Serum angiotensin-converting enzyme in sarcoidosis and psoriasis

Summary Untreated pulmonary sarcoidosis is associated with an increased level of serum angiotensin-converting enzyme (SACE), which is regarded as a valuable method of diagnosing sarcoidosis and measuring the activity of the disease. The level of SACE in cutaneous sarcoidosis or other skin diseases has not been clearly established. We therefore examined SACE in 31 patients with systemic sarcoidosis, including cutaneous manifestations, and 12 patients with isolated cutaneous sarcoidosis. Also, 23 patients with psoriasis were studied. The level of SACE was generally elevated only in patients with untreated systemic sarcoidosis, whereas it was normal in cutaneous sarcoidosis and psoriasis. If the level of SACE is elevated in isolated cutaneous sarcoidosis, systemic disease must be strongly suspected.     

Serum angiotensin-converting enzyme activity in psoriasis

Conflicting data concerning the presence of enhanced serum angiotensin-converting enzyme (SACE) activity in psoriasis are reported in the literature. In order to verify whether this abnormality is a typical pattern of psoriasis, SACE levels were determined in 27 psoriatics as well as in 18 healthy subjects and in 30 patients with essential hypertension. We found that SACE levels were normal in patients affected by psoriasis independently of the presence or the absence of abnormalities in carbohydrate metabolism. Furthermore, SACE levels were not related to the severity of the skin lesions. We conclude that an elevated SACE activity is not a typical pattern of psoriasis, whereas, when present in a psoriatic, it might suggest the possibility of a coexisting unknown systemic sarcoidosis.     

Serum angiotensin-converting enzyme in leprosy

Serum angiotensin-converting enzyme activity was measured in 91 adult healthy and lepromatous armadillos before inoculation with M. leprae and at necropsises. Mean ACE values were significantly elevated in armadillos with leprosy and the degree of elevation was roughly proportional to the extent of infection. There was also significant difference in the serum ACE levels between Florida and Louisiana armadillos. The dapsone treatment resulted in bringing these levels to normal. Serial assays of serum, ACE provided information on the response of armadillos to dapsone therapy.     

Association of insertion/deletion polymorphism of the angiotensin-converting enzyme gene with psoriasis

BACKGROUND: Genetic factors are likely to be of fundamental importance in the pathogenesis of psoriasis. There are reports concerning the induction or/and exacerbation of psoriasis by angiotensin-converting enzyme (ACE) inhibitors, which have been attributed to the ACE inhibitor-induced augmentation of kinin levels in skin. However, to the best of our knowledge there has been no molecular genetic study investigating whether ACE insertion/deletion (I/D) polymorphism may contribute to the genetic background in psoriasis. OBJECTIVES: To assess the role of ACE I/D polymorphism in psoriasis. METHODS: A group of 86 patients with psoriasis and 154 control subjects were analysed for ACE I/D polymorphism by polymerase chain reaction. RESULTS: The distribution of ACE I/D polymorphism and allele frequencies in psoriatic patients was not significantly different from controls. Further analyses of psoriasis patients showed that ACE I/D polymorphism was not associated with age at onset of disease, clinical type of psoriasis or gender. However, the frequency of the I allele was significantly higher in patients with a positive family history of psoriasis than in those with no family history (sporadic psoriasis) (48% vs. 32%; P =0.03). In addition, the I allele was found significantly more frequently in type I psoriasis patients (onset < 40 years and positive family history) than in type II psoriasis patients (onset >/= 40 years, no family history) (48% vs. 27%; P = 0.04). CONCLUSIONS: Our results suggest that the presence of the I allele may confer susceptibility to development of psoriasis in individuals from psoriatic families.     

Tissue angiotensin-converting enzyme and lysosomal enzyme levels in skin diseases

The activities of tissue angiotensin-converting enzyme (ACE) were investigated in several skin diseases. Biopsy specimens were taken from 49 patients with granulomatous lesions, including sarcoidosis, 16 patients with nongranulomatous lesions, and 13 normal individuals. The ACE level was measured fluorometrically and the lysosomal enzyme levels were measured by established techniques. It was found that ACE activity increased in all granulomatous skin lesions, but not in other inflammatory lesions. The enzyme activity showed an increase that paralleled the time course of the disease. In contrast, lysosomal enzymes increased in various types of skin lesions, suggesting that they reflect nonspecific inflammation. These findings indicate that the tissue ACE level may be a marker for granulomatous inflammation, but one that is not specific for sarcoidosis.     

Psoriasis related to angiotensin-converting enzyme inhibitors

Two mechanisms have been proposed for the pathogenesis of eruptions induced by angiotensin-converting enzyme (ACE) inhibitors: (1) an allergic, immune-mediated reaction and (2) a pharmacologic, dose-dependent response. Two cases of palmoplantar psoriasis are presented, which can be attributed to the induction (case 1) and exacerbation (case 2) of ACE inhibitors. The first patient developed his eruption 2 months after he had received captopril, probably as a result of an allergic immunologic mechanism. This has been based mainly on circumstantial evidence and is further strengthened by the positive result of the mast cell degranulation test. The second patient developed an atenolol-induced, mild plantar psoriasis. She experienced a dramatic flare-up of her psoriatic lesions shortly after she had received an ACE inhibitor. It is suggested that her reaction occurred as a result of the enalapril-induced augmentation of kinin levels in the skin. These 2 patients represent deductive and unusual examples of the two different mechanisms that are responsible for the cutaneous complications of ACE inhibitors.     

Serum carotene and serum retinol in psoriasis

The serum carotene and retinol levels were determined in 25 male psoriatic patients and 25 healthy male controls. No difference was observed in carotene level, however, retinol level was found lower in psoriatic patients as compared to controls.     

Widespread foreign-body granulomas and elevated serum angiotensin-converting enzyme

A patient had extensive foreign-body granulomatous inflammation of multiple skin sites and of the inguinal lymph nodes with splenomegaly, cutaneous anergy to common skin antigens, and peripheral blood eosinophilia. The patient had an elevated serum angiotensin-converting enzyme level. Histologically, the granulomas were of the foreign-body type with lymphocytes, histiocytes, eosinophils, and giant cells, some that contained doubly refractile crystalline material. Electron-probe x-ray microanalysis identified silicon, magnesium, iron, calcium, phosphorus, zinc, titanium, and chromium in the crystalline material. These findings suggest talc, cement, and inorganic pigment as possible sources of the crystals. This case is reported for its unusual clinical, laboratory, and morphologic features.     

Stratum corneum chymotryptic enzyme in psoriasis

Abstract Stratum corneum chymotryptic enzyme (SCCE) is a serine protease which may function in the turnover of the stratum corneum by means of degradation of intercellular adhesive structures between corneocytes. It is also potentially an epidermal activating enzyme for cytokines such as interleukin-1β. The aim of this work was to study the expression of SCCE in psoriatic epidermis by means of immunohistochemistry, and to elucidate the nature of the SCCE present in psoriatic scales by means of biochemical analyses. In comparison to normal skin the number of cell layers expressing SCCE in psoriatic lesions was consistently increased. In nonlesional psoriatic skin the pattern of SCCE expression varied. It was similar to the pattern in normal skin in some biopsies, whereas in other biopsies evidence of an increased expression of SCCE was found. By means of zymography and immunoblotting, extracts of psoriatic scales were found to contain active SCCE as well as enzymatically inactive SCCE precursor. Also the effects of inhibitors on the activity towards a chromogenic protease substrate in the extracts after partial purification by gel exclusion chromatography were compatible with the presence of enzymatically active SCCE. We conclude that the expression of SCCE in psoriasis may be upregulated, and that the conversion of inactive SCCE-precursor to active SCCE occurs in the psoriatic lesion. The possible role of SCCE in the pathophysiology of psoriasis remains to be elucidated, but should be considered in future studies. Received: 24 April 1998 / Received after revision: 1 October 1998 / Accepted: 16 October 1998     

Serum prolidase activity in psoriasis patients

This study aimed to evaluate serum prolidase activity and the effects of gender, body mass index (BMI), disease severity and duration, and therapy type on prolidase activity in patients with psoriatic as well as the relationship between serum NO· and prolidase levels in these patients. The study included 29 clinically documented plaque patients with psoriasis and 24 healthy volunteers. Data such as age, sex, BMI, duration and severity of disease, and type of therapy were assessed. NO· levels were determined by the Griess reaction. Serum prolidase assay is based on a colorimetric determination of proline by Chinard’s reagent. We did not determine any difference in serum NO· levels of psoriatic patients when compared to controls. Serum prolidase levels in psoriasis patients were significantly higher than those in controls. There was no significant difference in prolidase activity between male and female. No statistically significant correlations were found between serum prolidase levels and BMI, PASI and disease duration. When compared between topical treatment group and systemic treatment group, there was no significant difference in serum prolidase activity. In conclusion, patients with psoriasis exhibit higher serum prolidase activity independent of gender, BMI, disease severity or duration, type of treatments or NO· level. However, further studies are needed to verify these findings as well as altered collagen synthesis in patients with psoriasis.     

The angiotensin-converting enzyme insertion/deletion and the endothelin -134 3A/4A gene polymorphisms in patients with chronic plaque psoriasis

BACKGROUND: Psoriasis is a common chronic inflammatory skin disease. Vasoactive peptides such as endothelin-1 (ET-1) and bradykinin have previously been implicated in the pathogenesis of chronic plaque psoriasis. The angiotensin-converting enzyme (ACE) gene carries a 287-base pair insertion/deletion (I/D) gene polymorphism, which is associated with plasma concentrations of bradykinin-degrading ACE. A functional polymorphism (EDN1 -134 3A/4A) in the gene encoding ET-1 has been shown to affect ET-1 expression. The purpose of the present study was thus to investigate a hypothesized association between these gene polymorphisms and the presence of chronic plaque psoriasis. METHODS: The present case-control study comprised 207 patients with chronic plaque psoriasis (136 with early onset and 71 with late onset disease) and 182 control subjects. Genotypes of EDN1 and ACE were determined by a 5' exonuclease assay (Taqman). RESULTS: The prevalence of the homozygous ACE II genotype was significantly higher in patients with early-onset psoriasis than among control subjects (30.9% vs 19.2%, P = 0.016), yielding an odds ratio of 1.88 [95% confidence interval (CI): 1.12-3.15] for early-onset disease. For late-onset psoriasis, presence of the ACE II genotype was associated with a non-significant odds ratio 1.54 (95% CI: 0.81-2.92). As for the EDN1 -134 3A/4A gene polymorphism, no significant differences in genotype distributions were found between patients with either early- or late-onset psoriasis and control subjects (EDN1 -134 4A/4A: 9.6% in early-onset and 5.6% late-onset psoriasis vs 7.7% in controls; P > 0.05). CONCLUSIONS: Our data suggest that homozygosity for the ACE I allele may affect susceptibility to early-onset psoriasis.     

Serum lipids in patients with psoriasis.

In 13 patients with psoriasis a lower total cholesterol (TC) concentration was found compared to healthy controls of the same population. No differences in the concentration of serum triglyceride (TG) or phospholipids (PL) were detected between these two groups. In the same patients, serum triglyceride fatty acid analyses showed a reduced concentration of linoleic acid and a raised level of palmitoleic and myristic acids. No differences were detected in the major phospholipid fractions. The increase in plasma free fatty acids (FFA) following intravenous heparin was comparable in the psoriatic patient and in the controls. It is concluded that no basic abnormality of serum lipids exists and that the changes described were due to a selective loss via the scales or due to malabsorption.     

Serum lipoproteins in middle-aged men with psoriasis

Elevated serum triglyceride and low serum HDL cholesterol levels have been reported to be risk factors for occlusive vascular disease. In 20 middle-aged men with psoriasis the serum lipoprotein pattern was compared with that in a group of healthy middle-aged men. In thirteen of the 20 patients the psoriasis was mild to moderate and in seven patients it was severe and widespread. Both groups of patients had elevated levels of both VLDL and LDL triglycerides. They also showed a tendency towards higher VLDL and lower HDL cholesterol levels than the controls. The abnormalities were more pronounced in patients with severe psoriasis. The lipoprotein pattern found in this study may possibly indicate that psoriasis is associated with an increased risk of occlusive vascular disease.