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Raynaud's disease and phenomenon [keywords]
- Antiphosphatidylserine and antiphosphatidylethanolamine antibodies in systemic lupus erythematosus: occurrence and association with clinical disease manifestations. [JOURNAL ARTICLE]
- Pol Arch Med Wewn 2014 Jun 20.
INTRODUCTION Antiphosphatidylethanolamine antibodies (aPE) and antiphosphatidylserine antibodies (aPS) belong to a group of antiphospholipid antibodies (aPL) that occur in patients with antiphospholipid syndrome (APS) and systemic lupus erythematosus (SLE). OBJECTIVES The aim of this study was to examine the relationship among the elevated serum concentration of aPE/aPS, the clinical manifestations of SLE, and the presence of other autoantibodies. PATIENTS AND METHODS The study group consisted of 71 SLE patients. The control group was made up of 36 healthy volunteers. In both groups aPS/aPE serum concentration was measured with enzyme immunoassays. Data, including clinical manifestations and the laboratory markers of SLE, were obtained from medical documentation. RESULTS The study revealed a higher prevalence of aPE in SLE patients than in the controls (54.93% vs. 5.56%). Compared with aPE, aPS occurred in the study group less frequently (12.68%) and were absent in the controls. Anticardiolipin antibodies (aCL) and APS were found to be related to aPS presence. Among aPS-positive SLE patients, thrombocytopenia, Raynaud's phenomenon, and myocardial infarction were observed more frequently. The study revealed that aPE presence predisposes the patient to mucosal ulcers. A positive correlation between aPS and ESR was also revealed. The serum concentration of aPE correlated negatively with red blood count (RBC) and positively with erythrocyte sedimentation rate (ESR). CONCLUSIONS The presence of aPS in SLE patients was found to be associated with thrombocytopenia, Raynaud's phenomenon, and cardiac complications.
- Partial fingertip necrosis following a digital surgical procedure in a patient with primary Raynaud's phenomenon. [JOURNAL ARTICLE]
- Int Wound J 2014 Sep 9.
Raynaud's phenomenon is a common clinical disorder consisting of recurrent, long-lasting and episodic vasospasm of the fingers and toes often associated with exposure to cold. In this article, we present a case of partial fingertip necrosis following digital surgical procedure in a patient with primary Raynaud's phenomenon.
- Guillain-Barré syndrome presenting with Raynaud's phenomenon: a case report. [Journal Article]
- BMC Neurol 2014; 14(1):174.
Guillain-Barré syndrome is an immune mediated acute inflammatory polyradiculo-neuropathy involving the peripheral nervous system. Commonest presentation is acute or subacute flaccid ascending paralysis of limbs. Rarely autonomic dysfunction can be the presenting feature of Guillain-Barré syndrome. Raynaud's phenomenon, although had been described in relation to many disease conditions, has not been described in association with Guillain-Barré syndrome up to date.We report the first case of Guillain-Barré syndrome presenting with Raynaud's phenomenon in a 21-year-old previously well boy. New onset Raynaud's phenomenon was experienced followed by acute ascending flaccid paralysis of lower limbs and upper limbs together with palpitations and postural giddiness. Nerve conduction studies showed acute inflammatory demyelinating polyneuropathy with cerebrospinal fluid cyto-protein dissociation. He was treated with intravenous immunoglobulin and showed a satisfactory clinical recovery of muscle weakness, Raynaud's phenomenon and autonomic disturbances.Guillain-Barré syndrome presenting with Raynaud's phenomenon is not being reported in literature previously. Although the underlying mechanism is not fully understood, Raynaud's phenomenon should prompt the physician to consider Guillain-Barré syndrome with a complimentary clinical picture.
- Postural orthostatic tachycardia syndrome: a dermatologic perspective and successful treatment with losartan. [Journal Article]
- J Clin Aesthet Dermatol 2014 Aug; 7(8):41-7.
The postural orthostatic tachycardia syndrome is a disease characterized by excessively increased heart rate during orthostatic challenge associated with symptoms of orthostatic intolerance including dizziness, exercise intolerance, headache, fatigue, memory problems, nausea, blurred vision, pallor, and sweating, which improve with recumbence. Postural orthostatic tachycardia syndrome patients may present with a multitude of additional symptoms that are attributable to vascular vasoconstriction. Observed signs and symptoms in a patient with postural orthostatic tachycardia syndrome include tachycardia at rest, exaggerated heart rate increase with upright position and exercise, crushing chest pain, tremor, syncope, loss of vision, confusion, migraines, fatigue, heat intolerance, parasthesia, dysesthesia, allodynia, altered traditional senses, and thermoregulatory abnormalities. There are a number of possible dermatological manifestations of postural orthostatic tachycardia syndrome easily explained by its recently discovered pathophysiology. The author reports the case of a 22-year-old woman with moderate-to-severe postural orthostatic tachycardia syndrome with numerous dermatological manifestations attributable to the disease process. The cutaneous manifestations observed in this patient are diverse and most noticeable during postural orthostatic tachycardia syndrome flares. The most distinct are evanescent, hyperemic, sharply demarcated, irregular patches on the chest and neck area that resolve upon diascopy. This distinct "evanescent hyperemia" disappears spontaneously after seconds to minutes and reappears unexpectedly. Other observed dermatological manifestations of this systemic disease include Raynaud's phenomenon, koilonychia, onychodystrophy, madarosis, dysesthesia, allodynia, telogen effluvium, increased capillary refill time, and livedo reticularis. The treatment of this disease poses a great challenge. The author reports the unprecedented use of an oral angiotensin II type 1 receptor antagonist resulting in remarkable improvement.
- The association between vibration and vascular injury in rheumatic diseases: A review of the literature. [JOURNAL ARTICLE]
- Autoimmunity 2014 Aug 12.:1-8.
Abstract Vascular manifestations can be seen early in the pathogenesis of inflammatory rheumatic diseases. Animal experiments, laboratory and clinical findings indicated that acute or long-term vibration exposure can induce vascular abnormalities. Recent years, in addition to Raynaud's phenomenon (RP), vibration as a risk factor for other rheumatic diseases has also received corresponding considered. This review is concentrated upon the role of vibration in the disease of systemic sclerosis (SSc). In this review, we are going to discuss the main mechanisms which are thought to be important in pathophysiology of vascular injury under the three broad headings of "vascular", "neural" and "intravascular". Aspects on the vibration and vascular inflammation are briefly discussed. And the epidemiological studies related to vibration studies in SSc and other rheumatic diseases are taken into account.
- IgG4-related skin disease. [JOURNAL ARTICLE]
- Br J Dermatol 2014 Jul 26.
Immunoglobulin G4 (IgG4)-related disease (IgG4-RD) is a recently established clinical entity characterized by high levels of circulating IgG4 and tissue infiltration of IgG4(+) plasma cells. IgG4-RD exhibits a distinctive fibro-inflammatory change involving multiple organs, such as pancreas, and salivary and lacrimal glands. The skin lesions of IgG4-RD have been poorly characterized and may stem from not only direct infiltration of plasma cells but also IgG4-mediated inflammation. Based on the documented cases together with ours, we categorized the skin lesions into seven subtypes: (1) cutaneous plasmacytosis (multiple papulonodules or indurations on the trunk and proximal part of limbs), (2) pseudolymphoma and angiolymphoid hyperplasia with eosinophilia (plaques and papulonodules mainly on the periauricular, cheek, and mandible regions), (3) Mikulicz's disease (palpebral swelling, sicca syndrome, and exophthalmos), (4) psoriasis-like eruption (strikingly mimicking psoriasis vulgaris), (5) unspecified maculopapular or erythematous eruptions, (6) hypergammaglobulinemic purpura (bilateral asymmetrical palpable purpuric lesions on the lower extremities) and urticarial vasculitis (prolonged urticarial lesions occasionally with purpura), and (7) ischemic digit (Raynaud's phenomenon and digital gangrene). It is considered that the subtypes (1)-(3) are induced by direct infiltration of IgG4(+) plasma cells, while the other (4)-(7) types are caused by the secondary mechanisms. IgG4-related skin disease is defined as IgG4(+) plasma cell-infiltrating skin lesions that form plaques, nodules or tumors (1-3), but may manifest secondary lesions caused by IgG4+ plasma cells and/or IgG4 (4-7). This article is protected by copyright. All rights reserved.
- Old medications and new targeted therapies in systemic sclerosis. [REVIEW]
- Rheumatology (Oxford) 2014 Jul 26.
SSc is a multiorgan disease with significant morbidity that is associated with poor health-related quality of life. Treatment of this condition is often organ based and non-curative. However, there are newer, potentially disease-modifying therapies available to treat certain aspects of the disease. This review focuses on old and new therapies in the management of SSc in clinical practice.
- Therapeutic potentials of phosphodiesterase-5 inhibitors in cardiovascular disease. [Journal Article]
- Rev Cardiovasc Med 2014; 15(2):158-67.
Phosphodiesterase-5 (PDE5) inhibitors have been approved by the US Food and Drug Administration for the treatment of erectile dysfunction and more recently for pulmonary arterial hypertension (World Health Organization functional class I). PDE5 inhibitors can induce vasodilation; in addition, through a complex pathway involving nitric oxide, cyclic guanosine monophosphate, and protein kinase G, it can reduce apoptosis and suppress cell proliferation. The presence of PDE5 inhibitors in various tissues and systemic vasculature make them potential targets in a variety of cardiovascular diseases. In many in vitro and in vivo studies, PDE5 inhibitors have been shown to have positive effects in systolic and diastolic congestive heart failure, ischemic heart disease, doxorubicin cardiomyopathy, and pulmonary arterial hypertension. They also improved vasoconstriction in Raynaud phenomenon, peripheral artery disease, and hypoxic brain conditions. This article reviews the therapeutic potentials of PDE5 inhibitors in different cardiovascular diseases.
- [In Process Citation]. [Journal Article]
- MMW Fortschr Med 2014 Jun 12; 156(11):32.
- Combined use of ursodeoxycholic acid and bosentan prevents liver toxicity caused by endothelin receptor antagonist bosentan monotherapy: two case reports. [JOURNAL ARTICLE]
- J Med Case Rep 2014 Jul 11; 8(1):250.
Pulmonary arterial hypertension is a fatal disease characterized by progressive remodeling of the pulmonary arteries and an increase in pulmonary vascular resistance. Up to 50% of patients with systemic sclerosis have pulmonary arterial hypertension, which significantly affects the prognosis. The endothelin receptor antagonist bosentan is used for the treatment of pulmonary arterial hypertension and shows a great beneficial effect. However, the most frequent side effect of bosentan is liver toxicity, which often requires dose reduction and discontinuation.We report two cases (a 64-year-old Japanese woman and a 69-year old Japanese woman) of systemic sclerosis, both with severe Raynaud's phenomenon and pulmonary arterial hypertension. Both patients had initially received bosentan monotherapy, which caused liver toxicity as indicated by increased levels of alanine aminotransferase, alkaline phosphatase, and gamma-glutamyltransferase. After dose reduction or discontinuation of bosentan, these liver function abnormalities were normalized and the patients subsequently received retreatment with a combination of bosentan and ursodeoxycholic acid. The results of liver function tests did not show any abnormalities after this combination therapy.These reports suggest the usefulness of ursodeoxycholic acid for preventing liver toxicity caused by bosentan. Thus, the addition of ursodeoxycholic acid to the treatment protocol is expected to be useful when liver toxicity emerges as a side effect of bosentan.