD), plasma 1α,25(OH)2D and, in some studies, calcium balance were measured. Vitamin D2, 250 μg a day for 12 d, produced little, if any, change in mean plasma 1α,25(OH)2D and in urinary calcium in the normals and in the patients with normal calcium metabolism. In contrast, vitamin D2 produced increases in plasma 1α,25(OH)2D from concentrations which were within the normal range (20-55 pg/ml) to abnormal values and increased urinary calcium in two patients with abnormal calcium metabolism. In an abbreviated study in the third patient, vitamin D2, 250 μg a day for 4 d, also increased plasma 1α,25(OH)2D abnormally from a normal value. There was a highly significant correlation between plasma 1α,25(OH)2D and urinary calcium. Serum 25-OHD and serum calcium remained within the normal range in all subjects and patients. These findings provide evidence that the defect in calcium metabolism in sarcoidosis probably results from impaired regulation of the production and(or) degradation of 1α,25(OH)2D.
Symptoms of Sarcoidosis
Elevated 1,25-D
Sarcoidosis always results in dysregulated vitamin D metabolism and abnormally high levels of dihydoxyvitamin-D (1,25-D), a powerful hormone which affects many other hormones.
Symptoms of too much vitamin D (hypervitaminosis-D) in inflammatory disease may cause may adverse symptoms including:
Calcium deposits in the kidneys, lungs, blood vessels, heart and other soft tissues
High blood calcium levels
Irregular heartbeat
High blood pressure
High cholesterol
See Vitamin D.
Elevated serum calcium
Hypervitaminosis-D is associated with hypercalcemia.
Approximately 6% of sarcoidosis patients have elevated serum calcium (hypercalcemia). This abnormal calcium homeostasis is not simply caused by increased gut absorption of calcium. Elevated 1,25-dihydroxyvitamin D3 stimulates intestinal calcium absorption and resorption of calcium and phosphates from bone. Calcium levels are normally regulated by the parathyroid hormone.
Endocrine and reproductive manifestations of sarcoidosis
Vitamin D and calcium metabolism
The association between sarcoidosis and hypercalcaemia is seen in 5–10% of cases. Hypercalcaemia is usually transient in subacute sarcoidosis, but may fluctuate in chronic sarcoidosis, depending on disease activity.3 The underlying mechanism is thought to involve high circulating concentrations of 1,25-dihydroxyvitamin D3 [1,25(OH)2-D3], produced by extrarenal 1α-hydroxylation of vitamin D in alveolar macrophages and sarcoid granulomas.4 Production of 1,25(OH)2-D3 by alveolar macrophages is stimulated in a dose-response fashion by γ-interferon,5 and it is possible that the increased 1,25(OH)2-D3 production is a compensatory mechanism mounted by the immune system to inhibit the inflammatory process. Granulomatous production of parathyroid-hormone related protein (PTH-rP) may also play a role in abnormal calcium metabolism,4 where tissue necrosis factor-alpha (TNF-α) and interleukin-6, produced by macrophages, increase PTH-rP gene expression.4 PTH-rP, the usual aetiological agent of humoral hypercalcaemia of malignancy, was reported in one series to be present in 85% of biopsies of granulomatous tissue from patients with sarcoidosis.6
The important targets of 1,25(OH)2-D3 are the intestinal epithelium and bone, where the hormone acts to increase intestinal calcium and phosphate absorption, increase osteoclastic recruitment and bone resorption, and modulate an increase in osteoblastic bone formation.7 Although hypercalcaemia has long been recognized as a complication of sarcoidosis, the presence of hypercalciuria is three times more common, occurring in approximately 40–50% of patients with sarcoidosis.7 The mechanism of hypercalciuria is multifactorial, including: (i) increased absorption of calcium with a high urinary calcium/creatinine ratio, associated with elevated serum 1,25(OH)2-D3 levels;
Calcium metabolism in sarcoidosis and its clinical implications
Objective. To examine the clinical implications of disturbed calcium metabolism in sarcoidosis and how the pathophysiology affects management strategies.
Methods. The literature concerning calcium metabolism in sarcoidosis was reviewed.
Results. Dysregulated calcium metabolism is a well‐recognized complication of sarcoidosis, resulting in hypercalcaemia (prevalence 5–10%), hypercalcuria (40–62%) and reduced bone density (40–55%). Extrarenal synthesis of calcitriol [1,25(OH)2D3] is central to the pathogenesis of abnormal calcium homeostasis, but alterations in parathyroid hormone (PTH) activity and the expression of PTH‐related peptide have also been demonstrated. The immunosuppressive properties of calcitriol suggest that the raised levels seen in sarcoidosis could represent an adaptive response to the undefined antigen that causes sarcoidosis.
En als we dan ook je gevoeligheid voor zonlicht erbij pakken lijkt het ook te in het Sarcoïdose/1.25(OH)/hypercalcemie plaatje te passen als ik de volgende publicaties zo lees:
Precipitation of hypercalcaemia in sarcoidosis by foreign sun holidays: report of four cases.
Hypercalcaemia after foreign sun holidays in four patients is described. Although only one was a known case, all had sarcoidosis. The pathogenic mechanisms are discussed and the implications of excessive sun exposure for the mode of presentation and the management of sarcoidosis are highlighted.
The association between sunlight exposure and
hypercalcaemia in sarcoidosis, although long
recognized,' has not been much emphasized. The
mechanism whereby hypercalcaemia occurs in sarcoidosis
has been clarified,2 allowing an understanding
of the pathological role of sunlight
exposure and of the therapeutic role of corticosteroids.
We describe four patients who, during
or after foreign holidays in the sun, developed
hypercalcaemia, in all of whom symptoms were
sufficiently severe to require hospital admission.
For three patients it was the mode of presentation
of their sarcoidosis.
Discussion
Disorders of calcium metabolism are well-recognized
in sarcoidosis. Hypercalcaemia occurs in
10% of patients2 and hypercalciuria in up to 60%.3
These patients illustrate the spectrum of the clinical
consequences of hypercalcaemia, from troublesome
malaise during the summer months to lifethreatening
acute haemorrhagic pancreatitis. The
cause of hypercalcaemia in sarcoidosis has recently
been unravelled.2 It had been accepted that endorgan
hypersensitivity to the effects of vitamin D
was the basis of hypercalcaemia in this condition.
The finding of increased levels of 1,25-dihydroxyvitamin
D3, the active hormone, in hypercalcaemic
sarcoidosis suggested, however, a quantitative
rather than a qualitative increase in vitamin D
action.34 Furthermore, a similar finding in an
anephric patient with sarcoidosis and hypercalcaemia
pointed to extra-renal generation of 1,25-di- hydroxyvitamin D3.5 The pivotal study by Adams
et al. demonstrated that cultured alveolar sarcoid
macrophages metabolize 25-hydroxyvitamin D3 to
1,25-dihydroxyvitamin D3.6 A similar reaction was
subsequently shown in sarcoid lymph node
homogenate.7 Sunlight exposure through its antirachitic
action increases the substrate for this
reaction, resulting in increased circulating active
hormone and hypercalcaemia. Glucocorticoids inhibit
this reaction in sarcoid tissue. They rapidly
lower levels of 1,25-dihydroxyvitamin D3 in
sarcoidosis (before lowering calcium levels) without
affecting 25-hydroxyvitamin D3 levels;8 thus,
their therapeutic efficacy in this situation.
In each of the patients described above, there
was a clear-cut relationship between exposure to
the intense and prolonged solar radiation of
foreign sun holidays and the development of
symptomatic hypercalcaemia.
Duidelijke taal lijkt me zo dus disproportionele blootstelling aan zonlicht doet de hypercalcemie bij Sarcoïdose als gevolge van 1.25(OH) toenemen wat voor flinke symptoomverergering zorgt. Hier nog wat overige publicaties die ook over de gevoeligheid voor zonlicht bij Sarcoïdose en Hypercalcemie gaan:
Hypercalcemia due to sun exposure in a patient with multiple myeloma and elevated parathyroid hormone-related protein
A patient with multiple myeloma who developed hypercalcemia during three different stages of his
disease, with a different hypercalcemic agent elevated in his serum on each occasion, is described.
The initial episode of hypercalcemia was associated with high serum interleukin-6 (IL-6). After treatment
for myeloma normocalcemia was achieved. Subsequently, a relapse of hypercalcemia occurred,
this time characterized by frankly elevated plasma parathyroid hormone-related protein (PTHrP) but
normal IL-6. Monotherapy with pamidronate infusions resulted in remission of the hypercalcemia
and a significant fall in PTHrP levels. A third spell of hypercalcemia characterized by an acute rise
in serum 25-hydroxyvitamin D and 1,25-dihydroxyvitamin D to abnormally high levels occurred
during the summer season after prolonged and intense exposure to the sun.
SARCOIDOSIS WITH PHOTOSENSITIVE LESIONS: A RARE VARIANT
We had also considered lupus erythematosus in this case, but other clinical and serological features were absent. Sarcoid lesions mimicking lupus have been reported before.[5] Case 2 closely resembled granuloma annulare, but photosensitivity, negative Mantoux test, classical naked granuloma without any necrobiosis and raised SACE helped to exclude it.
In a recently published study of 23 Indian sarcoid patients, photosensitive skin lesions have not been documented.[6] The preferential distribution of skin lesions in photo-exposed areas and the significant clearing with hydroxychloroquine sulphate are the two aspects that make the cases special. A French article describes a Tunisian woman with papular erythema of the face, unresponsive to topical steroids.[7] She was histologically diagnosed to be a case of cutaneous sarcoid and the authors opined that photo-induced sarcoid is a distinct entity. Our cases further strengthen the view.
Seasonal cutaneous sarcoidosis: a photo-induced variant.
Sarcoidosis is a multisystem granulomatous disease, with cutaneous involvement in up to 35% of cases. Owing to its heterogeneous clinical presentation, sarcoidosis is often referred to as the 'great imitator' of dermatological disease. A rare variant of photosensitive cutaneous sarcoidosis has been infrequently reported in the literature. We describe an unusual case of recurrent, photo-distributed cutaneous sarcoidosis presenting only during the summer months.
Great imitator? Hmmmm waar heb ik die term ook alweer eerder gehoord.....hmmmmm???
CUTANEOUS SARCOIDOSIS - A GREAT MASQUERADER: A REPORT OF THREE INTERESTING CASES
It is a known fact that cutaneous sarcoidosis is a great imitator in dermatology. We report three cases of cutaneous sarcoidosis without systemic involvement and with varied dermatologic presentation with regard to age and morphology. Lesions mimicked various common dermatologic conditions, causing great confusion for the diagnosis and posing problems for management. Awareness of these varied morphologic presentations is essential for the early diagnosis and management of the master mimicker - cutaneous sarcoidosis.
Sarcoidosis is a great imitator of other dermatologic diseases because the cutaneous manifestations are quite variable and occur in both localized as well as generalized forms. Greater awareness about the not so rare occurrence of sarcoidosis and its varied manifestations mimicking the most common dermatologic conditions like psoriasis (as in case 2) and its association with common conditions like lichen planus (as in case 1) will help prevent misdiagnosis of sarcoidosis and helps in appropriate therapy.
A great masquerader, great imitator???
paperwhite schreef:Het is begonnen met lyme.Na de standaardbehandeling (21 dagen doxy) kreeg ik problemen met de zon. Als ik in de zon kwam ,viel mijn haar met plukken uit. Ik kreeg ook een lupusachtige uitslag, maar alle lupustesten waren negatief. 2 lupusspecialisten sloten ook seronegatieve lupus uit. Ik werd getest op syfilis want dat geeft haaruitval (oh nee van lyme kon het niet zijn want die was zgn. adequaat behandeld) uiteraard was dat negatief.
Sindsdien bescherm ik mij tegen de zon. 5 jaar geleden brak de late lyme uit. Na 6 maanden wachten kreeg ik ab, maar de problemen met de zon werden nog erger. Wel stopte de haaruitval na ab. Zelfs na 2 minuten zon, komen al lymeklachten opzetten...Ab heeft daar kennelijk geen effect op, ik denk dat het een immuunreactie is.
Prof.Dm had het over vit D, maar deed er niks mee.
Lupusachtige uitslagen en haaruitval?
Sarcoidal alopecia mimicking discoid lupus erythematosus: Report of a case and review of the literature
Sarcoidal alopecia is a subtype of plaque-forming cutaneous sarcoidosis that may resemble discoid lupus erythematosus (DLE). Because the clinical appearance of the two lesions is similar, the correct diagnosis may be missed. The systemic involvement and progressive nature of sarcoidosis, make it important to differentiate sarcoidal alopecia from DLE, so that proper treatment can be initiated and potential long-term sequelae avoided. We present the case of a 57-year-old Taiwanese woman with sarcoidal alopecia of the scalp that mimicked DLE.
Bij mijn vader is vorig jaar Sarcoïdose in de longen en zijn hart vastgesteld en hij is hoogstwaarschijnlijk door die Sarcoïdose longcomplicaties begin dit jaar plotseling te komen overlijden.
Dus ik heb nog een openstaande rekening die nog vereffend moet worden ivm Sarcoïdose. En mijn vader was al sinds de jaren 70 praktisch compleet kaal (Alopecia). Zelfs zijn wenkbrauwen vielen soms compleet uit.Maar ook als je in Google zoekt naar Lupus Rash en Sarcoidosis Rash dan zie je bij veel gevallen duidelijke overeenkomsten.
Officieel is de oorzaak van Sarcoïdose nog niet bekend maar er bestaan erg sterke aanwijzingen dat Sarcoidose een gevolg is van bacteriële infecties. Laten we de officiële Wikipedia pagina er eens bijpakken:
Een onderzoek (2002) uit Zweden meldt dat in de weefselmonsters van een serie van 30 sarcoïdosepatiënten in vrijwel alle gevallen het micro-organisme Rickettsia helvetica aanwezig zou zijn.[7] In een vervolgonderzoek werden echter bij 20 Zweedse sarcoïdosepatiënten in geen enkel geval antistoffen tegen dit micro-organisme aangetoond.[8] Er is een uitgebreide discussie van de vele en tegenstrijdige beschikbare gegevens over de rol van micro-organismen bij sarcoïdose gepubliceerd.[9]
Dus ze hebben het over dit artikel waar ze bij sarcoïdosepatiënten Rickettsia helvetica aantroffen. En andere studie hierop vond hiervoor geen bewijs. Ook een Deense studie kon het eerder Zweedse onderzoek niet staven. Maar bij de eerste studie gebruikte ze vooral PCR als detectie methode en bij de andere studies lag de nadruk op antilichamen.
Maar ook dus de grote imitator Lyme wordt in verband gebracht met Sarcoïdose:
Borrelia burgdorferi infection may be the cause of sarcoidosis.
Serum antibody to Borrelia burgdorferi was measured in 33 patients with sarcoidosis which was confirmed clinically and pathologically. The results showed that 81.8% of the patients were positive for anti-B. burgdorferi antibody. In addition, a strain of B. burgdorferi was isolated from a patient's blood. Fifteen patients received ceftriaxone 2g per day or penicillin 12 million U per day. The antibody titers of the patients decreased to nearly normal levels rapidly. Serum angiotensin converting enzyme (SACE) turned to normal range after the treatment. According to the findings mentioned above, we consider that B. burgdorferi infection may be the cause of sarcoidosis and sarcoidosis might be a specific type of Lyme disease.
SEROPREVALENCE OF ANTI-BORRELIA ANTIBODIES AMONG PATIENTS WITH CONFIRMED SARCOIDOSIS IN A REGION OF JAPAN WHERE LYME BORRELIOSIS IS ENDEMIC.
Sarcoidosis is a multisystemic granulomatous disease of unknown etiology, while Lyme borreliosis is a multisystemic disorder caused by Borrelia burgdorferi. The purpose of this study is to evaluate the relationship between sarcoidosis and Lyme borreliosis in a region of Japan where Lyme borreliosis is endemic.
We determined the seroprevalence of anti-Borrelia burgdorferi antibodies as well as antibodies three Japanese Borrelia strains by enzyme-linked immunosorbent assay and dotblot assay using purified Borrelia-specific proteins in 46 patients with confirmed sarcoidosis and 150 controls (50 disease controls and 100 healthy controls) in Hokkaido, the affected region.
Fifteen patients with sarcoidosis (32.6%) tested positive for Borrelia spirochete in both assays, compared with two disease controls (4.0%) and two healthy controls (2.0%). The seroprevalence of anti-Borrelia antibodies in patients with sarcoidosis was much higher in the affected region than in the region in our previous study were Lyme borreliosis is non-endemic.
In a region where Lyme borreliosis is endemic, Borrelia infection may be partially associated with sarcoidosis.
High prevalence of 'Borrelia-like' organisms in skin biopsies of sarcoidosis patients from Western Austria.
BACKGROUND:
Sarcoidosis is a multisystem granulomatous disorder of unknown aetiology with frequent skin involvement.
OBJECTIVE:
To investigate the frequency of 'Borrelia-like' organisms in cutaneous sarcoidosis (CS) by focus-floating microscopy (FFM).
METHODS:
Retrospective analysis of 38 CS specimens by immunohistochemistry with polyclonal anti-Borrelia antibody and assessment by FFM.
RESULTS:
Specimens of 34.2% CS were positive for 'Borrelia-like' organisms by FFM. Usually single spirochetes, rarely pairs or small clusters of bacteria were observed between collagen bundles or at the periphery of granulomas. Polymerase chain reaction (PCR) was performed in addition in 11 cases and was negative in all biopsies. Samples of erythema migrans served as positive controls: 92.3% of 39 samples were positive by FFM, but only 46.6% gave positive results by PCR. Of 61 negative controls only one specimen was falsely positive by immunohistochemistry.
CONCLUSION:
Detection of 'Borrelia-like' organisms by FFM in tissue sections of CS underlines the possibility that such microorganism maybe involved in the pathogenesis of some cases of CS.
Dus met die focus-floating microscopy (FFM) techniek werden er veelvuldig borrelia achtige spirocheten waargenomen bij dermale sarcoïdose. Maar met PCR methodes werd niets aangetroffen.
Die focus-floating microscopy (FFM) techniek is overigens erg interessant. Hier nog wat informatie erover.
Maar goed volgende keer meer over Sarcoïdose en diens mogelijke bacteriële oorzaken.
Het is daarnaast lastig om een conclusie te verbinden aan een paar wetenschappelijk publicaties, vaak is er toch een meta-analyse nodig.
. De waarde van mijn 1,25OH was 137. Volgens de referentiewaarden van het lab is dit een mooie waarde (referentiewaarden 47-203). Toch geeft de berekening op de site van het Marshall protocoll iets anders aan. 