Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0042384 (vasculitis)
 20,525 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Many pathophysiological process components are known to be implicated in lower limb ulcerations, among which vascular lesions have a major role. Vasculitis denotes a heterogeneous group of clinical entities which all are characterized by the inflammatory process of arterial and venous walls of any size and in any organ, quite frequently in the skin. Vasculopathy, on the other hand, refers to vascular and capillary lesions caused by, for example, some medications. The classification of vasculitides according to the size of the blood vessels involved serves for proper understanding the issue among clinicians and researchers, and not as a diagnostic tool. According to histologic finding obtained by examination of blood vessel biopsy specimen, vasculitides are divided into three groups: lymphocytic, leukocytoclastic and granulomatous. Livedoid vasculitis (livedo reticularis) most commonly affects women and is generally localized on lower extremities. The etiology oflivedoid vasculitis may imply autoimmune diseases, capillary obstruction with cryoglobulins, or antiphospholipid syndrome. Livedoid vasculopathy is a hyalinization disease of the vasculature, with thromboses and ulcerations on lower extremities, and of unknown etiology. Livedoid vasculopathy has been singled out as a separate disease that usually does not occur consequentially to other primary diseases. Livedoid vasculopathy typically affects women (71%) at a mean age of 45 (range 10-85) years; bilateral involvement of both lower limbs is present in 80.8%, disease manifested with ulcerations in 68.9%, ulcerations followed by development of atrophie blanche in 71.1%, transcutaneous oximetry reduction is found in 74.1%, factor V mutation (Leiden heterozygotes) in 22.2%, reduced protein C activity in 13.3%, prothrombin gene mutation (G20210A) in 8.3%, positive lupus anticoagulant in 17.9%, positive anticardiolipin antibodies in 28.6%, and elevated homocysteine level in 14.3% cases; blood vessel histology shows intraluminal thrombosis in 97.8% of patients, while direct immunofluorescence of blood vessel specimen shows immunoglobulins and complement components in blood vessels on the surface, in the mid-dermis as well as deep in the dermis. The immunofluorescence pattern differs from that found in immune complex diseases. Some of the agents tried in the treatment of livedoid vasculopathy include pentoxifylline, low-molecular heparin, hyperbaric oxygen therapy, methylprednisolone i.v. with pentoxifylline, recombinant tissue plasminogen activator, intravenous immunoglobulins, phenformin (biguanide) and ethylestrenol (anabolic steroid) combination, warfarin, heparin, systemic photochemotherapy (PUVA with oral psoralen), and low-molecular dextran. Infected ulcerations are treated with antibiotics. Combined therapy with folic acid, vitamin B12 and vitamin B6 can also be used.
 ...
PMID:[Vasculitis and vasculopathy]. 2319 16

The array of diagnostic workup for pyrexia of unknown origin (PUO) generally revolves in searching for infections, inflammatory/autoimmune, and endocrine etiologies. A differential diagnosis of fever, hemolytic anemia, and thrombocytopenia can have etiologies varying from infections like malaria, dengue, cytomegalovirus, Ebstein barr virus, Parvovirus, infective endocarditis, to autoimmune disorder (systemic lupus erythromatosis), vasculitis, hemolytic uremic syndrome, thrombotic thrombocytopenic purpura (TTP), autoimmune hemolytic anemia/Evan's syndrome, paroxysmal nocturnal hemoglobinuri (PNH), or drugs. Nutritional deficiencies (especially vitamin B12 deficiency) as a cause of fever, hemolytic anemia, and thrombocytopenia are very rare and therefore rarely thought of. Severe vitamin B12 deficiency may cause fever and if accompanied by concurrent hyper-homocysteinemia and hypophosphatemia can sometimes lead to severe hemolysis mimicking the above-mentioned conditions. We present a case that highlights vitamin B12 and vitamin D deficiency as an easily treatable cause of PUO, hemolytic anemia, and thrombocytopenia, which should be actively looked for and treated before proceeding with more complicated and expensive investigation or starting empiric treatments.
...
PMID:Vitamin B12 and vitamin d deficiencies: an unusual cause of Fever, severe hemolytic anemia and thrombocytopenia. 2581 Oct 10

We report the case of a 53-year-old female patient who developed bilateral sudden visual acuity loss after 15 weeks from the initiation of Peg-Interferon and Ribavirin treatment for hepatitis C. Debut was simultaneous and asymmetric, reported in the morning, at awakening. No pain or other symptom was reported by the patient. Results. At presentation, visual acuity was 0.2 in RE and 3/ 50 in LE. Pupillary reflexes were sluggish and severe dyschromatopsia was documented in both eyes (Ishihara plates). Fundus examination revealed bilateral pale optic disc edema, more prominent in LE, with splinter hemorrhages in the RNFL around the optic disk. Visual field exam demonstrated severe defects in 3 quadrants of the RE, whereas in the LE, it was impossible to perform the investigation due to VA<0.1. Neurologic evaluation was normal; other possible causes of systemic vasculitis were excluded by negative lab tests. Acute inflammatory markers (fibrinogen and ESR) and mild pancytopenia were the only documented laboratory changes in this patient. Anamnesis cleared the traditional risk factors for conventional AION (hypertension, diabetes, ischemic heart disease, and hypercholesterolemia). Cranial and orbital CT scan and MRI findings were normal. Patient was withdrawn from the Interferon and Ribavirin treatment and was administered methyl prednisolone pulse therapy (1g/ day) for 3 days, continued with oral Prednisone (60 mg/ day) tapered slowly for over 12 weeks. VA increased to 0.8 during treatment in the RE, but visual recovery in the LE was not as spectacular (0.16) as in the fellow eye. Modified latencies and amplitudes in evoked visual potentials examination during 4 months time emphasized bilateral optic atrophy. Optic nerve sufferance was amplified by a low level of vitamin B12, detected by chance at the last eye visit. Due to the general condition, dietary supplementation was not possible. Conclusion. A case of a patient with bilateral and simultaneous NAION caused by IFN and Ribavirin treatment for hepatitis C, who was also vitamin B12 deficient, was analyzed. Therefore, a combined etiology for optic atrophy was explained.
 ...
PMID:Combined etiology for bilateral and simultaneous optic neuropathy in a patient with ciancobalamin deficit and hepatitis C treated with peg-interferon and ribavirin. 2945 Mar 47

Drug-resistant tuberculosis is an increasing healthcare challenge. Drug regimen building demands the use of different therapeutic groups, many of which harbor neurotoxicity as a side-effect, whether central or peripheral. Peripheral neuropathy is a major concern as it tends to be severe and usually irreversible. Anti-tubercular drugs that may contribute to peripheral neuropathy include INH, ethambutol, linezolid, cycloserine and para-amino salicylic acid. This potential adverse effect must be balanced against the intrinsically grave prognosis that drug resistant tuberculosis harbors. We present such a clinically challenging case of a 25 years-old female with extremely drug resistant tuberculosis whose treatment necessitated the use of several neurotoxic anti-tubercular drugs, leading to severe sensory peripheral neuropathy who did not improve despite the withdrawal of culprit drugs. She developed positive and negative sensory symptoms in both lower limbs. Nerve conduction studies were suggestive of sensory neuropathy affecting both lower limbs. Alternate causes of peripheral neuropathy including HIV, vasculitis, B12 deficiency and diabetes were ruled out. Despite drug withdrawal, the patient did not improve significantly. This case emphasizes the irreversibility of anti-tubercular therapy-induced peripheral neuropathy, demanding more rigorous clinical screening for the same while managing such patients.
 ...
PMID:Irreversible neuropathy in extremely-drug resistant tuberculosis: An unfortunate clinical conundrum. 3282 76


<< Previous 1 2