in multiple sclerosis
Livedo reticularis associated with rasagiline
Methylphenidate and dextroamphetamine-induced peripheral vasculopathy
Gefitinib
Obstruction of capillaries:
Cryoglobulinaemia – proteins in the blood that clump together in cold conditions
Antiphospholipid syndrome due to small blood clots
Hypercalcaemia (raised blood calcium levels which may be deposited in the capillaries)
Haematological disorders of polycythaemia rubra vera or thrombocytosis (excessive red cells or platelets)
Infections (infective endocarditis, syphilis, tuberculosis, Lyme disease)
Associated with acute kidney injury due to cholesterol emboli status after cardiac catheterization
Arteriosclerosis (cholesterol emboli) and homocystinuria (due to Chromosome 21 autosomal recessive Cystathionine beta synthase deficiency)
Intra-arterial injection (especially in drug addicts)
Ehlers-Danlos syndrome – connective tissue disorder, often with many secondary conditions, may be present in all types
Pheochromocytoma
Livedoid vasculopathy and its association with factor V Leiden mutation
FILS syndrome (polymerase ε1 mutation in a human syndrome with facial dysmorphism, immunodeficiency, livedo, and short stature)
Primary hyperoxaluria, oxalosis (oxalate vasculopathy)
Cytomegalovirus infection (very rare clinical form, presenting with persistent fever and livedo reticularis on the extremities and cutaneous necrotizing vasculitis of the toes)
Generalized livedo reticularis induced by silicone implants for soft tissue augmentation
As a rare skin finding in children with Down syndrome
Idiopathic livedo reticularis with polyclonal IgM hypergammopathy
CO2 angiography (rare, reported case)
A less common skin lesion of Churg–Strauss syndrome
Erythema nodosum-like cutaneous lesions of sarcoidosis showing livedoid changes in a patient with sarcoidosis and Sjögrens syndrome
Livedo vasculopathy associated with IgM antiphosphatidylserine-prothrombin complex antibody
Livedo vasculopathy associated with plasminogen activator inhibitor-1 promoter homozygosity and prothrombin G20210A heterozygosity
As a first sign of metastatic breast carcinoma (very rare)
Livedo reticularis associated with renal cell carcinoma (rare)
Buergers disease (as an initial symptom)
As a rare manifestation of Graves hyperthyroidism
Associated with pernicious anaemia
Moyamoya disease (a rare, chronic cerebrovascular occlusive disease of unknown cause, 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)
Associated with the use of a midline catheter
Familial primary cryofibrinogenemia.
Greig cephalopolysyndactyly syndrome is a disorder that affects development of the limbs, head, and face. The features of this syndrome are highly variable, ranging from very mild to severe. People with this condition typically have one or more extra fingers or toes (polydactyly) or an abnormally wide thumb or big toe (hallux). Presentation
The skin between the fingers and toes may be fused (cutaneous syndactyly). This disorder is also characterized by widely spaced eyes (ocular hypertelorism), an abnormally large head size (macrocephaly), and a high, prominent forehead. Rarely, affected individuals may have more serious medical problems including seizures and developmental delay. Pathophysiology
Greig cephalopolysyndactyly syndrome is a chromosomal condition related to chromosome 7. Mutations in the GLI3 gene cause Greig cephalopolysyndactyly syndrome. The GLI3 gene provides instructions for making a protein that controls gene expression, which is a process that regulates whether genes are turned on or off in particular cells. By interacting with certain genes at specific times during development, the GLI3 protein plays a role in the normal shaping (patterning) of many organs and tissues before birth.Different genetic changes involving the Gli3 gene can cause Greig cephalopolysyndactyly syndrome. In some cases, the condition results from a chromosomal abnormality, such as a large deletion or translocation of genetic material, in the region of chromosome 7 that contains the GLI3 gene. In other cases, a mutation in the GLI3 gene itself is responsible for the disorder. Each of these genetic changes prevents one copy of the gene in each cell from producing any functional protein.