1/42. calciphylaxis associated with cholangiocarcinoma treated with low-molecular-weight heparin and vitamin K.calciphylaxis is a rare disorder of small-vessel calcification and cutaneous infarction associated with chronic renal failure. Rare cases of calciphylaxis not associated with chronic renal failure have been reported with breast cancer, hyperparathyroidism, and alcoholic cirrhosis. To our knowledge, we report the first case of calciphylaxis without chronic renal failure associated with cholangiocarcinoma and the first attempt to treat calciphylaxis with vitamin K. A 56-year-old woman presented with necrotic leg ulceration. She was treated initially with low-molecular-weight heparin, with no effect. A coagulation work-up showed vitamin k deficiency. During vitamin K therapy, the patient had fulminant progression of the calciphylaxis. She died, and an autopsy showed metastatic cholangiocarcinoma. thrombosis and protein c deficiency have been implicated in the pathophysiology of calciphylaxis. Functional protein c deficiency may be one of several factors contributing to the development of calciphylaxis. Vitamin K therapy was ineffective in our patient and may have been detrimental.- - - - - - - - - - ranking = 1keywords = vessel (Clic here for more details about this article) |
2/42. Atypical hemorrhagic bullous pyoderma gangrenosum.A 55-year-old woman was seen in the Plastic and Reconstructive Surgery Clinic because of a nonhealing wound on her left leg of approximately 2 months' duration. She had an 8-month history of multiple wounds appearing on her arms and legs. The patient noted that the majority of the wounds had been treated and healed with the use of topical medications. One wound on her left leg had continued to enlarge rapidly despite topical treatments. Therefore, hyperbaric oxygen therapy had been administered for 15 sessions. No additional healing had occurred with this treatment. skin grafting was performed on the affected area. She developed ulcers and blistering lesions at surgical and nonsurgical sites after skin grafting. The patient was referred to the dermatology Department. Dermatologic examination revealed a deep, necrotic ulcer, 30 cm x 10 cm, with surrounding violaceous erythema on the donor area, ulceration (18 cm x 8 cm) on the graft area, a hemorrhagic bullous plaque (5 cm x 15 cm) over the right malleolus, scattered ecchymotic lesions and small hemorrhagic bullae on both legs, and small pustules around the staplers (Fig. 1a,b). Cutaneous biopsy of a new lesion revealed a focal, dense neutrophilic infiltrate, liquefaction degeneration in the center, lymphocytic and mild plasmacytic infiltration around the venules, and fibrinoid deposits in the walls and lumen of the vessels (Fig. 2a). In addition, excessive polymorphonuclear leukocytes and extravasated erythrocytes were present in the papillary and reticular dermis (Fig. 2b). The patient had a 14-year history of asthma bronchiale. physical examination did not reveal any abnormality, except for crackling rales at the base of each lung. Laboratory examinations were within normal limits, except for the sedimentation rate (55 mm/h). Protein electrophoresis, peripheral blood smear, abdominal ultrasound, and thorax and abdominopelvic computed tomography scans were all normal. Swab cultures from the ulcers were negative. Bullous pyoderma gangrenosum was diagnosed on clinical and histopathologic grounds. prednisolone 80 mg/day was started. Rapid epithelialization was observed within 2 months of treatment. The dose of prednisolone was gradually decreased to 20 mg/day, and was used as a maintenance dose for an additional 6 months. Complete improvement was achieved in 8 months. The patient has been followed up for approximately 1 year. There were no side effects observed during the treatment and in addition no new lesions developed at the follow-up.- - - - - - - - - - ranking = 1keywords = vessel (Clic here for more details about this article) |
3/42. Successful pharmacologic treatment of lower extremity ulcerations in 5 patients with chronic critical limb ischemia.BACKGROUND: Ischemic ulcerations of the distal lower extremities are a manifestation of chronic critical limb ischemia. Without restoration of arterial flow, subsequent gangrene and limb loss can ensue. Unfortunately, revascularization is not always possible. methods: A literature search of medline was performed and a case series of 5 patients with lower extremity ischemic ulcerations is described. RESULTS AND CONCLUSION: Five patients with severe peripheral artery disease had nonhealing lower extremity ischemic ulcerations. Because 3 patients were not ideal candidates for percutaneous or surgical intervention, and 2 refused invasive therapy, they were treated with cilostazol. Between 7 and 24 weeks after beginning cilostazol therapy, the ulcerations healed in all 5 patients. Three of the patients experienced resolution of concurrent ischemic rest pain. One patient underwent a posttreatment noninvasive arterial study that documented improved large- and small-vessel perfusion. The antiplatelet, antithrombotic, and vasodilatory effects, in addition to possible unrecognized actions of cilostazol, appeared to promote wound healing in this small group of patients with chronic critical limb ischemia. When revascularization is not ideal therapy for ischemic ulcers, a pharmacologic approach with cilostazol might induce healing and obviate limb amputation.- - - - - - - - - - ranking = 1keywords = vessel (Clic here for more details about this article) |
4/42. Cutaneous necrosis revealing the coexistence of an antiphospholipid syndrome with acquired protein s deficiency, factor v Leiden and hyperhomocysteinemia.We report an exceptional case of cutaneous necrosis due to the coexistence of 4 thrombophilic factors, inherited and acquired. We would like to draw attention to these unrecognized associations. CASE REPORT: A 72-year-old woman was admitted with a 5 month history of necrotic nonhealing, painful ulcer of both legs and recently a purple toe. She had a history of 3 deep venous thromboses of the leg complicated by pulmonary embolism. A skin biopsy of the ulcer and purple toe showed only thrombosis in the dermal vessel. Laboratory findings showed a circulating lupus anticoagulant, positive anticardiolipin antibodies, antinuclear antibodies (1/320 dilution) and an anti Sm. Moreover, activated protein c resistance associated with factor v Leiden mutation and hyperhomocysteinemia was found; protein S was transiently low. With iloprost, oral anticoagulant, vitamin B12 and folic acid, the evolution was good, with healing of ulcer. COMMENTS: cutaneous necrosis can reveal hypercoagulable states, sometimes complex. We find 4 thrombophilic factors in our case, i.e. antiphospholipid antibodies, factor v Leiden, protein s deficiency and hyperhomocysteinemia. This is exceptional but highlights the role of several constitutional and acquired thrombophilic factors in the genesis of thrombosis. Extended protein C pathway disturbances could explain the mechanism that leads to cutaneous necrosis, in this patient, with an antiphospholipid syndrome. This case shows that it is necessary in some circumstances to make a complete hemostatic laboratory search to detect several thrombophilic factors. If they are present they can justify an oral anticoagulant treatment and a familial screening.- - - - - - - - - - ranking = 1keywords = vessel (Clic here for more details about this article) |
5/42. Leg ulcers and hydroxyurea: report of three cases with essential thrombocythemia.CASE 1: A 65-year-old woman with essential thrombocythemia (ET) had been taking oral hydroxyurea (HU), 1,000 mg daily, for 7 years. Six months ago, she developed an ulcer on the outer part of her left ankle, which healed spontaneously within 2 months. She presented with a new, tender, shallow ulcer, 2 cm x 2 cm in size, at the same site. Doppler examination revealed thrombosis of the left common femoral vein and a calcified atheroma plaque of the left common femoral artery. The dosage of HU was decreased to 500 mg daily when the platelet counts were found to be within normal levels. The ulcer completely healed within 2 months with occlusive wound dressings, and has not recurred within the follow-up period of 1 year. CASE 2: A 56-year-old women presented with multiple, painful, leg ulcers of 1 year duration. She had been diagnosed as having ET and had been on HU therapy, 1,500 mg/day, for the past 5 years. interferon-alpha-2b was started 3 months ago, in addition to HU, which was tapered to 1,000 mg daily. She had suffered from hypertension for 20 years treated with nifedipine and enalapril, and had recently been diagnosed with diabetes mellitus which was controlled by diet. Examination revealed three ulcers located on the lateral aspects of both ankles and right distal toe. Arterial and venous Doppler examinations were within normal limits. Histopathology of the ulcer revealed nonspecific changes with a mixed inflammatory cell infiltrate around dermal vessels. The ulcers completely healed within 10 weeks with topical hydrocolloid dressings. After healing, she was lost to follow-up. A year later, it was learned that she had developed a new ulcer at her right heel, 3 months after her last visit (by phone call). This ulcer persisted for 8 months until HU was withdrawn. CASE 3: A 64-year-old woman with ET presented with a painful leg ulcer of 6 months' duration. She had been taking oral HU for 5 years. She had a 20-year history of hypertension treated with lisinopril. Examination revealed a punched-out ulcer of 2 cm x 2 cm over the right lateral malleolus. Doppler examination of the veins revealed insufficiency of the right greater saphenous and femoral veins. angiography showed multiple stenoses of the right popliteal and femoral arteries. As her platelet count remained high, HU was continued. During the follow-up period of 13 months, the ulcer showed only partial improvement with local wound care.- - - - - - - - - - ranking = 1keywords = vessel (Clic here for more details about this article) |
6/42. Type I cryoglobulinemia presenting as hemorrhagic crusted leg ulcers.cryoglobulins (CGs) are serum proteins that reversibly precipitate when the serum is cooled below 37 degrees C. Cryoglobulinemias are associated with a variety of diseases, including hematologic, autoimmune, and infectious. Isolation of CGs requires handling the specimen with extreme care. We describe a 70-year-old man, recently diagnosed with chronic lymphocytic leukemia, who developed hemorrhagic crusted skin ulcers on his legs that were pruritic and painful. Results of skin biopsies showed dilated superficial, mid-dermal and deep-dermal blood vessels containing pink amorphous material and red blood cells. cryoglobulinemia was suspected; however, an initial search for CGs was negative. There was concern about suboptimal handling of the specimen, and the test was repeated. Two percent CGs with IgM kappa specificity were detected. This case illustrates the importance of the proper handling of specimens for evaluation of cryoglobulinemia.- - - - - - - - - - ranking = 7.9937512028828keywords = blood vessel, vessel (Clic here for more details about this article) |
7/42. Phakomatosis pigmentovascularis IIb with hypoplasia of the inferior vena cava and the right iliac and femoral veins causing recalcitrant stasis leg ulcers.We present a patient with phakomatosis pigmentovascularis (PPV) type IIb accompanied with venous hypoplasia, from the inferior vena cava to the superficial femoral vein. Although it is not obvious whether this vascular anomaly, which is probably congenital, is coincidental or not, it is possible that the 2 diseases have some relationship each other, because PPV is thought to result from abnormal vasomotor activity during the embryonic period. In the diagnosis of type II PPV, careful examination and several studies are required to determine systemic involvement that may include large vessel changes.- - - - - - - - - - ranking = 1keywords = vessel (Clic here for more details about this article) |
8/42. Intractable leg ulceration caused by cutaneous cholesterol embolism.OBJECTIVE: To present a case of chronic intractable leg ulceration caused by cholesterol crystal embolism. CLINICAL FEATURES: A 76-year-old Caucasian male with a history of ischaemic heart disease had repeated hospital admissions for diagnosis and treatment of recurrent leg ulceration of more than three years' duration. INTERVENTION AND OUTCOME: Definitive diagnosis was made after the third biopsy when the specimen obtained included subcutaneous arteries. Complete healing occurred within three weeks of excision and a skin graft, and subsequent treatment which included systemic steroids. CONCLUSION: cholesterol crystal embolism is probably an underdiagnosed cause of intractable leg ulceration and can be identified by a biopsy specimen which includes vessels in subcutaneous fat. Systemic steroids may be helpful in its treatment.- - - - - - - - - - ranking = 1keywords = vessel (Clic here for more details about this article) |
9/42. Intractable livedoid vasculopathy successfully treated with hyperbaric oxygen.We describe a new method for treating livedoid vasculopathy. The typical presentation of livedoid vasculopathy includes chronic, recurrent painful ulcers, satellite scar-like atrophy and telangiectasia involving the lower extremities. Histologically, these lesions show areas of ulceration and dermal vessel occlusion without frank inflammatory cell infiltration. There is currently no satisfactory therapy available for this disease. Hyperbaric oxygen (HBO) has recently established itself as one of the most effective methods of treating ischaemic wounds, including diabetic ulcers. We used this therapy in two patients whose lesions were resistant to multiple therapeutic modalities. Not only did their ulcers respond rapidly to the HBO therapy, but the disturbing wound pain also resolved at the same time. To our knowledge, this is the first successful trial of HBO therapy in livedoid vasculopathy. We believe this to be a very promising new therapy for livedoid vasculopathy and to be worth further investigation.- - - - - - - - - - ranking = 1keywords = vessel (Clic here for more details about this article) |
10/42. pyoderma gangrenosum-like ulcer in a patient with large granular lymphocytic leukemia.Large granular lymphocytic leukemia refers to a clonal expansion of lymphocytes that have abundant cytoplasm and azurophilic granules. The disease is characterized clinically by chronic neutropenia and it may be associated with recurrent pyogenic infections. Except for these infections, cutaneous manifestations of this disease have not been well characterized. We describe a patient with large granular lymphocytic leukemia, which was confirmed by molecular genetics studies, who had a pyoderma gangrenosum-like ulcer on his leg. Results of an evaluation of the histologic characteristics and the leukocytic immunophenotype of a skin biopsy specimen from the ulcer demonstrated large granular lymphocytes within the blood vessels. Cutaneous ulceration may be a manifestation of large granular lymphocytic leukemia, and this disease should be considered when diagnosing patients with otherwise unexplained pyoderma gangrenosum-like ulcers of the skin.- - - - - - - - - - ranking = 7.9937512028828keywords = blood vessel, vessel (Clic here for more details about this article) |
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