Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.4.15.1 (ACE)
 18,300 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The biochemical problems of psoriasis are discussed, especially two modern hypothesis about the pathogenesis of this skin disease. 1. DHEA-deficiency leading to an increase of G-6-PDH inaugurated by Holzmann et al. 2. cAMP deficiency in psoriatic lesions as a cause of psoriasis hypothized by Voorhees and Duell. A synopsis of the physiology of the steroid hormone DHEA (synthesis, regulation, conjugation and excretion) is given. There are doubts that this hypothesis is correct. Recent findings have indicated, that there is no decrease of cAMP in the psoriatic lesion--in contrast there is an increase of this cyclic nucleotid. It means that this theory is also doubtfull. Treatment of an hypothetical decrease of cAMP by AMP is not possible, because this AMP will not penetrate in the cell and cannot be metabolized to cAMP.
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PMID:[Psoriasis: A general disease? Can psoriasis be explained biochemically?]. 19 71

All-trans retinoic acid and its derivative retinoid, two new compounds with expanding therapeutic spectrum in dermatology, were investigated in biochemical assays. Both substances provoke an increase in oxygen consumption of rat skin whereas in human skin only retinoid was found active in this respect. In resting yeast cells, both substances failed to exert any significant influence on oxygen consumption.--Pure G-6-PDH was inhibited by retinoic acid and retinoid in concentrations as low as 5 mug/ml. In human skin homogenates, LDH-, GAPDH-, and G-6-PDH-activities were inhibited by retinoic acid whereas GOT-, LAP-, and ALD-activites remained practically unchanged following an incubation with retinoic acid in concentrations between 1 and 100 mug/ml for 60 min.--The data collected in this study were briefly discussed with regard to the use of retinoic acid and its derivatives in psoriasis.
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PMID:Influences of retinoic acid and retinoid on skin metabolism. Investigations of oxygen consumption and enzymatic activities of human skin. 98 76

The aim of the study was to determine a biochemical basis for the augmented oxidative metabolism found in mononuclear leukocytes (MNL) of patients with active psoriasis. Dehydroepiandrosterone (DHEA) is known to inhibit glucose-6-phosphate dehydrogenase (G-6-PDH). We determined the activity of G-6-PDH as well as the penetration and metabolism of DHEA - diminished plasma concentrations of which have been found in psoriatics previously - in 16 patients with active psoriasis and 16 controls. MNL in patients with psoriasis possessed 52% more (p less than 0.05) G-6-PDH activity, based on cell number, and 34% more (p less than 0.05) activity, based on soluble protein. No difference in DHEA penetration and metabolism in MNL was found between psoriatics and controls, in contrast with previous findings of reduced penetration and increased reduction in erythrocytes of psoriatics. We conclude that the enhanced G-6-PDH activity in MNL of patients with active psoriasis is not due to altered DHEA penetration or metabolism.
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PMID:Augmented glucose-6-phosphate dehydrogenase activity and normal penetration and metabolism of dehydroepiandrosterone in mononuclear leukocytes in psoriasis. 294 86

Serum angiotensin converting enzyme activity is frequently increased in patients with active sarcoidosis. In spite of a reported association between sarcoidosis and psoriasis, serum angiotensin converting enzyme activities have not been reported for patients with psoriasis. We found the mean (SD) angiotensin-converting enzyme activity for 51 healthy subjects was 18.6 (5.8) kU/l, but for 52 patients with psoriasis without coexisting sarcoidosis, it was 28.3 (6.7) kU/l. There is a significant difference between these means (p less than 0.01). Forty-two percent (22/52) of the psoriasis patients had an increased serum angiotensin converting activity. Other diseases sometimes associated with an increased serum angiotensin converting enzyme activity were excluded as possible causes of a elevated activity in our patients with psoriasis. We conclude that almost half of the patients with psoriasis will have an elevated serum angiotensin converting enzyme activity, even when coexisting sarcoidosis is absent.
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PMID:Serum angiotensin converting enzyme activity in patients with psoriasis. 299 46

Angiotensin-converting enzyme (ACE) is identical to the dipeptidyl carboxypeptidase kininase II, which inactivates bradykinin. That is why captopril, an orally active ACE inhibitor, alters the kallikrein-kinin-arachidonic acid system. It is suggested that this mechanism could be responsible for the dosage-dependent incidence of polymorph cutaneous eruptions during therapy with captopril. A 42-year-old female patient with no previous personal or family history of psoriasis developed an eruptive-exanthematous type of psoriasis vulgaris 1-2 weeks after the beginning of captopril therapy. It is suggested that the onset of the dermatosis was produced by a blockade of bradykinin inactivation. This might have increased the production of arachidonic acid and led to elevated concentrations of inflammatory mediators.
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PMID:[Initial manifestation of eruptive exanthematous psoriasis vulgaris caused by captopril medication]. 352 65

Although psoriasis has been recognized at least since Biblical times new forms, associations and influences continue to be described in the twentieth century. New forms include the rupioid erythema annulare centrifugum-like and follicular patterns. Associations with vitiligo bullous pemphigoid and lupus erythematosus have been recently described. Endoscopic surgery has increased para umbilical psoriasis while Sun Smart campaign have reduced photo-aggravated psoriasis. Infections such as paediatric perianal streptococcal cellulitis and drugs including angiotensin converting enzyme inhibitors and cytokines exacerbate psoriasis.
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PMID:Psoriasis: changing clinical patterns. 871 7

Pustular eruptions caused by anti-hypertension drugs are relatively rare. They have been reported with beta-adrenergic blocking agents, calcium channel blocker and angiotensin converting enzyme (ACE) inhibitors. Angiotensin II type 1 (AT 1) receptor antagonists, as a new class of drug for hypertension, has become an established and popular treatment. We describe a patient with generalized pustular psoriasis induced by candesartan cilexetil (AT1 receptor antagonist), who was previously diagnosed as flexural psoriasis. It is known that AT1 receptor antagonists do not increase the bradykinin level, inhibiting the renin-angiotensin system more potently than ACE inhibitor. But our results suggest that AT 1 receptor antagonists could have some ACE inhibitor potency as an up-regulator for bradykinin in our patient, with pustular eruptions developing on the psoriatic background. To the best of our knowledge, there have been no reported cases of pustular psoriasis associated with AT1 receptor antagonists.
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PMID:Candesartan cilexetil induced pustular psoriasis. 1294 27

Angiotensin-II, a product of angiotensin converting enzyme (ACE) action, regulates vascular tone, stimulates the release of pro-inflammatory cytokines, activates NFkappaB, increases oxidant stress, and suppresses nitric oxide synthesis. Thus, angiotensin-II is pro-inflammatory in nature. Hence, increase in ACE activity and the concentrations of angiotensin-II initiate and perpetuate inflammation. Since ACE is present in many tissues including: the uterus, placenta, vascular tissue, heart, brain, adrenal cortex and kidney, leukocytes, alveolar macrophages, peripheral monocytes, neuronal cells and epididymal cells, this suggests that angiotensin-II may have a role in atherosclerosis, congestive cardiac failure, stroke, bipolar disorder, schizophrenia, dementia, Alzheimer's disease, psoriasis, atopic and non-atopic dermatitis, eczema, several acute and chronic inflammatory diseases, and cancer, conditions in which inflammation is known to play a significant role. This suggests that ACE inhibitors and/or angiotensin-II receptor blockers could be of significant benefit in the management of these conditions. Alternatively, structural analogues of presently available ACE inhibitors and angiotensin-II receptor blockers could be developed such that they are not only useful in the treatment of hypertension and CHF but also possess anti-inflammatory actions.
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PMID:Is angiotensin-II an endogenous pro-inflammatory molecule? 1587 6

Psoriasis is a chronic, inflammatory skin disorder that is induced and aggravated by a number of endogenous and exogenous factors. Traditionally lithium, beta blockers, NSAIDs, ACE inhibitors and antimalarials have been associated with psoriasis, but interferon can also be a triggering factor. We present two patients with multiple sclerosis who suffered from activation of psoriasis in relation to interferon-beta treatment. In one of the patients, psoriasiform injection site lesions persisted six years after termination of the interferon treatment.
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PMID:[Activation of psoriasis in patients undergoing treatment with interferon-beta]. 1610 99

Angiotensin-II regulates vascular tone, stimulates the release of pro-inflammatory cytokines, activates NF-kappaB, increases oxidant stress, and suppresses nitric oxide synthesis, and thus, it functions as an inflammatory molecule. Since ACE is present in many tissues, this suggests that angiotensin-II may play a significant role in atherosclerosis, congestive cardiac failure, stroke, bipolar disorder, schizophrenia, dementia, Alzheimer's disease, psoriasis, atopic and non-atopic dermatitis, eczema, several acute and chronic inflammatory diseases, and cancer, conditions in which inflammation is an aetiopathogenic factor. Thus, ACE inhibitors and/or angiotensin-II receptor blockers could be of benefit in these conditions. Furthermore, structural analogues of ACE inhibitors and angiotensin-II receptor blockers could be developed that possess anti-inflammatory actions without significant action on the cardiovascular system.
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PMID:Angiotensin-II behaves as an endogenous pro-inflammatory molecule. 1612 58


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