Livedo reticularis: a side effect of interferon therapy in a pediatric patient with melanoma

Livedo reticularis is a lacy mottling of the skin that can have many etiologies. We report a case of an 8-year-old boy with a diagnosis of melanoma who developed persistent livedo reticularis during treatment with interferon alpha-2B. To our knowledge, this is the first case report of livedo reticularis occurring as a side effect of interferon treatment for pediatric melanoma. Given the increasing incidence of pediatric melanoma, it is important that dermatologists be aware of potential side effects of interferon therapy to optimize care and education for these patients.     

Livedo reticularis associated with increased titers of anticardiolipin antibodies in systemic lupus erythematosus

Seventy-eight consecutive patients with systemic lupus erythematosus were assessed for the presence of livedo reticularis. The possible association of livedo reticularis with other clinical and laboratory features including anticardiolipin antibodies was explored. Thirty-eight patients had livedo reticularis. Four cases were severe, 11 moderate, and 23 mild. There was a statistically significant association between the combined moderate and severe livedo reticularis group and elevated levels of anticardiolipin antibodies. The recognized association of anticardiolipin antibodies with thrombotic events suggests a possible pathogenetic role. The presence or history of central nervous system disease, renal disease, vasculitis, or lupus inhibitor was significantly associated with the moderate and severe livedo reticularis group. Livedo reticularis may be a cutaneous marker for the later development of important systemic events in systemic lupus erythematosus.     

Livedo reticularis in a patient with systemic lupus erythematosus and anticardiolipin antibodies

This report describes a case of livedo reticularis associated with increased titres of anticardiolipin antibodies (aCL) in a patient with systemic lupus erythematosus. A 38-year-old woman presented with fever, malaise, arthritis and livedo reticularis in a severe form. Antibodies to native DNA and an increased level of aCL were found. A significant positive correlation exists between livedo reticularis and elevated serum antiphospholipid activity in patients with systemic lupus erythematosus. aCL are shown to play a possible pathogenetic role in thrombotic events. This suggests that thrombosis is the underlying cause of livedo in these patients. A biopsy performed in a patient at the site where livedo was most marked showed no evidence of thrombi. It is postulated that the mechanism of livedo in lupus patients with aCL consists of both thrombosis and dysfunction in the regulation of the tone of the peripheral vascular bed.     

HEPARIN-ASSOCIATED THROMBOCYTOPENIA AND THROMBOSIS (HATT) PRESENTING WITH LIVEDO RETICULARIS

Background. Heparin-associated thrombocytopenia and thrombosis (HATT) is an infrequently encountered syndrome characterized by ischemic necrosis of soft tissue and vital organs following anticoagulation with heparin. The syndrome is thought to be due to heparin-dependent platelet aggregation and thrombosis, which is mediated by pathologic immunoglobulins. Case Report. A 60-year-old man developed truncal livedo reticularis and ischemic necrosis of the left foot associated with thrombocytopenia, disseminated intravascular coagulopathy (Die), and microangiopathic hemolytic anemia during intravenous heparin therapy. Skin biopsy from an area of livedo reticularis revealed fibrin thrombi in dermal blood vessels, which is characteristic of HATT. The diagnosis of HATT prompted discontinuation of heparin and a resulting rapid resolution of the livedo reticularis and hematologic abnormalities. No other potential causes of Die were identified, and, other than stopping heparin, no specific therapy was employed. Conclusions. Periodic monitoring of platelets should be performed on all patients receiving treatment with heparin, as early detection of heparin-induced thrombocytopenia followed by discontinuation of the drug may prevent life threatening thrombotic complications. HATT should be included in the differential diagnosis of patients with livedo reticularis that occurs during heparin therapy.     

Livedo reticularis

A middle-aged woman was admitted to the hospital with livedo reticularis of the extremities in addition to nonspecific symptoms and signs of hypothyroidism. The livedo reticularis disappeared with treatment of the hypothyroidism. Although livedo reticularis has been reported previously to be associated with thyroid disease, this association is rare. We review the literature and present the conditions associated with livedo reticularis.     

Vasculitis racemosa hemoplegica]

The secondary symptomatic forms of livedo reticularis can follow cerebrovascular incidents with consecutive hemiplegia; this is rarely known. A further patient is described who developed an asymmetrical livedo reticularis on the hemiplegic half of the body. The reason of the hemiplegia was an intracerebral hemorrhage.     

Criteria for the diagnosis of antiphospholipid syndrome in patients presenting with dermatologic symptoms

The antiphospholipid syndrome (APS) is an autoimmune disorder characterized by the occurrence of arterial and/or venous thromboembolic events and obstetric complications in the setting of circulating antiphospholipid antibodies. Dermatologic manifestations are commonly seen in APS with almost half of the patients exhibiting varied conditions such as ulceration, splinter hemorrhages, and livedo reticularis. In this paper, we report the case of a 12-year-old boy who was diagnosed with APS after presenting with livedo reticularis and positive antiphospholipid antibodies. We discuss the difficulty of diagnosing APS in patients presenting solely with dermatologic complaints, as these skin manifestations are not specific enough for APS to be included in the Sapporo diagnostic criteria. Proposed revisions to the Sapporo criteria to increase its specificity and sensitivity are also addressed.     

Persistent cutaneous manifestations of hyperoxaluria after combined hepatorenal transplantation

A 30-year-old woman with primary hyperoxaluria type I (PHI) developed livedo reticularis with overlying ulcerations on her legs 16 months after receiving a liver-kidney transplant. A skin biopsy of the lesion showed deposits of calcium oxalate. To our knowledge, there have been no reported cases of livedo reticularis in patients with PH1 after a combined liver-kidney transplant.     

Primary oxalosis—an unusual cause of livedo reticularis

A young woman presented with renal failure and skin lesions of livedo reticularis (LR) due to primary oxalosis. Primary oxalosis is a rare autosomal-recessive error of metabolism characterized by accumulation of calcium-oxalate crystals in the kidneys, eyes, heart and skin. This unusual cause of intravascular obstruction resulting in livedo reticularis should be considered in patients with renal impairment. An approach to the diagnosis of LR is presented.     

网状青斑伴木村病1例并文献复习

患者男,56岁,双耳垂肿胀伴痒10余年.患者既往有网状青斑50余年.皮损组织病理示:真皮内淋巴细胞增生,见多量淋巴滤泡样结构,伴间质血管增生及大量嗜酸性粒细胞浸润.外周血示嗜酸性粒细胞增多,血清IgE水平明显升高.诊断:网状青斑伴木村病.     

Livedo reticularis, cerebrovascular disorders and mitral disease: a new cause of Sneddon's syndrome?

Sneddon's syndrome consists of livedo reticularis and cerebral vascular accidents with no evidence of systemic disease responsible for the livedo. The syndrome has been assimilated to a subgroup of systemic lupus erythematosus (SLE) with presence of antibodies directed against phospholipids. Recently, a significant increase in the frequency of cardiac valve diseases has been demonstrated in some SLE patients with livedo reticularis, cerebral vascular accidents and antiphospholipid antibodies. We report the case of a 26-year old woman who had been presenting for 6 years with idiopathic livedo reticularis. Her history was remarkable for the occurrence of 2 cerebral ischaemic accidents at the ages of 23 and 26 years, generalized convulsive seizures at 22 years, and hypertension of pregnancy with 2 miscarriages. Biopsy of the livedo showed normal histological patterns, but electron microscopy detected an obliterating endothelial proliferation and endothelial cells with numerous Weibel-Palade bodies. Laboratory signs of SLE, as well as antiphospholipid antibodies were absent. At the age of 26 years, cardiac abnormalities were heard at auscultation for the first time, and echocardiography showed that they were due to a fairly loose mitral stenosis. According to Burton's criteria our patient had all the typical features of Sneddon's syndrome. The finding of mitral stenosis--an emboligenic cardiopathy that is potentially responsible for cerebral vascular accidents--raises the problem of its relationship with Sneddon's syndrome. The association does not seem to be fortuitous, since our case is very similar to the cases of SLE or antiphospholipid antibody syndrome associated with cardiac valve lesions. However, this case is particular in that 6 years after the onset of the disease there was still no sign of SLE and of antiphospholipid antibodies.(ABSTRACT TRUNCATED AT 250 WORDS)     

Livedo reticularis and cerebrovascular accidents

The authors report the case of three middle-aged women admitted to the hospital because of cerebro-vascular accidents, in whom examination disclosed idiopathic livedo reticularis. This association has only been described recently, but does not seem fortuitous; some of the clinical manifestations are characteristic, but the histology is usually nonspecific and the basic abnormality remains unknown. The main problem is prognostic and therapeutic. In an attempt to prevent the neurological defects, tobacco and contraception should not be permitted to female patients showing widespread acquired livedo reticularis; high blood-pressure should be treated systematically.     

Livedo reticularis and neurological lesions

Two patients with extensive livedo reticularis have developed multiple severe neurological lesions over a 6-year period. The possible pathogenesis is discussed. The presence of livedo reticularis has been described in conjunction with many diseases (Rook, Wilkinson & Ebling, 1979). A rare association between this condition and neurological syndromes has also been reported (Sneddon, 1965; Quimby & Perry, 1980). We report two cases which add further support to this association.     

青斑样血管病64例皮损特点分析

【摘要】 目的 分析青斑样血管病网状青斑和紫癜性皮损的特点、分布规律。方法 回顾中国医学科学院皮肤病医院2017年7月至2020年10月诊治的64例青斑样血管病患者的临床资料。结果 64例中男23例,女41例;年龄13 ~ 54岁,发病年龄7 ~ 51岁,48例25岁前发病;病程6个月至10年。49例夏季发病或病情加重,皮损基本表现为坏死性不规则紫癜、紫癜性皮病样红斑、不规则溃疡、网状青斑、毛细血管扩张、不规则的白色萎缩性瘢痕和色素沉着。64例溃疡和坏死性紫癜多为不规则形,发生于足背和踝关节周围。40例有紫癜性皮病样的皮损表现,其中32例表现为色素性紫癜,8例表现为毛细血管扩张性紫癜。4例出现麻木刺痛等神经末梢受损的症状。结论 青斑样血管病的皮损表现多样,对于出现广泛网状青斑、紫癜样皮病样皮损、麻木等症状的患者,需做好鉴别诊断。     

Livedo reticularis associated with hereditary protein C deficiency and recurrent thromboembolism

We report the occurrence of livedo reticularis in a patient with symptomatic hereditary type 1 protein C deficiency. Antithrombin III deficiency and the antiphospholipid syndrome may also be associated with livedo reticularis, and we suggest that a thrombophilia screen may be a useful investigation in a patient with otherwise unexplained livedo, particularly if there is a personal or family history of thromboembolism.     

Livedo reticularis with ulceration: response to azathioprine therapy

Livedo reticularis is common as a symptomatic expression of underlying disease, or as an entity without discoverable cause. With livedo reticularis, leg ulceration of painful and intractible type can occur. A patient is described, in whom such ulcers improved rapidly and almost completely, with Azathioprine and Prednisolone therapy.     

Livido racemosa in detection of anti-phospholipid antibodies

Livedo reticularis and antiphospholipid antibodies have previously been found to be associated with a subgroup of patients with systemic lupus erythematosus. We present a case of livedo reticularis accompanied by antiphospholipid antibodies, in which no other signs of any systemic or cutaneous disease could be detected.     

Amantadine-induced livedo reticularis - Case report

Livedo reticularis is a spastic-anatomical condition of the small vessels which translates morphologically by a reticular pattern, interspersing cyanosis, pallor and erythema. The same can be congenital or acquired. Among the acquired, we highlight the physiological livedo reticularis and the idiopathic livedo by vasospasm; the latter configures the most common cause. The drug-induced type is less common. The drugs amantadine and norepinephrine are often implicated. Cyanosis is usually reversible if the causative factor is removed, however, with chronicity, the vessels may become permanently dilated and telangiectatic. We report a case of a patient diagnosed with Parkinson’s disease with chronic livedo reticularis associated with the use of amantadine and improvement after discontinuation of the drug.     

Livedo reticularis and massive thoracoabdominal aneurysm

Cholesterol crystal embolization arising from an atheromatous aortic aneurysm is a potentially treatable condition. We report a 55-year old man with a sudden onset of painful livedo reticularis of the buttocks and lower limbs secondary to a massive thoracoabdominal aortic aneurysm, discovered incidentally when the patient underwent a liver ultrasound test. The diagnosis of cholesterol crystal embolization of the skin requires a high degree of clinical suspicion. Abdominal ultrasound should be considered in the routine assessment of lower limb livedo reticularis.     

Livedo reticularis in a child with moyamoya disease

Moyamoya disease is a rare, chronic cerebrovascular occlusive disease of unknown etiology. It is characterized by progressive stenosis of the arteries of the circle of Willis leading to an abnormal capillary network and resultant ischemic strokes or cerebral hemorrhages. The association of moyamoya disease with livedo reticularis has been described in a previously reported patient with a factor V Leiden mutation, leading to hypercoagulation. We describe a girl with livedo reticularis and moyamoya disease with extensive cardiovascular malformations, but without a primary coagulopathy.