A systemic non-thrombocytopenic purpura caused by HYPERSENSITIVITY VASCULITIS and deposition of IGA-containing IMMUNE COMPLEXES within the blood vessels throughout the body, including those in the kidney (KIDNEY GLOMERULUS). Clinical symptoms include URTICARIA; ERYTHEMA; ARTHRITIS; GASTROINTESTINAL HEMORRHAGE; and renal involvement. Most cases are seen in children after acute upper respiratory infections.
Purplish or brownish red discoloration, easily visible through the epidermis, caused by hemorrhage into the tissues. When the size of the discolorization is >2-3 cm it is generally called Ecchymoses (ECCHYMOSIS).
Thrombocytopenia occurring in the absence of toxic exposure or a disease associated with decreased platelets. It is mediated by immune mechanisms, in most cases IMMUNOGLOBULIN G autoantibodies which attach to platelets and subsequently undergo destruction by macrophages. The disease is seen in acute (affecting children) and chronic (adult) forms.
An acquired, congenital, or familial disorder caused by PLATELET AGGREGATION with THROMBOSIS in terminal arterioles and capillaries. Clinical features include THROMBOCYTOPENIA; HEMOLYTIC ANEMIA; AZOTEMIA; FEVER; and thrombotic microangiopathy. The classical form also includes neurological symptoms and end-organ damage, such as RENAL FAILURE.
A severe, rapidly fatal reaction occurring most commonly in children following an infectious illness. It is characterized by large, rapidly spreading skin hemorrhages, fever, or shock. Purpura fulminans often accompanies or is triggered by DISSEMINATED INTRAVASCULAR COAGULATION.
Purplish or brownish red discoloration of the skin associated with increase in circulating polyclonal globulins, usually GAMMA-GLOBULINS. This syndrome often occurs on the legs of women aged 20 to 40 years.
Removal of plasma and replacement with various fluids, e.g., fresh frozen plasma, plasma protein fractions (PPF), albumin preparations, dextran solutions, saline. Used in treatment of autoimmune diseases, immune complex diseases, diseases of excess plasma factors, and other conditions.
Surgical procedure involving either partial or entire removal of the spleen.
The number of PLATELETS per unit volume in a sample of venous BLOOD.
A family of membrane-anchored glycoproteins that contain a disintegrin and metalloprotease domain. They are responsible for the proteolytic cleavage of many transmembrane proteins and the release of their extracellular domain.

Familial Mediterranean fever--renal involvement by diseases other than amyloid. (1/225)

BACKGROUND: In patients with familial Mediterranean fever (FMF) renal involvement is usually in the form of AA amyloidosis. There is increasing evidence that renal involvement may be due to diseases other than amyloid as well. METHODS: Amongst 302 children with FMF we observed and followed 28 with typical clinical and laboratory features of vasculitis. The diagnosis of FMF was established according to the Tel Hashomer criteria. RESULTS: Polyarteritis nodosa, protracted febrile attacks and Henoch-Schonlein purpura were diagnosed in 4, 13, and 11 patients, respectively. The presentation was often difficult to distinguish from FMF attacks, but protracted febrile attacks lasting several weeks, hypertension, thrombocytosis, and dramatic responses to corticosteroid therapy that were observed in many cases were different from what is observed in classical FMF. CONCLUSIONS: We suggest that FMF, perhaps as a consequence of impaired control of inflammatory responses, predisposes to vasculitis with renal involvement.  (+info)

Deletion polymorphism of the angiotensin converting enzyme gene predicts persistent proteinuria in Henoch-Schonlein purpura nephritis. (2/225)

OBJECTIVE: To study the influence of deletion/insertion polymorphism in the 16th intron of the angiotensin converting enzyme (ACE) gene on clinical manifestations of Henoch-Schonlein purpura nephritis. STUDY DESIGN: Cross sectional study. ACE gene polymorphism was determined in patients (4-15 years old at onset) with Henoch-Schonlein purpura nephritis (n = 40) and compared with that in patients with IgA nephropathy (n = 79). MAIN OUTCOME MEASURES: ACE genotypes, systemic blood pressures, urine protein excretion rate, haematuria, creatinine clearance, serum ACE activities. RESULTS: The initial clinical manifestations of both Henoch-Schonlein purpura nephritis and IgA nephropathy were no different among homozygotes for insertion (II) and deletion (DD), and heterozygotes (ID) for the ACE gene. In patients with Henoch-Schonlein purpura nephritis, the incidence of moderate to heavy proteinuria at four and eight years after onset was more than five times higher in the DD genotype than in the II or ID genotypes. No such trend was seen in patients with IgA nephropathy. The number of patients with Henoch-Schonlein purpura nephritis in whom proteinuria resolved at four and eight years after onset was significantly lower in the DD genotype compared with the II genotype, whereas no differences were detected among the three different genotypes in patients with IgA nephropathy. Plasma ACE activities in patients with the DD genotype were significantly higher than in those with non-DD genotypes. CONCLUSIONS: The ACE DD genotype predicts persistent proteinuria in Henoch-Schonlein purpura nephritis. The proteinuria might be related to a defective angiotensin system which is genetically determined by the D/I polymorphism.  (+info)

Pulmonary function abnormalities in children with Henoch-Schonlein purpura. (3/225)

Henoch-Schonlein purpura (HSP) is a widespread necrotizing vasculitis affecting small vessels characterized by nonthrombocytopenic purpura. Pulmonary involvement is a rare fatal complication with diffuse alveolar haemorrhage. The objective of this study was to evaluate possible early lung function abnormalities and to establish any relationship with the clinical activity of the disease. Fifteen children with HSP and without clinical or radiological evidence of lung involvement underwent pulmonary function study at the onset of the disease. A sample of 28 subjects matched by age, height, and weight was chosen as a control group. After a mean of 21 months (range 12-43) lung function tests were repeated in 10 of the previously studied children. During the acute phase of the disease the transfer factor for carbon monoxide, measured by steady-state (TL,COss) and single-breath (TL,COsb) methods, was found to be significantly lower in children with HSP than control subjects. There was no significant relationship between pulmonary function tests with symptoms and signs at onset, nor was there any correlation between variables and serum immunoglobulin A (IgA) concentration. In all but two patients, clinical recovery was observed within 6 weeks from the onset of the disease. In one case relapses of purpuric skin lesions were observed during the first 3 months of follow-up. The second case had relapses of purpuric skin lesions and microscopical haematuria during the 12 months following the onset of the disease with characteristic IgA mesangial deposition on renal biopsy. Although the overall mean value of TL,COsb improved from baseline to the second investigation, in both patients the recurrences of clinical signs were associated with a slight impairment of TL,COsb at the second evaluation. These data suggest an early subclinical lung impairment in children with Henoch-Schonlein purpura during the active phase of the disease. The presence of isolated pulmonary function abnormalities was not associated with the subsequent development of lung disease.  (+info)

Successful treatment of adult-onset Henoch-Schonlein purpura nephritis with high-dose immunoglobulins. (4/225)

A 26-year-old woman was admitted for the evaluation of edema and massive proteinuria. She had a history of purpura of the lower extremities, abdominal pain and melena. Laboratory investigations showed hypoalbuminemia, hypercholesterolemia and proteinuria of over 10 g/day. Renal biopsy showed moderate proliferative glomerulonephritis with mesangial immunoglobulin A (IgA) deposition. She was diagnosed as having Henoch-Schonlein purpura nephritis. Oral prednisolone, dipyridamole and intravenous heparin treatment were not effective. Steroid pulse therapy induced a partial improvement of proteinuria to 2-3 g/day. High-dose intravenous immunoglobulin (i.v.-IG) treatment was introduced and a dramatic improvement of proteinuria was noted. I.v.-IG should be fully considered in patients with steroid-resistant Henoch-Schonlein purpura nephritis.  (+info)

Red-man syndrome after vancomycin: potential cross-reactivity with teicoplanin. (5/225)

We report a patient with infective endocarditis who developed a severe form of Red-man syndrome after vancomycin. On substituting the antibiotic to teicoplanin, the patient went on to develop a dramatic pyrexia which settled only after the teicoplanin was discontinued. This suggested that there may be an element of cross-reactivity between teicoplanin and vancomycin in such patients and that teicoplanin may not be the most appropriate substitute in all cases of vancomycin-induced Red-man syndrome.  (+info)

Binding sites for carrier-immobilized carbohydrates in the kidney: implication for the pathogenesis of Henoch-Schonlein purpura and/or IgA nephropathy. (6/225)

BACKGROUND: Henoch-Schonlein purpura is a common vasculitis of childhood affecting the skin, joints, gastrointestinal tract, and kidney. The mesangial deposition of IgA1 is the most critical factor for the prognosis of patients with this disease. The aberrant glycosylation of the IgA1 subclass with the absence of terminally located galactose and presence of only alpha-N-acetylgalactosamine in O-linked oligosaccharides in the hinge region of IgA1 represents a prominent difference from the normal IgA1. These alterations prompt the supposition that the sugar part may guide IgA deposition by recognition of endogenous lectins on the mesangium. METHODS: Owing to the limited knowledge about the expression of carbohydrate-binding sites in the human kidney we initiated the study of this aspect with a class of tools which are suitable to map the lectinome of cells. Employing biotinylated neoglycoconjugates, glycosaminoglycans, and sulphated polysaccharides we monitored the presence of accessible carbohydrate-binding sites in control kidneys represented by tumour-free areas of kidneys with Grawitz tumour and in biopsies from patients with Henoch-Schonlein purpura-associated IgA nephropathy. RESULTS: Using frozen sections, no expression of any tested carbohydrate-binding site(s) was observed in the endothelial and the mesangial cells in glomeruli of the control kidneys as well as in the biopsies from Henoch-Schonlein purpura IgA nephropathic kidneys, in contrast to the tubules. The N-acetylgalactosamine-binding sites were expressed only in the inner layer of Bowman's capsule of 20% of glomeruli of the control kidney from one patient with Grawitz tumour and one biopsy from a patient with Henoch-Schonlein purpura-associated IgA nephropathy. However, the macrophages in the glomeruli of patients with IgA nephropathy and interstitial macrophages from both studied groups, i.e. without and with IgA nephropathy, harbour capacity to recognize carrier-immobilized alpha-N-acetylgalactosamine. Access to this binding site for the neoligand conjugate can be blocked by the monoclonal antibody MEM-18 recognizing CD14 antigen. CONCLUSION: The possibility for a participation of macrophage deposition of IgA1 in mesangium via a lectin mechanism involving this binding capacity warrants further studies.  (+info)

Primary renal vasculitis in Norfolk--increasing incidence or increasing recognition? (7/225)

BACKGROUND: The incidence of renal vasculitis has previously been estimated using histological definitions or only a single clinical diagnosis, e.g. Wegener's Granulomatosis (WG). Our hospital is the single referral centre for the former Norwich Health Authority (NHA) which encompasses a stable, homogeneous, well-defined and studied population. We estimated the overall incidence of primary renal vasculitis and the incidence within individual clinical disease classifications. METHODS: All cases of primary renal vasculitis diagnosed within the NHA over 66 months (1992-1997) were identified by review of renal biopsies, the Norfolk Vasculitis Register, hospital discharge summaries and plasmapheresis records. Patients were classified using the 1990 American College of Rheumatology criteria for Polyarteritis Nodosa (PAN), Churg Strauss Syndrome (CSS) and Henoch-Schonlein Purpura; the Chapel Hill Consensus Conference Definitions for Microscopic Polyangiitis (mPA) and the Lanham criteria for CSS. Incidence figures were calculated using the NHA adult population of 413747 (1994). Ninety-five per cent confidence intervals (C.I.) were calculated using the poisson distribution. RESULTS: The overall annual incidence for primary renal vasculitis was 18/million (C.I. 12.9-24.4). The annual incidence of renal involvement of individual diseases was as follows: WG 7.9/million (95% C.I. 4.7-12.5); mPA 7.5/million (95% C. I. 4.4-12.0); PAN 7.0/million (95% C.I. 4.0-11.4); HSP 3.1/million (95% C.I. 1.2-6.3); CSS 1.3/million (95% C.I. 0.3-3.9). CONCLUSIONS: The annual incidence for primary renal vasculitis overall and the individual subtypes in Norfolk is much higher than previous European estimates. This may reflect an increasing incidence in primary renal vasculitis with time or underestimation in previous studies. However the incidence of renal vasculitis in our population is markedly lower than reported in Kuwait. There may therefore be true variation in incidence between populations which could have implications for the aetiology of primary vasculitis.  (+info)

Systemic vasculitis and atypical infections: report of two cases. (8/225)

Two cases of systemic vasculitis are described; one presenting with adult Henoch-Schonlein purpura secondary to a concomitant Chlamydia infection and the other with leucocytoclastic vasculitis and mesangioproliferative glomerulonephritis secondary to a recent parvovirus B19 infection. Association of chlamydial infection has not previously been described with Henoch-Schonlein purpura and this infection should, perhaps, be added to the list of aetiologies of this disease. Parvovirus B19 causing significant urinary sediment abnormalities associated with mesangioproliferative glomerulonephritis and leucocytoclastic vasculitis has also not been described previously.  (+info)

Henoch-Schönlein purpura (HSP) is a type of small vessel vasculitis, which is a condition characterized by inflammation of the blood vessels. HSP primarily affects children, but it can occur in adults as well. It is named after two German physicians, Eduard Heinrich Henoch and Johann Schönlein, who first described the condition in the mid-19th century.

The main feature of HSP is a purpuric rash, which is a type of rash that appears as small, red or purple spots on the skin. The rash is caused by leakage of blood from the small blood vessels (capillaries) beneath the skin. In HSP, this rash typically occurs on the legs and buttocks, but it can also affect other parts of the body, such as the arms, face, and trunk.

In addition to the purpuric rash, HSP is often accompanied by other symptoms, such as joint pain and swelling, abdominal pain, nausea, vomiting, and diarrhea. In severe cases, it can also affect the kidneys, leading to hematuria (blood in the urine) and proteinuria (protein in the urine).

The exact cause of HSP is not known, but it is thought to be related to an abnormal immune response to certain triggers, such as infections or medications. Treatment typically involves supportive care, such as pain relief and fluid replacement, as well as medications to reduce inflammation and suppress the immune system. In most cases, HSP resolves on its own within a few weeks or months, but it can lead to serious complications in some individuals.

Purpura is a medical term that refers to the appearance of purple-colored spots on the skin or mucous membranes, caused by bleeding underneath the skin due to various factors such as blood clotting disorders, vasculitis (inflammation of the blood vessels), severe thrombocytopenia (low platelet count), or use of certain medications. These spots can vary in size and shape, ranging from small pinpoint hemorrhages (petechiae) to larger, irregularly shaped patches (ecchymoses). The bleeding is usually not caused by trauma or injury to the area. It's important to consult a healthcare professional if you notice any unexplained purpuric spots on your skin or mucous membranes, as they can indicate an underlying medical condition that requires further evaluation and treatment.

Idiopathic Thrombocytopenic Purpura (ITP) is a medical condition characterized by a low platelet count (thrombocytopenia) in the blood without an identifiable cause. Platelets are small blood cells that help your body form clots to stop bleeding. When you don't have enough platelets, you may bleed excessively or spontaneously, causing purpura, which refers to purple-colored spots on the skin that result from bleeding under the skin.

In ITP, the immune system mistakenly attacks and destroys platelets, leading to their decreased levels in the blood. This condition can occur at any age but is more common in children following a viral infection, and in adults after the age of 30-40 years. Symptoms may include easy or excessive bruising, prolonged bleeding from cuts, spontaneous bleeding from the gums or nose, blood blisters, and small red or purple spots on the skin (petechiae).

Depending on the severity of thrombocytopenia and the presence of bleeding symptoms, ITP treatment may include observation, corticosteroids, intravenous immunoglobulin (IVIG), or other medications that modify the immune system's response. In severe cases or when other treatments are ineffective, surgical removal of the spleen (splenectomy) might be considered.

Thrombotic thrombocytopenic purpura (TTP) is a rare but serious blood disorder. It's characterized by the formation of small blood clots throughout the body, which can lead to serious complications such as low platelet count (thrombocytopenia), hemolytic anemia, neurological symptoms, and kidney damage.

The term "purpura" refers to the purple-colored spots on the skin that result from bleeding under the skin. In TTP, these spots are caused by the rupture of red blood cells that have been damaged by the abnormal clotting process.

TTP is often caused by a deficiency or inhibitor of ADAMTS13, a protein in the blood that helps to regulate the formation of blood clots. This deficiency or inhibitor can lead to the formation of large clots called microthrombi, which can block small blood vessels throughout the body and cause tissue damage.

TTP is a medical emergency that requires prompt treatment with plasma exchange therapy, which involves removing and replacing the patient's plasma to restore normal levels of ADAMTS13 and prevent further clotting. Other treatments may include corticosteroids, immunosuppressive drugs, and rituximab.

Purpura fulminans is a severe, life-threatening condition characterized by the rapid progression of hemorrhagic purpura (discoloration of the skin due to bleeding under the skin) and disseminated intravascular coagulation (DIC), leading to thrombosis and necrosis of the skin and underlying tissues. It can be classified into two types: acute infectious purpura fulminans, which is caused by bacterial infections such as meningococcus or pneumococcus; and chronic purpura fulminans, which is associated with autoimmune disorders or protein C or S deficiencies. The condition can lead to serious complications such as sepsis, organ failure, and death if not promptly diagnosed and treated.

Hyperglobulinemic purpura is a medical condition characterized by the presence of purple-colored spots on the skin (purpura) due to bleeding under the skin caused by an abnormal increase in certain types of proteins called globulins in the blood. This condition is often associated with various underlying diseases, such as autoimmune disorders, infections, or cancer, that can lead to excessive production of these proteins.

The increased levels of globulins can cause damage to the walls of small blood vessels (capillaries), leading to leakage of red blood cells and plasma into the surrounding tissues. This results in the characteristic purpuric lesions on the skin, which may vary in size and distribution. In addition to skin manifestations, hyperglobulinemic purpura can also affect other organs, such as the kidneys, leading to further complications.

It is important to note that hyperglobulinemic purpura is a relatively rare condition, and its diagnosis typically requires a thorough evaluation of the patient's medical history, physical examination, laboratory tests, and imaging studies to identify the underlying cause and determine appropriate treatment.

Plasma exchange, also known as plasmapheresis, is a medical procedure where the liquid portion of the blood (plasma) is separated from the blood cells. The plasma, which may contain harmful substances such as antibodies, clotting factors, or toxins, is then removed and replaced with fresh plasma or a plasma substitute. This process helps to remove the harmful substances from the blood and allows the body to replenish its own plasma with normal components. Plasma exchange is used in the treatment of various medical conditions including autoimmune diseases, poisonings, and certain types of kidney diseases.

A splenectomy is a surgical procedure in which the spleen is removed from the body. The spleen is an organ located in the upper left quadrant of the abdomen, near the stomach and behind the ribs. It plays several important roles in the body, including fighting certain types of infections, removing old or damaged red blood cells from the circulation, and storing platelets and white blood cells.

There are several reasons why a splenectomy may be necessary, including:

* Trauma to the spleen that cannot be repaired
* Certain types of cancer, such as Hodgkin's lymphoma or non-Hodgkin's lymphoma
* Sickle cell disease, which can cause the spleen to enlarge and become damaged
* A ruptured spleen, which can be life-threatening if not treated promptly
* Certain blood disorders, such as idiopathic thrombocytopenic purpura (ITP) or hemolytic anemia

A splenectomy is typically performed under general anesthesia and may be done using open surgery or laparoscopically. After the spleen is removed, the incision(s) are closed with sutures or staples. Recovery time varies depending on the individual and the type of surgery performed, but most people are able to return to their normal activities within a few weeks.

It's important to note that following a splenectomy, individuals may be at increased risk for certain types of infections, so it's recommended that they receive vaccinations to help protect against these infections. They should also seek medical attention promptly if they develop fever, chills, or other signs of infection.

A platelet count is a laboratory test that measures the number of platelets, also known as thrombocytes, in a sample of blood. Platelets are small, colorless cell fragments that circulate in the blood and play a crucial role in blood clotting. They help to stop bleeding by sticking together to form a plug at the site of an injured blood vessel.

A normal platelet count ranges from 150,000 to 450,000 platelets per microliter (µL) of blood. A lower than normal platelet count is called thrombocytopenia, while a higher than normal platelet count is known as thrombocytosis.

Abnormal platelet counts can be a sign of various medical conditions, including bleeding disorders, infections, certain medications, and some types of cancer. It is important to consult with a healthcare provider if you have any concerns about your platelet count or if you experience symptoms such as easy bruising, prolonged bleeding, or excessive menstrual flow.

ADAM (A Disintegrin And Metalloprotease) proteins are a family of type I transmembrane proteins that contain several distinct domains, including a prodomain, a metalloprotease domain, a disintegrin-like domain, a cysteine-rich domain, a transmembrane domain, and a cytoplasmic tail. These proteins are involved in various biological processes such as cell adhesion, migration, proteolysis, and signal transduction.

ADAM proteins have been found to play important roles in many physiological and pathological conditions, including fertilization, neurodevelopment, inflammation, and cancer metastasis. For example, ADAM12 is involved in the fusion of myoblasts during muscle development, while ADAM17 (also known as TACE) plays a crucial role in the shedding of membrane-bound proteins such as tumor necrosis factor-alpha and epidermal growth factor receptor ligands.

Abnormalities in ADAM protein function have been implicated in various diseases, including cancer, Alzheimer's disease, and arthritis. Therefore, understanding the structure and function of these proteins has important implications for the development of novel therapeutic strategies.

... associated with Henoch-Schoenlein purpura: a case report and a review of adult cases of GCKD". Clinical Nephrology. Dustri- ...
... purpura, schoenlein-henoch MeSH C20.543.520.910.952 - vasculitis, allergic cutaneous MeSH C20.673.430.500 - IgA deficiency MeSH ...
... purpura MeSH C15.378.100.802.250 - purpura, hyperglobulinemic MeSH C15.378.100.802.375 - purpura, schoenlein-henoch MeSH ... purpura, hyperglobulinemic MeSH C15.378.463.835.580 - purpura, schoenlein-henoch MeSH C15.378.463.835.800 - scurvy MeSH C15.378 ... purpura, thrombocytopenic MeSH C15.378.100.805.600 - purpura, thrombocytopenic, idiopathic MeSH C15.378.100.805.680 - purpura, ... purpura, thrombocytopenic MeSH C15.378.140.855.700.600 - purpura, thrombocytopenic, idiopathic MeSH C15.378.140.855.700.680 - ...
Purpura Schönlein-Henoch, also known as "anaphylactoid purpura", "purpura rheumatica", and "Schönlein-Henoch purpura) Blasius ... Schönlein, Schoenlein may refer to: Johann Lukas Schönlein (1793, Bamberg - 1864), a German professor of medicine Henoch- ... Schoenlein, Schonlein. If an internal link intending to refer to a specific person led you to this page, you may wish to change ...
... purpura, hyperglobulinemic MeSH C14.907.934.580 - purpura, schoenlein-henoch MeSH C14.907.934.800 - scurvy MeSH C14.907.934.810 ... purpura, schoenlein-henoch MeSH C14.907.940.910.952 - vasculitis, allergic cutaneous MeSH C14.907.940.897.249.750 - ... purpura, thrombotic thrombocytopenic MeSH C14.907.355.830.850 - thromboembolism MeSH C14.907.355.830.850.213 - intracranial ...
... an allergic non-thrombopenic purpura rash that became known as Henoch-Schönlein purpura, though now known as IgA vasculitis. He ... Lucas Schoenlein von der Hirnmetamorphose, Inauguralabhandlung, Würzburg, Gedruckt bey F. E. Nitribitt, Universitätsbuchdrucker ... Schönlein-Henoch purpura at Who Named It? Schönlein's tricophyton at Who Named It? Schönlein, J.L. (1832). Allgemeine und ... Jones, J V (Dec 1973). "Letter: Schönlein versus Henoch". Br Med J. 4 (5893): 677-8. doi:10.1136/bmj.4.5893.677-e. ISSN 0007- ...
Henoch-Schoenlein purpura (HSP) affects approximately 20 in 100,000 children per year and twice as many boys than girls are ...
Henoch-Schoenlein purpura ISO. IL5 (Homo sapiens). 9068941. protein:increased expression:serum. RGD. PMID:16787590 and REF_RGD_ ...
... also referred to as Schönlein-Henoch purpura, anaphylactoid purpura, or purpura rheumatica) is an acute immunoglobulin A (IgA)- ... Prenzel F, Pfaffle R, Thiele F, Schuster V. Decreased factor XIII activity during severe Henoch-Schoenlein purpura -- does it ... 23] In addition to Henoch-Schönlein purpura, IgAV has also been referred to as Schönlein-Henoch purpura, anaphylactoid purpura. ... encoded search term (IgA Vasculitis (Henoch-Schonlein Purpura)) and IgA Vasculitis (Henoch-Schonlein Purpura) What to Read Next ...
... also referred to as Schönlein-Henoch purpura, anaphylactoid purpura, or purpura rheumatica) is an acute immunoglobulin A (IgA)- ... Prenzel F, Pfaffle R, Thiele F, Schuster V. Decreased factor XIII activity during severe Henoch-Schoenlein purpura -- does it ... encoded search term (IgA Vasculitis (Henoch-Schonlein Purpura)) and IgA Vasculitis (Henoch-Schonlein Purpura) What to Read Next ... A 9-year-old boy with IgA vasculitis (Henoch-Schönlein purpura). Note confluence of purpura around the ankles. Image courtesy ...
3. Henoch-Schoenlein purpura and other forms of vasculitis. 4. Familial fever syndromes (FMF, TRAPS, CAPS) and other ...
... associated with Henoch-Schoenlein purpura: a case report and a review of adult cases of GCKD". Clinical Nephrology. Dustri- ...
Lanzkowsky, S., Lanzkowsky, L., & Lanzkowdky, P. (1992). Henoch-Schoenlein Purpura. Pediatrics in Review, 13(4), 130-137. ...
Henoch-Schoenlein purpura - blood vessel inflammation that causes bleeding in the capillaries of the skin, kidneys and other ...
Henoch-Schönlein Purpura (Childhood Immunoglobulin A Vasculitis) Caused by Dental Infection in One of Fraternal Twins: A Case ...
... , Fengying Wang, Xiaozhong Li, Lusheng ... Henoch-Schoenlein purpura, Children. Introduction. Henoch-Schoenlein Purpura (HSP) is a major disease in the capillaries of ... Upregulation of SOCS1 and SOCS3 in pediatric patients with Henoch-Schoenlein purpura. Fengying Wang1, Xiaozhong Li1*, Lusheng ... This study aimed to investigate the expression of SOCS1 and SOCS3 in the development of Henoch-Schoenlein Purpura (HSP) in ...
Purpura, Schoenlein-Henoch 1 0 Systemic Inflammatory Response Syndrome 1 0 Diabetes Mellitus 1 0 ...
Purpura, Schoenlein-Henoch. IgA Vasculitis. Rapid Mix. Hydraulic Rapid Mix. Regional Plans. Regional Environmental Plans. ...
Henoch-Schoenlein purpura. Inflammatory bowel disease. Angioectasia. Small bowel varices and/or portal hypertensive enteropathy ... Henoch-Schoenlein purpura, neurofibromatosis, malignant atrophic papulosis, and other inherited polyposis syndromes. A family ...
Purpura, Schoenlein-Henoch. A systemic non-thrombocytopenic purpura caused by HYPERSENSITIVITY VASCULITIS and deposition of IGA ... MembranoproliferativeDiabetic NephropathiesImmune Complex DiseasesPurpura, Schoenlein-HenochNephritisGlomerulosclerosis, Focal ... Schoenlein-HenochNephritisMicroscopy, ElectronAntigens, Thy-1Glomerulosclerosis, Focal SegmentalKidney DiseasesImmunoglobulin G ... Basement MembraneAntigen-Antibody ComplexKidneyJuxtaglomerular ApparatusDiabetic NephropathiesImmune Complex DiseasesPurpura, ...
Henoch-Schoenlein purpura.. *Essential cryoglobulinemic vasculitis.. *ANCA-associated: *Granulomatosis with polyangiitis ( ...
Schoenlein-Henoch purpura. *Scleroderma. *Secondary syphilis. *Seizure disorders. *Sensorineural hearing loss. *Septal ...
... allergic purpura, Henoch-Schoenlein purpura, purpura allergic, Henoch- Schonlein purpura, Henoch Schonlein purpura More ... Synonyms (terms occurring on more labels are shown first): anaphylactoid purpura, Henoch-Schonlein purpura, Henoch-Schonlein, ... Henoch-Schonlein purpura. Definition: A systemic non-thrombocytopenic purpura caused by HYPERSENSITIVITY VASCULITIS and ...
Successful treatment of severe gastrointestinal involvement in adult-onset Henoch-Schönlein purpura. ... Successful treatment of severe gastrointestinal involvement in adult-onset Henoch-Schönlein purpura. Together they form a ...
Purpura, Hyperglobulinemic C14.907.934.550 C14.907.454.550. Purpura, Schoenlein-Henoch C14.907.934.580. Putamen A8.186.211.730. ...
Purpura, Hyperglobulinemic C14.907.934.550 C14.907.454.550. Purpura, Schoenlein-Henoch C14.907.934.580. Putamen A8.186.211.730. ...
Purpura, Hyperglobulinemic C14.907.934.550 C14.907.454.550. Purpura, Schoenlein-Henoch C14.907.934.580. Putamen A8.186.211.730. ...
Purpura, Hyperglobulinemic C14.907.934.550 C14.907.454.550. Purpura, Schoenlein-Henoch C14.907.934.580. Putamen A8.186.211.730. ...
Purpura, Hyperglobulinemic C14.907.934.550 C14.907.454.550. Purpura, Schoenlein-Henoch C14.907.934.580. Putamen A8.186.211.730. ...
Purpura, Hyperglobulinemic C14.907.934.550 C14.907.454.550. Purpura, Schoenlein-Henoch C14.907.934.580. Putamen A8.186.211.730. ...
Purpura, Hyperglobulinemic C14.907.934.550 C14.907.454.550. Purpura, Schoenlein-Henoch C14.907.934.580. Putamen A8.186.211.730. ...
Purpura, Hyperglobulinemic C14.907.934.550 C14.907.454.550. Purpura, Schoenlein-Henoch C14.907.934.580. Putamen A8.186.211.730. ...
Purpura, Hyperglobulinemic C14.907.934.550 C14.907.454.550. Purpura, Schoenlein-Henoch C14.907.934.580. Putamen A8.186.211.730. ...
Purpura, Hyperglobulinemic C14.907.934.550 C14.907.454.550. Purpura, Schoenlein-Henoch C14.907.934.580. Putamen A8.186.211.730. ...
Henoch-Schoenlein purpura, and hemolytic uremic syndrome [8, 9]. Therefore, it is important to find the etiological causes of ...
Schoenlein-Henoch Purpura Medicine & Life Sciences 48% * Langerhans Cell Histiocytosis Medicine & Life Sciences 46% ... Henoch Schonlein Purpura, systemic lupus erythematosus, scleroderma, sarcoidosis, dermatomyositis and immune thrombocytopenic ... Henoch Schonlein Purpura, systemic lupus erythematosus, scleroderma, sarcoidosis, dermatomyositis and immune thrombocytopenic ... Henoch Schonlein Purpura, systemic lupus erythematosus, scleroderma, sarcoidosis, dermatomyositis and immune thrombocytopenic ...

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