https://en.wikipedia.org/wiki/Capillary_leak_syndrome
Cyclophosphamide (CP), also known as cytophosphane among other names,[3] is a medication used as chemotherapyand to suppress the immune system.[4] As chemotherapy it is used to treat lymphoma, multiple myeloma, leukemia, ovarian cancer, breast cancer, small cell lung cancer, neuroblastoma, and sarcoma.[4] As an immune suppressor it is used in nephrotic syndrome, granulomatosis with polyangiitis, and following organ transplant, among other conditions.[4][5]It is taken by mouth or injection into a vein.[4]
Most people develop side effects.[4] Common side effects include low white blood cell counts, loss of appetite, vomiting, hair loss, and bleeding from the bladder.[4] Other severe side effects include an increased future risk of cancer, infertility, allergic reactions, and pulmonary fibrosis.[4] Cyclophosphamide is in the alkylating agent and nitrogen mustard family of medications.[4] It is believed to work by interfering with the duplication of DNA and the creation of RNA.[4]
Cyclophosphamide was approved for medical use in the United States in 1959.[4] It is on the World Health Organization's List of Essential Medicines.[6]
https://en.wikipedia.org/wiki/Cyclophosphamide
Granulomatosis with polyangiitis (GPA), previously known as Wegener's granulomatosis (WG),[1][2][3][4][5] is a rare long-term systemic disorder that involves the formation of granulomas and inflammation of blood vessels(vasculitis). It is a form of vasculitis that affects small- and medium-size vessels in many organs but most commonly affects the upper respiratory tract, lungs and kidneys.[6] The signs and symptoms of GPA are highly varied and reflect which organs are supplied by the affected blood vessels. Typical signs and symptoms include nosebleeds, stuffy nose and crustiness of nasal secretions, and inflammation of the uveal layer of the eye.[3]Damage to the heart, lungs and kidneys can be fatal.
The cause of GPA is unknown. Genetics have been found to play a role in GPA though the risk of inheritance appears to be low.[7]
GPA treatment depends on the severity of the disease.[8] Severe disease is typically treated with a combination of immunosuppressive medications such as rituximab or cyclophosphamide and high-dose corticosteroids to control the symptoms of the disease and azathioprine, methotrexate, or rituximab to keep the disease under control.[1][7][8]Plasma exchange is also used in severe cases with damage to the lungs, kidneys, or intestines.[9]
The number of new cases of GPA each year is estimated to be 2.1–14.4 new cases per million people in Europe.[3]GPA is rare in Japanese and African-American populations but occurs more often in people of Northern European descent.[7] GPA is estimated to affect 3 cases per 100,000 people in the United States and equally affects men and women.[10]
https://en.wikipedia.org/wiki/Granulomatosis_with_polyangiitis
ANCAs are associated with small vessel vasculitides including granulomatosis with polyangiitis, microscopic polyangiitis, primary pauci-immune necrotizing crescentic glomerulonephritis (a type of renal-limited microscopic polyangiitis), eosinophilic granulomatosis with polyangiitis and drug induced vasculitides. PR3 directed c-ANCA is present in 80-90% of granulomatosis with polyangiitis, 20-40% of microscopic polyangiitis, 20-40% of pauci-immune crescentic glomerulonephritis and 35% of eosinophilic granulomatosis with polyangiitis. c-ANCA (atypical) is present in 80% of cystic fibrosis (with BPI as the target antigen) and also in inflammatory bowel disease, primary sclerosing cholangitis and rheumatoid arthritis (with antibodies to multiple antigenic targets). p-ANCA with MPO specificity is found in 50% of microscopic polyangiitis, 50% of primary pauci-immune necrotizing crescentic glomerulonephritis and 35% of eosinophilic granulomatosis with polyangiitis. p-ANCA with specificity to other antigens are associated with inflammatory bowel disease, rheumatoid arthritis, drug-induced vasculitis, autoimmune liver disease, drug induced syndromes and parasitic infections. Atypical ANCA is associated with drug-induced systemic vasculitis, inflammatory bowel disease and rheumatoid arthritis.[2][4] The ANCA‐positive rate is much higher in patients with type 1 diabetes mellitus than in healthy individuals.[5]
Levamisole, which is a common adulterant of cocaine, can cause an ANCA positive vasculitis.[6]
The presence or absence of ANCA cannot indicate presence or absence of disease and results are correlated with clinical features. The association of ANCA and disease activity remains controversial; however, the reappearance of ANCA after treatment can indicate a relapse.[7][8]
https://en.wikipedia.org/wiki/Anti-neutrophil_cytoplasmic_antibody#Disease_associations
Arteriosclerosis obliterans is an occlusive arterial disease most prominently affecting the abdominal aorta and the small- and medium-sized arteries of the lower extremities, which may lead to absent dorsalis pedis, posterior tibial, and/or popliteal artery pulses.[1]: 842
It is characterized by fibrosis of the tunica intima and calcification of the tunica media.
https://en.wikipedia.org/wiki/Arteriosclerosis_obliterans
Superficial thrombophlebitis is a thrombosis and inflammation of superficial veins which presents as a painful indurationwith erythema, often in a linear or branching configuration forming cords.[2]: 826–7 [3]
Superficial thrombophlebitis is due to inflammation and/or thrombosis, and less commonly infection of the vein. It is generally a benign, self-limited disorder, however, it can be complicated by deep vein thrombosis (DVT) and even pulmonary embolism (PE)[4] Migratory superficial thrombophlebitis is known as Trousseau's syndrome.[5]
https://en.wikipedia.org/wiki/Superficial_thrombophlebitis
https://www.cancer.gov/publications/dictionaries/cancer-terms/def/capillary
Angiostrongyliasis is an infection by a roundworm of the Angiostrongylus type. Symptoms may vary from none, to mild, to meningitis.[1]
Infection with Angiostrongylus cantonensis (rat lungworm) can occur after ingestion of raw or undercooked snails or slugs, and less likely unwashed fruits and vegetables.
In humans, A. cantonensis is the most common cause of eosinophilic meningitis or meningoencephalitis.[2] Frequently the infection will resolve without treatment or serious consequences, but in cases with a heavy load of parasites the infection can be so severe it can cause permanent damage to the central nervous system or death.[3]
https://en.wikipedia.org/wiki/Angiostrongyliasis
Meningoencephalitis (/mɪˌnɪŋɡoʊɛnˌsɛfəˈlaɪtɪs, -ˌnɪndʒoʊ-, -ən-, -ˌkɛ-/;[3][4] from Greek μῆνιγξ meninx, "membrane", ἐγκέφαλος, enképhalos "brain", and the medical suffix -itis, "inflammation"), also known as herpes meningoencephalitis, is a medical condition that simultaneously resembles both meningitis, which is an infectionor inflammation of the meninges, and encephalitis, which is an infection or inflammation of the brain.
Signs and symptoms[edit]
Signs of meningeoncephalitis include unusual behavior, personality changes, and thinking problems.[5][6]
Symptoms may include headache, fever, pain in neck movement, light sensitivity, and seizure.[7]
Causes[edit]
Causative organisms include protozoans, viral and bacterial pathogens.[citation needed]
Specific types include:
Bacterial[edit]
Veterinarians have observed meningoencephalitis in animals infected with listeriosis, caused by the pathogenic bacteria L. monocytogenes. Meningitis and encephalitis already present in the brain or spinal cord of an animal may form simultaneously into meningeoencephalitis.[8] The bacterium commonly targets the sensitive structures of the brain stem. L. monocytogenes meningoencephalitis has been documented to significantly increase the number of cytokines, such as IL-1β, IL-12, IL-15, leading to toxic effects on the brain.[9]
Meningoencephalitis may be one of the severe complications of diseases originating from several Rickettsia species, such as Rickettsia rickettsii (agent of Rocky Mountain spotted fever (RMSF)), Rickettsia conorii, Rickettsia prowazekii (agent of epidemic louse-borne typhus), and Rickettsia africae. It can cause impairments to the cranial nerves, paralysis to the eyes, and sudden hearing loss.[10][11] Meningoencephalitis is a rare, late-stage manifestation of tick-borne ricksettial diseases, such as RMSF and Human monocytotropic ehrlichiosis (HME), caused by Ehrlichia chaffeensis (a species of rickettsiales bacteria).[12]
Other bacteria that can cause it are Mycoplasma pneumoniae, Tuberculosis, Borrelia (Lyme disease) and Leptospirosis.
Viral[edit]
- Tick-borne encephalitis
- West Nile virus
- Measles
- Epstein-Barr virus
- Varicella-zoster virus
- Enterovirus
- Herpes simplex virus type 1
- Herpes simplex virus type 2
- Rabies virus
- Adenovirus, although meningoencephalitis is almost solely seen in heavily immunocompromised patients.[13]
- Mumps, a relatively common cause of meningoencephalitis. However, most cases are mild, and mumps meningoencephalitis generally does not result in death or neurologic sequelae.[14]
- HIV, a very small number of individuals exhibit meningoencephalitis at the primary stage of infection.[15][16]
Autoimmune[edit]
- Antibodies targeting amyloid beta peptide proteins which have been used during research on Alzheimer's disease.[17]
- Anti-N-methyl-D-aspartate (anti-NMDA) receptor antibodies, which are also associated with seizures and a movement disorder, and related to Anti-NMDA receptor encephalitis.
- NAIM or "Nonvasculitic autoimmune inflammatory meningoencephalitis" (NAIM).[18] They can be divided into GFAP- and GFAP+ cases. The second is related to the Autoimmune GFAP Astrocytopathy.
Protozoal[edit]
Animal[edit]
This nematode is an exceptionally rare cause of meningoencephalitis.[19]
Other/multiple[edit]
Other causes include granulomatous meningoencephalitis and vasculitis. The fungus, Cryptococcus neoformans, can be symptomatically manifested within the CNS as meningoencephalitis with hydrocephalus being a very characteristic finding due to the unique thick polysaccharide capsule of the organism.[citation needed]
https://en.wikipedia.org/wiki/Meningoencephalitis
https://en.wikipedia.org/wiki/Cryptococcus_neoformans
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