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Livedo reticularis is a vascular abnormality of the skin resulting in an erythematous reticular rash. The combination of livedo reticularis and stroke-like episodes in adults is known as Sneddon syndrome [Sneddon, IB (1965). Br J Dermatol 77:180-188]. A similar combination of stroke-like episodes and livedo reticularis has been reported to occur in children [Baxter P et al. (1993). Dev Med Child Neuro 35:917-926]. We present here a 7-year-old male with congenital livedo reticularis, obesity, developmental delay, stroke-like episode, hypertension and cystic kidneys. We summarize our patient's findings and family history, and compare his disorder to other possibly related conditions.
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PMID:Livedo reticularis, developmental delay and stroke-like episode in a 7-year-old male. 954 37

Sneddon syndrome is a systemic non inflammatory arteriopathy characterized by the association of livedo reticularis, thrombotic cerebrovascular disease, coronary artery disease and hypertension. Middle age females are usually affected. It should be considered in the differential diagnosis of acute ischemic attacks in younger patients. It has been related to the antiphospholipid antibody syndrome. Treatment is based on control of hypertension and cardiovascular risk factors along with antiplatelet agents. Two cases meeting the clinical criteria outlined above are reported.
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PMID:[Sneddon syndrome. Presentation of 2 cases]. 972 83

Sneddon syndrome is characterized by the association of livedo reticularis and cerebral ischemic arterial events (stroke or transient ischemic attack). Reported prevalence of antiphospholipid antibodies is highly variable. We conducted this study to compare the clinical and pathologic features of patients with Sneddon syndrome according to the presence or absence of antiphospholipid antibodies. Forty-six consecutive patients with Sneddon syndrome were analyzed. All were examined by the same dermatologist who classified the livedo of the trunk according to the regularity of the fishnet reticular pattern and according to the thickness of the fishnet reticular pattern (> or = 10 mm = large; < 10 mm = fine). Skin biopsies were systematically performed, from both the center and the violaceous netlike pattern in 38 patients. Antiphospholipid antibodies-positive Sneddon syndrome was defined by the presence of lupus anticoagulant or abnormal titers of anticardiolipin antibodies on repeated determinations. Group I consisted of 27 antiphospholipid antibodies-negative patients and Group II, of 19 antiphospholipid antibodies-positive patients. All patients except I in Group II had irregular livedo reticularis. Large livedo racemosa was more frequently observed in Group I (89%) than in Group II (21%, p < 0.001). On skin biopsy, arteriolar obstruction was detected in only 8 patients (4 in each group). The following parameters were not statistically different between the 2 groups: gender, mean age at detection of livedo, mean age at first clinical cerebral event, hypertension, Raynaud phenomenon, patients with extracerebral and extracutaneous arterial or arteriolar thrombosis or stenosis, patients with venous thrombosis, and women with 2 fetal losses or more. In contrast, seizures (11% in Group I versus 37% in Group II, p < 0.05), mitral regurgitation on echocardiogram (19% versus 53%, p = 0.02), and thrombocytopenia < 150,000/muL (0% versus 42%, p < 0.005) were more frequently observed in Group II. The number of events per year of follow-up was lower with antiplatelet therapy (0.08 versus 0.5) in Group I, but was not different with anticoagulation (0.056 versus 0.06). Antiphospholipid antibodies-negative and -positive patients with Sneddon syndrome belong to close but different subsets of Sneddon syndrome.
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PMID:Sneddon syndrome with or without antiphospholipid antibodies. A comparative study in 46 patients. 1042 3

Antiphospholipid antibodies (APA) were studied in 30 women with a history of recurrent fetal losses. An increased level of anticardiolipin antibodies was found in 7(23.3%) of them, being high and moderate in 4 women. Lupus anticoagulant was present in 9(30.0%) examinees. None cases of SLE were diagnosed. Diagnostically significant APA levels were associated with moderate symptomless thrombocytopenia. 12 of 13 women with antiphospholipid syndrome markers had definite (livedo reticularis, damage of cardiac valves, recurrent thrombophlebitis, leg ulcers, stroke, migraine) and possible (moderate arterial hypertension, proteinuria, retina angiopathy) extragenital features of this disorder. The most serious vascular complications took place in the group with high and moderate levels of anticardiolipin antibodies IgG.
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PMID:[Antiphospholipid syndrome in females with recurrent fetal losses]. 1048 65

The term vasoneuroses comprises functional disorders of peripheral vessels, in particular arterioles, manifested by vasospasms on the periphery of the upper and lower extremities, more rarely the nose and ears. The main representant of these diseases is a disorder manifested by episodic attacks of ischaemia of the fingers, in particular of the upper extremities--Raynaud's phenomenon (RP) which has two forms: primary RP (Raynaud's disease) where no other basic disease is diagnoses during a two-year period. secondary RP (Raynaud's phenomenon) as an associated symptom of other, in particular systemic diseases. The etiology and pathology of Raynaud's phenomenon has not been elucidated satisfactorily so far. With regard to the variety and scope of detected functional and morphological abnormalities RP is rather multifactorial, caused by an unbalanced action of local and systemic factors affecting the sensitivity of the vascular wall to spastic stimuli. Treatment therefore remains symptomatic. It is restricted to administration of vasodilatating agents, in more severe cases sympathectomy is considered; it is important to rule out another basic disease. Vasoneuroses include also acrocyanosis, livedo reticularis and erythromelalgia. In the case of erythromelalgia it is important to rule out secondary causes (hypertension and polycythemia vera), otherwise it is not necessary to use pharmacological means to influence these diseases because of their relatively harmless course.
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PMID:[Vasoneuroses]. 1104 64

Sneddon's syndrome is a rare disease with strong gender prevalence of females. This syndrome is characterized by livedo racemosa and cerebrovascular lesions. Since no specific test is available, the clinical differentiation from other disorders with similar symptomatology may raise difficulties. The cerebral involvement includes strokes with cases of more than one ischaemic event having been reported. Associations with convulsions, heart valve disease, systemic hypertension, and renal impairment have been described. We report the case of a 5-year-old boy who was anaesthesized for dental surgery. Due to the fact that 50% of Sneddon's syndrome patients develop mental retardation, even minor procedures require general anaesthesia. A review of the literature is added and specific anaesthesiological aspects of the perioperative care of Sneddon's syndrome are discussed.
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PMID:Anaesthesiological considerations in patients with Sneddon's syndrome. 1111 4

We report a case of Sneddon's syndrome with the triad of livedo reticularis, hypertension, and neurologic symptoms. The procedures for diagnosis and the tests to delineate clotting abnormalities are examined.
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PMID:Sneddon's syndrome: a case report. 1127 Feb 93

Polyarteritis nodosa (PAN) is a necrotizing arteritis of small and medium-sized vessels. It may present with hypertension and/or renal insufficiency. Peripheral neuropathy, myopathy, joint pains, testicular pain, and ischemic myalgias may also be seen. Gastrointestinal involvement may lead to gangrene of the bowel, peritonitis, perforation, intra-abdominal hemorrhage, and pancreatitis. The cutaneous manifestations include tender subcutaneous nodules grouped along the course of superficial arteries of the lower extremities, with or without an overlying livedo reticularis. Although multisystem involvement is characteristic, sometimes only one organ or system may be involved. Associations with viral hepatitis (both B and C) and streptococcal infection have been established for PAN. Recurrent strep infections of the upper respiratory tract, streptococcal glomerulonephritis and rheumatic fever have previously been linked to PAN. This report extends the spectrum of associated streptococcal infections to include necrotizing fasciitis.
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PMID:Cutaneous polyarteritis nodosa after streptococcal necrotizing fasciitis. 1151 22

Cholesterol emboli are being increasingly recognized as an important cause of renal dysfunction in an aging US population. Irregularly shaped atheroemboli typically cause partial obstruction of small renal vessels resulting in ischemia. A vasculitis-like picture often evolves with an inflammatory reaction and giant cell formation. Cholesterol emboli may be temporally related to vascular manipulation, anticoagulant, or thrombolytic drug use. Spontaneous cases have been reported. Patients with cholesterol emboli may present with a spectrum of acute renal failure varying from mild and asymptomatic to life-threatening disease. The differential diagnosis includes radiocontrast nephropathy, endocarditis with left-sided emboli, vasculitis, and thrombotic emboli. The physical examination findings suggestive of cholesterol emboli include extrarenal emboli and livedo reticularis. The urinalysis is typically unremarkable. Some patients have hematuria and/or non-nephrotic proteinuria. Serology and hematology results may suggest an inflammatory-like picture with elevated erythrocyte sedimentation rate, hypocomplementemia, eosinophilia, and eosinophiluria. In the setting of a clear precipitating factor and suggestive physical findings, cholesterol emboli can be established purely on clinical grounds. Demonstration of cholesterol crystals by biopsy of the kidney, skin (if lesion present), or muscle is diagnostic in unexplained cases. The kidney is the organ most frequently involved in this order. Therapy is supportive with particular emphasis on management of hypertension and hypercholesterolemia.
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PMID:Atheroembolic Renal Disease. 1186 88

Systemic lupus erythematosus (SLE) is an inflammatory multisystem disease of unknown etiology with immunologic aberrations. Many studies have shown that genetic and environmental factors are implicated in the development of SLE. Angiotensin-converting enzyme (ACE) affects various immune phenomena through the renin-angiotensin and kallikrein-kininogen systems by creating angiotensin II and inactivating bradykinin. We investigated the correlation between insertion/ deletion polymorphism of the ACE gene and the clinical manifestations of SLE, especially vascular involvement and lupus nephritis. Two-hundred and eleven Korean patients fulfilling the ACR criteria and 114 healthy subjects were enrolled. The ACE genotype was determined by polymerase chain reaction using genomic DNA from peripheral blood. The nephritis patients were classified by the WHO classification. In addition, the activity and chronicity index were used to assess the severity of renal involvement. We evaluated vascular involvement by the presence or absence of hypertension, Raynaud's phenomenon, livedo reticularis, antineutrophil cytoplasmic antibody and the SLICC/ACR Damage Index. The gene frequency of ACE gene polymorphism was as follows: II 39 vs 34%, ID 41 vs 50%, DD 20 vs 16% in SLE patients and controls, respectively. There was no difference in genotype frequency between both groups. There were no significant differences between the distribution of ACE gene genotypes and lupus nephritis and its related parameters, including WHO classification, activity index, chronicity index, renal dysfunction and amount of 24 h urinary protein. The ACE genotypes and alleles did not affect the presence of vascular manifestations evaluated, but the frequency of DD genotype was significantly low in SLE patients with Raynaud's phenomenon compared to those without Raynaud's phenomenon (P = 0.002 for ACE ID vs DD and II, OR 2.7, 95% CI 1.43-5.09; P=0.023 for ACE DD vs ID and II, OR 0.33, 95% CI 0.12-0.89). Also skewing from DD to II genotype was noted in patients with anti-Sm antibody compared to those without anti-Sm antibody (P = 0.025 for ACE DD vs ID and II, OR 0.21, 95% CI 0.05-0.93). The onset age of serositis was older in patients with the ID genotype than the others (ID= 34.5+/-10.8, II + DD = 25.6+/-10.2, P= 0.002). Also the onset age of malar rash was older in patients with II genotype than the others (II=26.7+/-8.4, ID+DD=21.3+/-9.0; P=0.021). The patients with I allele showed a significantly higher frequency of serositis (P = 0.022). Taken together, the I/D polymorphisms of ACE gene did not affect susceptibility of SLE, lupus nephritis and the vascular manifestations, including Raynaud's phenomenon, in Korean SLE patients, although the DD genotype was negatively associated with Raynaud's phenomenon among SLE patients. However, it would be valuable to evaluate the role of other genes potentially related to vascular events, such as endothelin, nitric oxide or angiotensin II receptor as well as ACE gene.
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PMID:Angiotensin-converting enzyme gene polymorphism and vascular manifestations in Korean patients with SLE. 1263 Jul 62


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