Did you mean: (Vasculitis hypersensitivity leuko cytoclastic )?
- A case of Henoch-Schonlein Purpura with dilated coronary arteries. [Case Reports]
- PRPediatr Rheumatol Online J 2018 Sep 04; 16(1):54
- CONCLUSIONS: Cardiac findings, while rare, can exist in HSP. Coronary dilation appeared to respond to our hospital protocol's Kawasaki Disease (KD) therapy, possibly indicating an overlap in HSP and KD pathophysiology. This case, along with prior reports of dilated coronaries in systemic juvenile idiopathic arthritis (SJIA), highlights the importance of considering other sources of systemic inflammation, in addition to KD, when coronary dilation is identified. The appropriate therapy, follow-up, and prognosis for our patient are not clear, as further studies are needed to determine the natural course of these findings.
- Cutaneous Vasculitis in Cogan's Syndrome: A Report of Two Cases Associated with Chlamydia Infection. [Case Reports]
- JNJ Nippon Med Sch 2018; 85(3):172-177
- Cogan's syndrome (CS) is defined by the combination of hearing loss, vertigo, and ocular inflammation of uncertain cause, and can be associated with variable vessel vasculitis. Vasculitic manifestati...
Cogan's syndrome (CS) is defined by the combination of hearing loss, vertigo, and ocular inflammation of uncertain cause, and can be associated with variable vessel vasculitis. Vasculitic manifestations may include arteritis (affecting large, medium or small arteries), aortitis, and aortic and mitral valvulitis. Cutaneous manifestations including erythema, papules, subcutaneous nodules, and purpura sometimes occur; however, to date, only six cases have been histologically confirmed to have genuine vasculitis. Here, we report two cases of CS, one of which involved a patient who developed the typical symptoms of Takayasu arteritis and purpuric lesions in the legs, with histologic findings consistent with small vessel vaculitis in the dermis. The second case involved a patient who developed subcutaneous nodules in the legs and the axilla, and histologic findings revealed a necrotizing vasculitis of the small arteries in the interlobular area. Both cases were successfully treated with systemic steroid therapy. Based on the clinical features and the examination data, there is a possibility that a Chlamydia trachomatis infection played a pivotal role in the pathogenesis of those vasculitides.
- A Unique Case Report on Hypersensitivity Vasculitis as an Allergic Reaction to the Herpes Zoster Vaccine. [Journal Article]
- VEVasc Endovascular Surg 2018 Aug 20; :1538574418794079
- Hypersensitivity vasculitis (HV) or leukocytoclastic vasculitis is a rare small-vessel vasculitis that may occur as a manifestation of the body's extreme allergic reaction to a drug, infection, or ot...
Hypersensitivity vasculitis (HV) or leukocytoclastic vasculitis is a rare small-vessel vasculitis that may occur as a manifestation of the body's extreme allergic reaction to a drug, infection, or other foreign substance. Characterized by the presence of inflammatory neutrophils in vessel walls, HV results in inflammation and damage to blood vessels, primarily in the skin. Histologically, when neutrophils undergo leukocytoclasia and release nuclear debris into the vasculature, vascular damage manifests as palpable purpura. The incidence of HV is unknown and its relationship and interaction with certain vaccinations is rare and poorly understood. Affected patients with HV generally have a good prognosis; however, fatality may occur if organs such as the central nervous system, heart, lungs, or kidneys are involved. We report a unique case of a 60-year-old man who presented with a serious case of HV after receiving the herpes zoster vaccine. A thorough literature review yielded only one similar case of vascular reaction to the varicella vaccine that was reported in the Annals of Internal Medicine in 1997; however, no other reported cases with regard to the herpes zoster vaccine have been found. Our case presents a rare glimpse into HV that may result from varicella vaccine administration.
- Case 2: Hemolacria, Hematochezia, and Hematuria in an 11-month-old Boy. [Case Reports]
- PRPediatr Rev 2018; 39(8):418-420
- Erythema elevatum diutinum. [Case Reports]
- ABAn Bras Dermatol 2018 Jul-Aug; 93(4):614-615
- Clindamycin-induced Maculopapular Exanthema with Preferential Involvement of Striae Distensae: A Koebner phenomenon? [Case Reports]
- ADActa Dermatovenerol Croat 2018; 26(1):61-63
- Clindamycin is a lincomycin-derived antibiotic useful for the treatment of anaerobic and Gram-positive aerobic bacterial infections. Cutaneous adverse reactions are usually maculopapular exanthemas, ...
Clindamycin is a lincomycin-derived antibiotic useful for the treatment of anaerobic and Gram-positive aerobic bacterial infections. Cutaneous adverse reactions are usually maculopapular exanthemas, although hypersensitivity syndrome, acute generalized exanthematous pustulosis, and Stevens-Johnson syndrome have also been reported (1). We report the case of a patient with a maculopapular rash triggered by clindamycin who developed cutaneous lesions on striae distensae (SD). A 47-year-old woman was referred to our clinic for pruritic cutaneous lesions which had started 6 days earlier. Her past clinical history included hypertension, hypothyroidism, hyperuricemia, cholecystectomy, caesarean section, and endometriosis-related abdominal surgery, and she was taking levothyroxine, allopurinol, imidapril, and omeprazole. The skin rash first developed on her neck and back on the 3rd day of clindamycin oral treatment (300 mg every 6 hours), which was prescribed as antibiotic prophylaxis for a tooth implant. General malaise (but not fever) was also reported. Physical examination revealed an erythematous maculopapular eruption symmetrically distributed on the neck, abdomen, and back (Figure 1, A), with isolated lesions involving the proximal upper and lower limbs (Figure 1, B). There was a striking vertical distribution of skin lesions along the SD on the lateral sides of the abdomen (Figure 1, C). No mucosal involvement was found, and laboratory studies showed no abnormalities. Clindamycin withdrawal was followed by prescription of a course of oral deflazacort, starting at 30 mg daily and tapering down during a 9-day period. On the 5th day of treatment, the rash had almost cleared with minimal desquamation (Figure 1, D). Eight weeks after clearance of the skin rash, informed consent was obtained in order to perform an allergological evaluation of clindamycin, including prick and intradermal (ID) tests on the forearm and patch tests on the upper back (2). For patch testing, powder of the commercial capsules (Dalacin®) was diluted in petrolatum (pet.) and water (aq.), resulting in a final 1% clindamycin dilution. Parenteral clindamycin preparations were used in therapeutic concentrations for prick tests (150 mg/mL) and dilutions in saline of 1/100 and 1/10 for the ID test. Other authors have reported that these concentrations do not seem to irritate the skin (3-6). Prick and ID tests were assessed after 20 min and 24 hours, respectively. Patch tests were removed after the 2nd day, and late reactions were evaluated on day 2 and day 4. Prick and ID test results after 20 min were negative. Late results of ID tests with clindamycin (1.5 and 15 mg/mL) were positive: erythematous infiltrated papules about 7×7 mm and 18×15 mm were observed at 24 hours and lasted until the 8th day. Patch tests with clindamycin 1% in pet. and 1% in aq. were also positive (+ on day 2 and day 4). Positive late skin tests suggested delayed-type non-IgE-mediated allergic clindamycin hypersensitivity. Oral challenge tests are considered to be the gold standard to establish or exclude drug hypersensitivity. Due to the positive result of late skin test to clindamycin, oral challenge was not performed in our patient (3,5). The Koebner isomorphic phenomenon has been described in cutaneous reactions induced by drugs, such as antibiotics and chemotherapy. Chronic pressure on the skin is probably involved in the onset of skin lesions in hand-foot eruptions induced by tyrosine kinase inhibitors (sorafenib and sutinib). Solar exposure and cutaneous trauma also seem to play a role in the location of papulopustular eruptions caused by endothelial growth factor receptor inhibitors (erlotinib) (7). More frequent involvement in traumatized skin and surgical scars has been reported in the context of linear IgA bullous dermatosis and leukocytoclastic vasculitis triggered by vancomycin and cefuroxime (8). SD are produced by non-penetrating physical trauma, similar to friction or pressure. Different dermatoses can develop along SD skin lesions (like plaque psoriasis, pustular psoriasis, lichen planus, vitiligo, discoid lupus erythematosus, lupus vasculitis, urticarial vasculitis, or chronic graft-versus-host disease) (9). Bevacizumab, etretinate, and corticosteroid-induced ulcers, hyperpigmentation caused by bleomycin, and urticariform lesions triggered by diclofenac are examples of different type of drug-induced abnormalities involving SD (10). In summary, we identified clindamycin as the cause of the cutaneous reactions that occurred in our patient on the basis of the results of the skin tests and clinical history. Our findings confirmed a delayed-type hypersensitivity reaction, possibly involving a T-cell-mediated immunologic mechanism. Intradermal and patch tests were found to be useful in order to confirm the diagnosis (4,5). We did not find reports in the literature of drug-induced cutaneous eruptions along the SD as a manifestation of a Koebner phenomenon. Clinical underreporting of this phenomenon could explain the scarce literature on this cutaneous adverse reaction.
- Xp11 translocation renal cell carcinoma paraneoplastic syndrome presenting as cutaneous vasculitis: first reported case of yet another mask. [Case Reports]
- BCBMJ Case Rep 2018 Apr 21; 2018
- Renal cell carcinoma is historically known as the 'great masquerader' with 40% of patients experiencing a paraneoplastic syndrome. Translocation carcinoma represents one-third of renal cancer in paed...
Renal cell carcinoma is historically known as the 'great masquerader' with 40% of patients experiencing a paraneoplastic syndrome. Translocation carcinoma represents one-third of renal cancer in paediatric patients but less than 3% of renal cancers in patients aged 18-45 years where the clinical course is often rapidly terminal. There are less than 10 reported cases of leucoclastic vasculitis associated with clear cell carcinoma reported in the literature and 10 case reports of translocation carcinoma in adults. To our knowledge, we present the first reported case of Xp11 translocation carcinoma presenting as cutaneous vasculitis, as part of a paraneoplastic syndrome, in an adult patient. Our case highlights that renal cell cancers are truly the 'great masquerader' and a rash can be the first sign of renal malignancy.
- Leukocytoclastic Vasculitis and Desensitization to High-dose Methotrexate in Primary Central Nervous System Lymphoma. [Journal Article]
- CLClin Lymphoma Myeloma Leuk 2018; 18(5):e197-e200
- StatPearls [BOOK]
- BOOKStatPearls Publishing: Treasure Island (FL)
- Leukocytoclastic vasculitis, also known as “hypersensitivity vasculitis” is a histopathologic diagnosis given to cutaneous, small vessel vasculitis, specifically a vasculitis of the dermal post-capil...
Leukocytoclastic vasculitis, also known as “hypersensitivity vasculitis” is a histopathologic diagnosis given to cutaneous, small vessel vasculitis, specifically a vasculitis of the dermal post-capillary venules. The vasculitis is most often idiopathic. However, there are many other triggers including, but not limited to, infections, neoplasms, inflammatory disorders, and drug-induced vasculitis. Key clinical features of leukocytoclastic vasculitis include palpable purpura, lower extremity location, small vessel involvement, and extracutaneous involvement in approximately 30% of patients. If leukocytoclastic vasculitis is suspected, a punch biopsy should be performed with direct immunofluorescence studies. If no systemic symptoms are present, laboratory testing including ESR, complete blood count (CBC), basic metabolic panel, liver function tests, and urinalysis should be done as well. If there is a concern for systemic involvement, a more extensive workup can be performed. Most cases of cutaneous, small vessel vasculitis are self-limited with 90% resolving in weeks to months of onset. Otherwise, treatment depends on the severity of disease and can range from an oral corticosteroid taper to various steroid-sparing agents.
New Search Next
- Complete resolution of erythema elevatum diutinum using oral sulfasalazine. [Case Reports]
- DODermatol Online J 2017 Oct 15; 23(10)
- Erythema elevatum diutinum (EED) is a rare, chronic small-vessel vasculitis that presents as firm, red, violaceous, or brown papules and nodules on the extensor surfaces of the limbs. Oral dapsone is...
Erythema elevatum diutinum (EED) is a rare, chronic small-vessel vasculitis that presents as firm, red, violaceous, or brown papules and nodules on the extensor surfaces of the limbs. Oral dapsone is considered first-line therapy for EED; in the current case report, a patient presenting with EED began dapsone treatment and symptoms subsided within two weeks. Seven months later, the patient became pregnant and stopped dapsone owing to her concerns with dapsone use during pregnancy, resulting in recurrence of EED symptoms. We present a novel treatment approach with oral sulfasalazine, which was given to the patient in lieu of dapsone and resulted in complete resolution of EED symptoms.