Angiotensin I converting enzyme in cerebrospinal fluid of patients with neurological diseases

Schweisfurth, H.; Schiöberg-Schiegnitz, S.; Kühn, Wilfried; Parusel, B.

doi:10.1007/bf01717829

Cited by 38 publications

(23 citation statements)

References 17 publications

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“…To date, several reports have described significantly increased ACE activity in cerebrospinal fluid and serum among patients with MS (Constantinescu, Goodman, Grossman, Mannon, & Cohen, 1997; Kawajiri et al., 2008; Schweisfurth, Schiöberg‐Schiegnitz, Kuhn, & Parusel, 1987). Furthermore, in our previous work with MS patients from Croatian and Slovenian populations, we demonstrated that the homozygous ACE‐DD genotype might contribute to an elevated MS risk among male patients (Lovrečić et al., 2006).…”

Section: Introductionmentioning

confidence: 99%

The lack of association between angiotensin‐converting enzyme gene insertion/deletion polymorphism and nicotine dependence in multiple sclerosis

et al. 2016

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ObjectiveBlood‐borne angiotensin II is generated from angiotensinogen via cleavage by renin and angiotensin‐converting enzyme (ACE), an enzymatic cascade known as the renin–angiotensin system (RAS). Several lines of evidence indicate that ACE, beyond its classical role of mediating blood pressure regulation, might contribute to the etiology of substance addictions by influencing dopaminergic signaling. A functional insertion/deletion (I/D) polymorphism of the ACE gene was associated with risk for being a smoker among individuals with depression and with smoking severity in studies comprising patients with depression and healthy controls. Several reports have described significantly increased ACE activity in cerebrospinal fluid and serum among MS patients. Furthermore, in our previous work with MS patients from Croatian and Slovenian populations, we demonstrated that the ACE‐I/D polymorphism contributes to an elevated MS risk among male patients. Here we investigated whether the ACE‐I/D polymorphism might influence smoking behavior among patients with MS.Patients and MethodsGenotyping was performed in 521 patients (males/females: 139/382) using polymerase chain reaction.ResultsWe revealed no significant differences in ACE genotype and allele frequencies between smokers and nonsmokers and no significant association between the ACE‐I/D polymorphism and either pack‐year smoking history or number of cigarettes smoked daily (p > .05, respectively).ConclusionThe ACE‐I/D polymorphism does not contribute either to risk for nicotine dependence or to smoking severity among MS patients. In the context of reports on the ACE‐I/D polymorphism and nicotine dependence among healthy controls and patients with depression, we may speculate that the mechanism by which this polymorphism influences nicotine dependence risk differs in MS compared to depression, although not compared to a healthy population. In addition to angiotensin II, other potential ACE substrates, such as substance P and neurotensin, which also influence dopaminergic neurotransmission (and are proposed to be associated with MS), may deserve study in future.

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Section: Introductionmentioning

confidence: 99%

The lack of association between angiotensin‐converting enzyme gene insertion/deletion polymorphism and nicotine dependence in multiple sclerosis

et al. 2016

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“…Furthermore, increases in the concentration of ACE (ref. 26,27,[33][34][35][36][37] ), IgG-index [38][39][40] , oligoclonal bands 38,39,41 , CD4/CD8 lymphocyte ratios 42 , lysosymes and beta 2-microglobulin concentrations 43 in CSF have been reported. Most studies report evidence of intrathecal synthesis of immunoglobulins with oligoclonal bands in about 30-40% of patients with NS (ref.…”

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confidence: 99%

Neurosarcoidosis: Two case reports with multiple cranial nerve involvement and review of the literature

Mijajlović¹,

Mirkovic²,

Mihailović-Vučinić³

et al. 2014

Biomed Pap Med Fac Univ Palacky Olomouc Czech Repub

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aBackground. Involvement of the central nervous system is registered in a relatively small number of patients with sarcoidosis. In this article we present two cases with various neurological symptoms that fulfill criteria for neurosarcoidosis (NS). In addition, we review the literature on NS with special attention to isolated cranial nerve involvement. Methods and Results. First patient: Neurological examination identified multiple cranial neuropathy, moderate rightsided hemiparesis, polyradiculoneuritis of the lower limbs and positive meningeal signs. Laboratory tests showed serum and cerebrospinal fluid (CSF) inflammatory abnormalities, with increased values of the angiotensin-converting enzyme (ACE). CSF analysis also showed presence of 9 oligoclonal IgG bands. Brain and spine magnetic resonance imaging (MRI) revealed diffuse meningopathy, and focal granulomatous lesion in the body of the L5 vertebra. Lung sarcoidosis was confirmed by additional diagnostic procedures. The patient was treated with Methylprednisolone and a tapering course of oral Prednisone, which reduced the pain in the back and legs and improved the strength of the right leg. However, the other neurological deficiencies remained. After confirming lung sarcoidosis, the patient received Methotrexate in addition to Prednisone but during the following 2 years the patient's condition progressively worsened and ended in death. Second patient: Neurological findings showed weakness of the right n. oculomotorius and the right n. trochlearis, as well as the right-side face weakness. We found raised level of the ACE in serum and CSF. Thorax high-definition computed tomography (HDCTT) showed ribbon-like domains of discrete changes in the pulmonary parenchyma. MRI of the brain showed multiple white matter lesions. This patient also received Methylprednisolone followed by Prednisone, and after two months, ocular motility normalized. Conclusion. The diagnosis of NS is always a challenge. For this rerason definitive diagnosis requires the exclusion of other causes of neuropathy. Multiple cranial neuropathies should always arouse suspicion of NS.

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“…They compared the CSF ACE levels of 11 patients with ‘probable’ neurosarcoidosis with 207 normal controls, using a radioassay. Schweisfurth et al [18]and Oksanen et al [19]found elevated levels of ACE in CSF in patients with untreated neurosarcoidosis compared with normal controls. They assumed ACE-producing granulomas to be the source.…”

Section: Discussionmentioning

confidence: 99%

Neurosarcoidosis: Clinical Experience and Diagnostic Pitfalls

Kellinghaus

Schilling

Lüdemann³

2004

Eur Neurol

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Objective: To describe a group of patients with neurosarcoidosis and to highlight diagnostic difficulties based on current diagnostic criteria. Methods: The patient database of a general neurological department was searched for patients with established or suspected diagnosis of neurosarcoidosis. Twenty-four patients were identified with definite (n = 3), probable (n = 10) and possible neurosarcoidosis (n = 10). History and clinical, laboratory and imaging data of patients with definite and probable neurosarcoidosis were analyzed. Results: Cranial nerve symptoms were a dominant clinical feature, with the optic nerve being affected most frequently. Cerebrospinal fluid pleocytosis was found in more than half of the patients. Intrathecal IgG synthesis and oligoclonal bands were less frequent. There was a wide array of MRI lesions in both groups. Chest X-ray was false negative in 2 of 5 patients who also underwent a thoracic CT. Therapy with prednisolone was initiated in all patients. After a median of 36 months, 6 of 8 patients with follow-up data of >24 months were still in remission. Aggravation of symptoms required therapy escalation in 2 patients. Conclusion: There is a wide range of clinical symptoms and test results in patients with ‘definite’ or ‘probable’ neurosarcoidosis. Because systemic involvement is a crucial diagnostic criterion, extensive medical work-up may be necessary. Prognosis under corticosteroid treatment may be better than previously thought.

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Angiotensin I converting enzyme in cerebrospinal fluid of patients with neurological diseases

Cited by 38 publications

References 17 publications

The lack of association between angiotensin‐converting enzyme gene insertion/deletion polymorphism and nicotine dependence in multiple sclerosis

The lack of association between angiotensin‐converting enzyme gene insertion/deletion polymorphism and nicotine dependence in multiple sclerosis

Neurosarcoidosis: Two case reports with multiple cranial nerve involvement and review of the literature

Neurosarcoidosis: Clinical Experience and Diagnostic Pitfalls

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