ARTICLE
ejd.2011.1455
Auteur(s) : Antonio Giovanni Richetta1 antoniorichetta@hotmail.com,
Carlo Mattozzi1, Laura Macaluso1, Carmen Cantisani1, Simona Giancristoforo1, Sara D’epiro1, Monica Salvi1, Marco Scarnò2, Stefano Calvieri1
1 Department of Dermatology, Policlinico “Umberto I”
University of Rome “La Sapienza”, Viale del Policlinico, 155, 00133
Rome, Italy
2 CASPUR Department of medical statistics, Italy
Hyperhomocysteinaemia represents an independent risk factor for
atherosclerotic cardiovascular disease, stroke, peripheral arterial
occlusive disease and venous thrombosis [1]. Psoriasis is a chronic
inflammatory skin disease associated with several comorbidities,
such as atherosclerosis, chronic ischemic heart disease, obesity
and diabete mellitus [2].
Elevated homocysteine levels may cause irritation of the blood
vessels; the endothelial injury of hyperhomocysteinaemia and the
cardiovascular risks that derive from it are gradual and
continuous. The authors investigated the relationship between
plasma homocysteine levels and the severity of chronic psoriasis in
a selected cohort of patients without known risk factors for
acquired hyperhomocysteinaemia.
Plasma homocysteine levels were analyzed in 70 patients
with psoriasis and in 30 controls, matched for sex, age and body
mass index. The distribution of variables in the study groups was
assessed by Kolmogorov-Simirnov test. Statistical differences
between data from the patients and control groups were determined
according to Student's t-test of Mann-Whitney U-test. P<0.05 was
considered significant.
The inclusion criteria for the case were
age >18 years, diagnosis of psoriasis made at least 1
year before enrolment and suspension of systemic and topical
steroid treatment respectively from 4 and 2 weeks. Exclusion
criteria were: intake of drugs known to cause
hyperhomocysteinaemia; intake of antipsoriatic drugs including
methotrexate with folic acid supplementation and acitretin;
presence of chronic renal and hepatic diseases; systemic lupus
erythematosus, hypothyroidism, stroke and peripheral vascular
disease. Severity of psoriasis was assessed according to the
Psoriasis Area Severity Index (PASI). Our patients were matched in
three subgroups according to the PASI score: 9 patients were
affected by mild psoriasis (PASI<10), 30 by moderate psoriasis
(PASI 10-20), and 31 by severe psoriasis (PASI>20) with a PASI
ranging from 4 to 60 (mean 18.9) (tables 1 and
2).
Table 1 Descriptive characteristics of cases and
controls.
|
| Patients with psoriasis (n=70) |
Controls(n=30) |
| Sex (M/F) |
36/34 |
13/17 |
| Age (years) |
52 |
48 |
| BMI (kg/m2) |
26.1 |
22.3 |
| Homocysteine (μmol/L) |
18.2 |
11.7 |
Table 2 Psoriatic patients with hyperhomocysteinaemia
|
| PASI |
MID homocyesteine |
| Mild psoriasis |
<10 |
8.6 μmol/L |
| Moderate psoriasis |
10-20 |
17.5 μmol/L |
| Severe psoriasis |
>20 |
21.6 μmol/L |
The results showed that patients with moderate to severe
psoriasis had plasma homocysteine levels higher than controls
(52.86% of cases vs 20% of controls having
hyperhomocysteinaemia (≥ 15 μmol/L)) (figure 1).
In psoriasic patients, homocysteine levels correlated directly with
psoriasis severity and consequently with the PASI score (p<0.05;
Pearson Index 0.85) (figure 2).
The control group showed normal ranges of homocysteine plasmatic
levels, with the exception of 6/30 controls with minimal increases
of plasmatic homocysteine (aminoacid concentration between 15 and
20 μmol/L).
All patients and controls underwent epiaortic ultrasound
examination. 35 patients with hyperhomocysteinaemia presented signs
of subclinical atherosclerosis; two of them developed severe
cardiovascular events after twenty years of disease.
Data from the literature confirm our results; several studies
have shown that the homocysteine plasmatic concentration in
psoriatic patients is higher than in healthy controls
[1, 3-5]; however, the correlation we found between
homocysteine serum levels and psoriasis severity measured by PASI
score has hardly ever been reported in the literature. Few studies
show a relationship between homocysteine blood levels and disease
activity [4, 6].
These studies also demonstrate that psoriatic patients often
present low levels of folic acid as a result of an increasing
vitamin utilization in the skin and/or reduced gut absorption
[4, 5]. Physicians must find a pharmacological treatment that
reduces the plasmatic homocysteine levels, even when these are only
moderately high; we know that folic acid, vitamin B6 and vitamin
B12 are all involved in breaking down homocysteine in the blood.
Therefore dietary supplementation with folic acid and vitamins B6
and B12 is recommended. Treatment of hyperhomocysteinaemia may not
only reduce atherosclerotic plaque areas, but also it may decrease
the risk of ischaemic heart disease, deep vein thrombosis and
stroke [4].
Based on their findings, the authors suggest that psoriatic
patients should be treated by a global management taking into
account cardiovascular risk factors.
Disclosure
Financial support: none. Conflict of interest: none.
References
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