On Jul 5, 6:18 am, "ironjust...@aol.com" <ironjust...@aol.com> wrote:
porphyria <<

Porphyria manifests hemolysis and a marker for this is d-dimer.
ANOTHER marker in lupus which they  .. disregard .. thereby
effectively eliminating a diagnosis OF .. hemolysis.

"D-dimer"

Arthritis Rheum. 2005 Jun 15;53(3):452-9. Links
Thrombosis in systemic lupus erythematosus: congenital and acquired
risk factors.
Afeltra A, Vadacca M, Conti L, Galluzzo S, Mitterhofer AP, Ferri GM,
Del Porto F, Caccavo D, Gandolfo GM, Amoroso A.
University Campus Bio-Medico, Rome, Italy. a.afeltra@unicampus.it

OBJECTIVE:
To investigate the thrombotic tendency in patients with systemic lupus
erythematosus (SLE) by evaluating congenital or acquired abnormalities
associated with an increased risk of venous and/or arterial
thrombosis.
METHODS:
A total of 57 patients with SLE were included in the study.
Twenty-one patients (37%) had a history of arterial and/or venous
thrombosis and 36 patients (63%) did not have such a history.
Sera from 50 healthy controls were examined.
Protein C, protein S, antithrombin, D-dimer, fibrinogen, homocysteine,
anticardiolipin antibodies (aCL), lupus anticoagulant (LAC),
prothrombin G20210A, and methylenetetrahydrofolate reductase (MTHFR)
C677T gene mutation were evaluated.
RESULTS:
Protein C, antithrombin, fibrinogen, D-dimer, and homocysteine levels
were significantly higher in patients with SLE than in controls.
A prothrombin mutation was observed in 2 (4%) of 50 controls and in 6
(11%) of 57 patients.
A significantly higher prevalence (P = 0.036) of MTHFR homozygous
mutation was observed in patients with SLE (14 [25%] of 57) in
comparison with controls (4 [8%] of 50). IgG-aCL and IgM-aCL levels
were significantly higher in patients with SLE than in controls (P <
0.0001).
The presence of medium-high (> or = 20 IgG phospholipid units/ml) IgG-
aCL antibody titers was significantly higher (P = 0.005) in patients
with thrombosis (11 [52%] of 21) than in patients without (5 [14%] of
36) thrombosis.
LAC was present in 22 (38.5%) of 57 patients and in none of 50
controls.
CONCLUSION:
In this study, we confirm the association between thrombosis and IgG-
aCL at medium-high titers and suggest that the coexistence of other
risk factors can affect the expression of thrombosis in patients with
SLE.

PMID: 15934123 [PubMed - indexed for MEDLINE]

--------------------------------------------------------------------------------

J Transl Med. 2004 11 9;2 (1):38 15535889 (P,S,E,B) Cited:1
The role of d-dimer as first marker of thrombophilia in women affected
by sterility: implications in pathophysiology and diagnosis of
thrombophilia induced sterility.

[My paper] Di Micco, D'Uva, Strina, Mollo, Amato, Niglio, De Placido
IV Divisione di Medicina Interna e Patologie Epato-Bilio-Metaboliche,
Seconda Università di Napoli, Naples, Italy. pdimicco@libero.it.
BACKGROUND:
D-dimer is considered a marker of hypercoagulable state and of
endogenous fibrinolysis, so increased d-dimer is detectable in
patients affected by thrombosis. Yet, several studies showed that also
infertility, in particular secondary infertility due to recurrent
fetal losses, has been often related to thrombotic events, in
particular in women carrying thrombotic risk factors such as inherited
thrombophilia (MTHFRC677T, PTHRA20210G, Factor V Leiden polimorphisms
and/or inhAfter this screening we selected 39erited protein C, protein
S, AT III deficiency) or acquired thrombophilia (primary
antiphospholipid syndrome, acquired protein C, protein S, AT III
deficiency, drugs induced thrombophilia).
However, because its high predictive negative value in case of
suspected thrombosis, increased d-dimer has been often associated to
subclinical thrombophilia.
The aim of this study is to investigate the role of d-dimer as first
marker of thrombophilia in women affected by unexplained infertility
and subsequently to search the cause of increased d-dimer, such as
inherited and/or acquired thrombophilia.
PATIENTS AND METHODS:
We selected 79 patients with unexplained primary or secondary
infertility.
We excluded 40 patients affected by hydrosalpinx, uterine fibroids,
uterine malformations, endocrinological and immunological diseases,
luteal insufficiency, cytogenetical alterations.
All remaining 39 patients were tested for d-dimer and divided in two
groups: the patients of group A (25 patients) showed increased plasma
d-dimer, in group B were included 14 patients with normal plasma level
of d-dimer.
After this step all 39 patients were screened for MTHFRC677T,
PTHRA20210G, Factor V Leiden polimorphisms, protein C, protein S, AT
III, anticardiolipin IgM and IgG, lupus anticoagulant.
In the control group were included 15 age matched women without
sterility problems referred to our outpatient's section of vascular
medicine for suspected deep venous thrombosis.
Statistical analysis was based on chi2 test, differences were
considered to be significant if p < 0.05.
RESULTS:
D-dimer was increased in 25/39 and 20/25 showed inherited/acquired
thrombophilia while patients with normal d-dimer showed inherited/
acquired thrombophilia in 7/14 (p: < 0.05, s).
DISCUSSION:
D-dimer is a well known marker of hypercoagulable state, in particular
its high predictive negative value in case of suspected thrombosis has
been recognised by several reports.
Yet, increased d-dimer has been identified also for subclinical
thrombophilia besides for vascular thrombosis.
Our data, in fact, for the first time suggest an interesting role of d-
dimer to identify women affected by unexplained primary or secondary
infertility and thrombophilia. So, probably there is a role for d-
dimer in these subjects for its predictive positive value.
Of course, further data on large based population are needed to
confirm our results, because these findings may speed up a diagnostic
screening in these patients also for a good cost/effectiveness of this
test.

Who loves ya.
Tom

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