Livedo Reticularis
Skin Diseases, Vascular
Sneddon Syndrome
Zona Reticularis
Embolism, Cholesterol
Antibodies, Antiphospholipid
Antibodies, Anticardiolipin
Antiphospholipid Syndrome
Reticular Formation
Adrenarche
Zona Fasciculata
Adrenal Cortex
Buerger's disease manifesting nodular erythema with livedo reticularis. (1/17)
We report a patient with Buerger's disease (BD) who showed painful nodular erythema with livedo reticularis as an initial symptom. The patient developed this cutaneous manifestation in both lower extremities, and a skin biopsy demonstrated perivascular infiltration of mononuclear cells in the border zone between the dermis and subcutaneous tissue. Both nodular erythema and livedo reticularis were successfully treated with oral prednisolone, but both feet developed necrosis with ulcerations and had to be amputated 1.5 years later because of acute gangrene. Histopathology of the amputated tissue showed acute inflammation and multiple thrombi with recanalization in the posterior tibial arteries, leading to a diagnosis of BD. This disease should be considered as a possible diagnosis in refractory patients with nodular erythema and livedo reticularis, particularly when ulcerations and necrosis rapidly worsen. (+info)Microembolization from an abdominal aortic aneurysm after thoracic aortic replacement. (2/17)
A 66-year-old man with thoracic and abdominal aortic aneurysm suffered from microembolism in the lower extremities after total arch replacement. He presented with livedo reticularis with palpable peripheral pulses, and the serum creatinine kinase level elevated up to 7,695. The abdominal aortic aneurysm, but not the thoracic aorta, was the origin of this complication. The morphological change of thrombus in the abdominal aorta detected by ultrasonography was the key to the diagnosis. Graft replacement of the abdominal aorta finally resolved his problem. (+info)Homocystinuria due to cystathionine beta synthase deficiency. (3/17)
A two year-old male child presented with cutis marmorata congenita universalis, brittle hair, mild mental retardation, and finger spasms. Biochemical findings include increased levels of homocysteine in the blood-106.62 micromol/L (normal levels: 5.90-16 micromol/L). Biochemical tests such as the silver nitroprusside and nitroprusside tests were positive suggesting homocystinuria. The patient was treated with oral pyridoxine therapy for three months. The child responded well to this therapy and the muscle spasms as well as skin manifestations such as cutis marmorata subsided. The treatment is being continued; the case is reported here because of its rarity. Homocysteinuria arising due to cystathionine beta-synthase (CBS) deficiency is an autosomal recessive disorder of methionine metabolism that produces increased levels of urinary homocysteine and methionine It manifests itself in vascular, central nervous system, cutaneous, and connective tissue disturbances and phenotypically resembles Marfan's syndrome. Skin manifestations include malar flush, thin hair, and cutis reticulata / marmorata. (+info)Differences in anti-phosphatidylserine-prothrombin complex antibodies and cutaneous vasculitis between regular livedo reticularis and livedo racemosa. (4/17)
(+info)Livedo racemosa, secondary to drug-induced systemic lupus erythematosus. (5/17)
We present a 40-year-old man with erythematous-to-violaceous, broken, reticulated patches on the upper chest, back, and extremities, which is consistent with livedo racemosa. The cutaneous findings appeared after an increase in dilantin dose and subsequently improved after a reduction in dilantin dose. Furthermore, antinuclear antibodies and antihistone antibodies were detected. We therefore believe that the livedo racemosa is a cutaneous manifestation of a drug-induced systemic lupus erythematosus. We review the distinctive features of livedo racemosa as well as its associations with several disorders. Although there are no effective treatments for livedo racemosa, patients often are placed on low-dose aspirin and counseled to avoid smoking in an effort to protect against their increased risk of stroke and arterial thrombosis. (+info)A patient with idiopathic cholesterol crystal embolization: effectiveness of early detection and treatment. (6/17)
A 72-year-old man was admitted to our hospital because of progressive renal dysfunction persisting for 1.5 months. Physical examination showed livedo reticularis of the toes of both feet, peripheral edema, and gait disturbance due to the toe pain. The levels of blood urea nitrogen (50.0 mg/dL) and creatinine (2.81 mg/dL) were elevated, and eosinophilia (10%, 870/microL) was noted. A biopsy of the area of livedo reticularis revealed cholesterin crystals. The patient had not undergone angiography, anticoagulation therapy, or antithrombotic treatment. Idiopathic cholesterol crystal embolization was diagnosed. Transesophageal echocardiography revealed intimal thickening of the aorta and plaque. Oral steroid therapy was started because of the progressive renal dysfunction. After steroid therapy, the symptoms improved. Early diagnosis and treatment are important. Renal dysfunction is a common symptom in elderly patients. Cholesterol crystal embolization should also be considered as a cause of unexplained renal dysfunction, especially in such patients. (+info)Livedoid vasculopathy: an intringuing cutaneous disease. (7/17)
(+info)Livedo reticularis associated with autoimmune hemolytic anemia: prolonged remission induced by peripheral blood stem cell transplantation relapse after 10 years and restoration of hemoglobin levels by rituximab. (8/17)
(+info)Livedo reticularis is a cutaneous manifestation characterized by a bluish-purple, netlike pattern of discoloration on the skin. It is caused by the abnormal dilation and constriction of blood vessels near the skin's surface, leading to impaired circulation in the affected areas.
The condition can be idiopathic (primary) or secondary to various underlying disorders such as autoimmune diseases, vasculitis, hematologic disorders, infections, or medications that affect the blood vessels. In some cases, livedo reticularis may be a sign of an underlying medical condition requiring further evaluation and treatment.
It is essential to differentiate livedo reticularis from other related conditions like livedo racemosa, which presents with more irregular and diffuse patterns, and is typically associated with vasculitis or severe systemic disorders. Additionally, livedo reticularis should not be confused with cutis marmorata, a physiological response to cold temperatures that resolves upon warming the affected area.
Vascular skin diseases are a group of medical conditions that affect the blood vessels in the skin. These disorders can be caused by problems with the structure or function of the blood vessels, which can lead to various symptoms such as redness, discoloration, pain, itching, and ulcerations. Some examples of vascular skin diseases include:
1. Rosacea: a chronic skin condition that causes redness, flushing, and visible blood vessels in the face.
2. Eczema: a group of inflammatory skin conditions that can cause redness, itching, and dryness. Some types of eczema, such as varicose eczema, are associated with problems with the veins.
3. Psoriasis: an autoimmune condition that causes red, scaly patches on the skin. Some people with psoriasis may also develop psoriatic arthritis, which can affect the blood vessels in the skin and joints.
4. Vasculitis: a group of conditions that cause inflammation of the blood vessels. This can lead to symptoms such as redness, pain, and ulcerations.
5. Livedo reticularis: a condition that causes a net-like pattern of discoloration on the skin, usually on the legs. It is caused by abnormalities in the small blood vessels.
6. Henoch-Schönlein purpura: a rare condition that causes inflammation of the small blood vessels, leading to purple spots on the skin and joint pain.
7. Raynaud's phenomenon: a condition that affects the blood vessels in the fingers and toes, causing them to become narrow and restrict blood flow in response to cold temperatures or stress.
Treatment for vascular skin diseases depends on the specific condition and its severity. It may include medications, lifestyle changes, and in some cases, surgery.
Sneddon syndrome is a rare medical condition characterized by the concurrence of livedo reticularis (a purplish, net-like discoloration of the skin) and recurrent strokes or transient ischemic attacks (TIAs). It primarily affects young to middle-aged women. The exact cause of Sneddon syndrome remains unknown, but it's thought to be an autoimmune disorder with potential involvement of the coagulation system.
The main diagnostic criteria for Sneddon syndrome are:
1. Livedo reticularis (fixed, persistent form)
2. One or more cerebrovascular events (strokes or TIAs)
Additional features may include cognitive impairment, migraine-like headaches, seizures, and other neurological symptoms. Diagnosis is often challenging due to its rarity and the need to exclude other conditions that can present with similar symptoms. Treatment typically involves anticoagulation therapy, antiplatelet agents, or immunosuppressive medications to manage symptoms and prevent further cerebrovascular events.
The zona reticularis is a layer of the adrenal cortex, which is the outer part of the adrenal gland. These glands are located on top of the kidneys and are responsible for producing several important hormones. The adrenal cortex itself has three distinct layers: the zona glomerulosa, the zona fasciculata, and the zona reticularis.
The zona reticularis is the innermost layer of the adrenal cortex. It is responsible for producing and releasing certain steroid hormones, particularly androgens such as dehydroepiandrosterone (DHEA) and its sulfate (DHEAS). These androgens are precursor hormones that can be converted into more potent androgens or estrogens in other parts of the body. The zona reticularis plays a crucial role in sexual development and function, as well as maintaining overall health and well-being.
Disorders related to the zona reticularis may result in abnormal hormone production, leading to conditions such as congenital adrenal hyperplasia, Cushing's syndrome, or Addison's disease. Proper diagnosis and treatment of these disorders typically involve endocrinologists, healthcare professionals specializing in hormonal and metabolic disorders.
Cholesterol embolism is a medical condition that occurs when cholesteral crystals or plaque debris from an atherosclerotic lesion in the aorta or its major branches dislodge and travel to smaller vessels, where they obstruct blood flow. This can lead to tissue damage or infarction in various organs, depending on the location of the embolism.
Cholesterol emboli are typically small, crystalline, and composed of cholesterol, calcium, and other debris from atherosclerotic plaques. They can cause inflammation and damage to the endothelial cells lining the blood vessels, leading to further narrowing or occlusion of the vessel lumen.
Symptoms of cholesterol embolism depend on the location and extent of the obstruction. Common sites for embolization include the kidneys, brain, eyes, skin, and extremities. Symptoms can range from mild to severe and may include sudden pain, weakness, or numbness in the affected area; skin discoloration or ulcerations; vision changes; kidney dysfunction; and stroke-like symptoms.
Cholesterol embolism is often a complication of invasive procedures such as angiography, coronary artery bypass grafting, or aortic surgery. It can also occur spontaneously in patients with advanced atherosclerosis or those who have recently undergone anticoagulation therapy.
Diagnosis of cholesterol embolism is often challenging due to its nonspecific symptoms and variable presentation. Imaging studies, such as angiography or CT scans, may be used to visualize the location and extent of the obstruction. Blood tests and biopsy of affected tissues can also provide diagnostic clues.
Treatment of cholesterol embolism is primarily supportive and aimed at managing symptoms and preventing further complications. Antiplatelet therapy, statins, and anti-inflammatory agents may be used to reduce the risk of recurrent embolization and improve outcomes. In severe cases, surgical intervention or endovascular procedures may be necessary to remove the obstruction or restore blood flow.
Antiphospholipid antibodies are a type of autoantibody that targets and binds to certain proteins found in the blood that attach to phospholipids (a type of fat molecule). These antibodies are associated with an increased risk of developing antiphospholipid syndrome, a disorder characterized by abnormal blood clotting.
There are several types of antiphospholipid antibodies, including:
1. Lupus anticoagulant: This type of antiphospholipid antibody can interfere with blood clotting tests and may increase the risk of thrombosis (blood clots) in both arteries and veins.
2. Anticardiolipin antibodies: These antibodies target a specific phospholipid called cardiolipin, which is found in the inner membrane of mitochondria. High levels of anticardiolipin antibodies are associated with an increased risk of thrombosis and pregnancy complications such as recurrent miscarriage.
3. Anti-β2 glycoprotein I antibodies: These antibodies target a protein called β2 glycoprotein I, which binds to negatively charged phospholipids on the surface of cells. High levels of anti-β2 glycoprotein I antibodies are associated with an increased risk of thrombosis and pregnancy complications.
The exact mechanism by which antiphospholipid antibodies cause blood clotting is not fully understood, but it is thought to involve the activation of platelets, the inhibition of natural anticoagulants, and the promotion of inflammation. Antiphospholipid syndrome can be treated with medications that thin the blood or prevent clots from forming, such as aspirin, warfarin, or heparin.
Anticardiolipin antibodies are a type of autoantibody that targets and binds to cardiolipin, a phospholipid component found in the inner mitochondrial membrane of cells. These antibodies are clinically significant because they have been associated with a variety of autoimmune disorders, including antiphospholipid syndrome (APS).
APS is a condition characterized by recurrent blood clots, pregnancy losses, and thrombocytopenia (low platelet count). Anticardiolipin antibodies are one of the three main types of autoantibodies found in APS, along with lupus anticoagulant and anti-β2 glycoprotein I antibodies.
The presence of high levels of anticardiolipin antibodies in the blood can lead to abnormal blood clotting, which can cause serious complications such as deep vein thrombosis, pulmonary embolism, and stroke. Anticardiolipin antibodies can also contribute to pregnancy losses by causing placental insufficiency or abnormal blood clotting in the placenta.
Anticardiolipin antibodies are typically detected through a blood test that measures their levels in the serum. A positive result is usually confirmed with a second test performed at least 12 weeks later to establish persistence. Treatment for anticardiolipin antibody-related disorders typically involves anticoagulation therapy to prevent blood clots and other complications.
Antiphospholipid syndrome (APS) is an autoimmune disorder characterized by the presence of antiphospholipid antibodies in the blood. These antibodies are directed against phospholipids, a type of fat molecule found in cell membranes and plasma lipoproteins. The presence of these antibodies can lead to abnormal blood clotting, which can cause serious complications such as stroke, heart attack, deep vein thrombosis, and pulmonary embolism.
APS can occur either on its own (primary APS) or in conjunction with other autoimmune disorders, such as systemic lupus erythematosus (secondary APS). The exact cause of APS is not fully understood, but it is believed to involve a combination of genetic and environmental factors.
Symptoms of APS can vary widely depending on the location and severity of the blood clots. They may include:
* Recurrent miscarriages or stillbirths
* Blood clots in the legs, lungs, or other parts of the body
* Skin ulcers or lesions
* Headaches, seizures, or stroke-like symptoms
* Kidney problems
* Heart valve abnormalities
Diagnosis of APS typically involves blood tests to detect the presence of antiphospholipid antibodies. Treatment may include medications to prevent blood clots, such as anticoagulants and antiplatelet agents, as well as management of any underlying autoimmune disorders.
The reticular formation is not a single structure but rather a complex network of interconnected neurons located in the brainstem, extending from the medulla oblongata through the pons and mesencephalon (midbrain) up to the diencephalon (thalamus and hypothalamus). It forms part of the reticular activating system, which is involved in regulating arousal, awareness, and sleep-wake cycles.
The reticular formation plays a crucial role in various functions such as:
1. Modulation of sensory input: The neurons in the reticular formation receive inputs from all senses (visual, auditory, tactile, etc.) and help filter and prioritize this information before it reaches higher cognitive areas.
2. Control of motor function: The reticular formation contributes to the regulation of muscle tone, posture, and locomotion by modulating the activity of motor neurons in the spinal cord.
3. Regulation of autonomic functions: The reticular formation is involved in controlling heart rate, blood pressure, respiration, and other visceral functions through its connections with the autonomic nervous system.
4. Consciousness and arousal: The ascending reticular activating system (ARAS) originates from the reticular formation and projects to the thalamus and cerebral cortex, where it helps maintain wakefulness and arousal. Damage to the ARAS can lead to coma or other states of altered consciousness.
5. Sleep-wake cycle regulation: The reticular formation contains cells that release neurotransmitters like histamine, serotonin, and orexin/hypocretin, which are essential for sleep-wake regulation. Dysfunction in these circuits has been implicated in various sleep disorders, such as narcolepsy and insomnia.
Adrenarche is a phase of development in which the adrenal glands begin to produce androgens, specifically DHEA (dehydroepiandrosterone) and its sulfate form DHEAS. This process usually begins between the ages of 6-8 in children, although it can vary. The androgens produced during adrenarche contribute to the development of secondary sexual characteristics such as pubic and underarm hair, but do not play a significant role in the growth spurt or reproductive function. It is important to note that adrenarche is separate from puberty, which is initiated by the hypothalamus and pituitary gland and involves the release of gonadotropins that stimulate the gonads to produce sex steroids.
The Zona Fasciculata is a region within the adrenal gland, which is a small gland located on top of the kidneys. It plays an essential role in endocrine function. The adrenal gland is divided into two main parts: the outer cortex and the inner medulla. The cortex itself is further divided into three zones: the Zona Glomerulosa, the Zona Fasciculata, and the Zona Reticularis.
The Zona Fasciculata is the middle layer of the adrenal cortex. It is primarily responsible for producing and releasing steroid hormones, particularly glucocorticoids such as cortisol. Cortisol helps regulate metabolism, immune response, and stress response, among other functions. The Zona Fasciculata contains large, column-shaped cells called fasciculated cells that contain lipid droplets filled with cholesterol esters. These cells convert cholesterol into pregnenolone, which is then converted into cortisol through a series of enzymatic reactions.
In summary, the Zona Fasciculata is a crucial region within the adrenal gland that produces and releases cortisol, a vital glucocorticoid hormone involved in various physiological processes.
The adrenal cortex is the outer portion of the adrenal gland, which is located on top of the kidneys. It plays a crucial role in producing hormones that are essential for various bodily functions. The adrenal cortex is divided into three zones:
1. Zona glomerulosa: This outermost zone produces mineralocorticoids, primarily aldosterone. Aldosterone helps regulate sodium and potassium balance and thus influences blood pressure by controlling the amount of fluid in the body.
2. Zona fasciculata: The middle layer is responsible for producing glucocorticoids, with cortisol being the most important one. Cortisol regulates metabolism, helps manage stress responses, and has anti-inflammatory properties. It also plays a role in blood sugar regulation and maintaining the body's response to injury and illness.
3. Zona reticularis: The innermost zone produces androgens, primarily dehydroepiandrosterone (DHEA) and its sulfate form (DHEAS). These androgens are weak compared to those produced by the gonads (ovaries or testes), but they can be converted into more potent androgens or estrogens in peripheral tissues.
Disorders related to the adrenal cortex can lead to hormonal imbalances, affecting various bodily functions. Examples include Addison's disease (insufficient adrenal cortical hormone production) and Cushing's syndrome (excessive glucocorticoid levels).
Livedo reticularis
Sneddon's syndrome
Amantadine
Erythema ab igne
Lupus
Polyarteritis nodosa
Livedoid vasculitis
Adenosine deaminase 2 deficiency
POEMS syndrome
Neuropathia mucinosa cutanea
Cholesterol embolism
Familial thoracic aortic aneurysm and aortic dissection
Cutaneous manifestations of COVID-19
Calciphylaxis
Cutis marmorata telangiectatica congenita
Livedo racemosa
Antiphospholipid syndrome
Ehlers-Danlos syndromes
Cold agglutinin disease
Systemic vasculitis
Thrombophilia
Cryoglobulinemia
Livedo
List of skin conditions
Vasculitis
Shock (circulatory)
Relapsing polychondritis
Cerebral vasculitis
Livedo reticularis - Wikipedia
Livedo Reticularis
Livedo reticularis: MedlinePlus Medical Encyclopedia
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Biomarkers Search
Sneddon syndrome - Getting a Diagnosis - Genetic and Rare Diseases Information Center
Cutis marmorata telangiectasia congenita with painful ulcerations - PubMed
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Atlas of dermatopathology: Collection of histological slides by prof. Werner Kempf
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Characterised by livedo reticularis and cerebrovascular1
- Sneddon's syndrome is an uncommon cause of stroke in young people, characterised by livedo reticularis and cerebrovascular disease. (bmj.com)
Rash4
- Livedoid dermatitis Livedo racemosa Perinatal gangrene of the buttock erythema ab igne (AKA livedo recticularis e calore) - a rash caused by prolonged heat exposure (e.g. hot water bottle or heat pad) List of cutaneous conditions Rapini, Ronald P. (wikipedia.org)
- Livedo reticularis is a rash that occurs when the blood supply is disrupted. (drtimpearce.com)
- WOMACK: When I got the vaccine, within a few minutes, I got something called Livedo Reticularis, which is basically like a rash - a red rash on my arms, intense facial flushing like a tomato, very, very bad headache. (ketr.org)
- They found that two-thirds of the children experienced additional symptoms not formally associated with antiphospholipid syndrome in adults , including low platelet counts, hemolytic anemia and livedo reticularis, a rash indicating abnormal blood flow to the skin. (michiganmedicine.org)
Idiopathic2
- No further test or examination confirms idiopathic livedo reticularis. (wikipedia.org)
- Other than identifying and treating any underlying conditions in secondary livedo, idiopathic livedo reticularis may improve with warming the area. (wikipedia.org)
Nodules1
- The skin is affected in over one-third of patients resulting in livedo reticularis , gangrene , cyanosis (' blue toe syndrome ' secondary to lack of oxygenated blood supply), ulceration , painful red nodules , and purpura (purple patches). (dermnetnz.org)
Racemosa1
- Secondary LR is also known as livedo racemosa. (medlineplus.gov)
Purplish4
- Livedo reticularis is a common skin finding consisting of a mottled reticulated vascular pattern that appears as a lace-like purplish discoloration of the skin. (wikipedia.org)
- Livedo reticularis is a purplish-colored lace pattern under the skin. (rawarrior.com)
- Livedo reticularis: a lacey, purplish discoloration of the skin on the legs with some leg swelling. (parkinson.org)
- Livedo reticularis - a purplish pattern on the skin of the hands and feet over the vascular reticular system. (bvfootclinic.com)
Discoloration1
- It was the discoloration and the livedo reticularis pattern albeit a fleeting example, which confirmed their suspicions. (drtimpearce.com)
Erythema1
- 5. Erythema ab igne mimicking livedo reticularis. (nih.gov)
Lesions1
- Sneddon's syndrome is characterized by livedo reticularis and cerebrovascular lesions. (cumhuriyet.edu.tr)
20211
- 2021). Livedo reticularis. (mhmedical.com)
Systemic1
- 10. Dexrazoxane for rapid extended livedo reticularis-like skin reaction due to systemic epirubicin diffusion during transcatheter arterial chemoembolization procedure for hepatocellular carcinoma. (nih.gov)
Pulses2
Peripheral1
- Peripheral edema, livedo reticularis, ataxia. (psychdb.com)
Vasculitis2
- Classic presentation includes livedo reticularis, vasculitis, and stroke. (nih.gov)
- And I immediately found pictures of livedo reticularis caused by vasculitis related to Rheumatoid disease (or Lupus). (rawarrior.com)
Eosinophilia1
- Livedo reticularis , kidney impairment, and eosinophilia (high numbers of circulating eosinophils in the blood). (dermnetnz.org)
Cardiac1
- Although not included in the diagnostic criteria, other clinical symptoms, such as livedo reticularis, nephropathy, thrombocytopenia, cardiac valvular disease, and neurological symptoms are commonly associated comorbidities. (medscape.com)
Ulcers1
- aCL assay is also indicated in cutaneous circulation disturbances without clear explanations, such as blue toe syndrome, ulcers resembling pyoderma gangrenosum, and livedo reticularis. (medscape.com)
Secondary1
- Physiologic livedo reticularis improves or disappears with warming, whereas secondary causes usually do not. (mhmedical.com)
Skin1
- Livedo reticularis (LR) is a skin symptom. (medlineplus.gov)
Piel1
- Afección caracterizada por la presencia de un patrón reticular en la piel de las extremidades inferiores y otras partes del cuerpo. (bvsalud.org)
Fever1
- Minocycline induced arthritis associated with fever, livedo reticularis, and pANCA. (globale-dermatologie.com)
Clinical1
- Livedo reticularis is diagnosed by its clinical appearance and history. (wikipedia.org)
Pattern2
- The causes and treatments for livedo reticularis are not fully understood, however it is believed that when some small blood vessels are blocked or no longer feed surface tissues, other vessels enlarge to compensate, creating the netted pattern. (rawarrior.com)
- Livedo Reticularis or "What is the Weird Blue Pattern on my Feet? (bvfootclinic.com)
Disease1
- Does livedo reticularis have anything to do with Rheumatoid disease? (rawarrior.com)
Cold1
- Physiologic livedo reticularis is a response to cold temperatures and is a common finding in infants, children, and adults prone to acrocyanosis. (mhmedical.com)
Patch1
- Livedo reticularis is a reactive macular, reticulated (net-like) patch of nonpalpable cutaneous vasodilatation due to normal physiologic variation, vasospasm, vessel wall damage, or intraluminal pathology. (mhmedical.com)
Figure1
- Livedo reticularis was confirmed by biopsy (see Figure 1). (medscape.com)