Cases reported "Vascular Diseases"

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1/20. Complex vascular lesions at autopsy in a patient with phentermine-fenfluramine use and rapidly progressing pulmonary hypertension.

    Anorectic agents, such as aminorex and fenfluramine derivatives, have been associated previously with the development of primary pulmonary hypertension. The combination diet drug phentermine-fenfluramine (or "phen-fen") was recently marketed in the united states. We describe a case of a 39-year-old woman with rapidly progressing, fatal pulmonary hypertension following administration of phentermine-fenfluramine. autopsy was remarkable for complex pulmonary vascular lesions most consistent with thrombotic arteriopathy.
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2/20. High flow priapism due to an arterial-lacunar fistula complicating initial veno-occlusive priapism.

    High flow or arterial priapism is rare, caused by unregulated arterial blood flow from a lacerated cavernous artery or branch entering directly into lacunar spaces, bypassing the protective, high resistance helicine arterioles and resulting in an arterial-lacunar fistula (ALF) and usually occurs following direct blunt or penetrating perineal trauma. Clinical features include delayed onset of a constant, painless, nontender erection of incomplete rigidity with potential for full rigidity with sexual stimulation. Colour duplex Doppler ultrasonography (CDU) is reliable in the diagnosis of arterial priapism. Treatment by arterial ligation, super-selective embolisation with autologous clot, gelatin sponge or microcoil, duplex guided compression, systemic or intracavernous administration of a variety of alpha-adrenergic agents or methylene blue, mechanical compression/ice packs or expectant management has been reported.
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3/20. Vascular events associated with alpha interferon therapy.

    Alpha Interferon (IFN) is a biological agent used for the therapy of an increasing number of diseases, either as an established effective therapeutic tool or in the context of clinical trials. The use of IFN may be complicated by serious adverse reactions. We describe here the clinical course of a variety of vasculopathic complications in association with IFN-therapy in 12 patients with the diagnosis of chronic myeloid leukemia and 1 patient with malignant melanoma treated at our institute. Vascular manifestations in these patients include Raynaud's phenomena, digital ulcerations and gangrene, pulmonary vasculitis, pulmonary hypertension and thrombotic thrombocytopenic purpura/hemolytic uremic syndrome (TTP/HUS). These reactions occurred after 3 months to 3 years of 3-10 million units (MU) daily IFN therapy. Concomitant administration of hydroxyurea (HU) was noted in 5 patients. Discontinuation of IFN and initiation of immunosuppressive therapy brought about a complete resolution or arrested progression of these reactions. IFN-therapy may be complicated by severe vasculopathic/vasospastic complications that usually improve after its discontinuation. Possible underlying mechanisms for these complications are discussed. The early diagnosis of these complications may be vital and IFN should be immediately discontinued when early signs of these complications become evident.
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4/20. sirolimus-induced thrombotic microangiopathy in a renal transplant recipient.

    A rare but well-documented serious adverse reaction to the administration of the calcineurin inhibitors tacrolimus and cyclosporine in renal transplant recipients is the development of medication-induced thrombotic microangiopathy. The recently introduced immunosuppressive medication sirolimus has a very similar molecular structure to tacrolimus and also binds to the same intracellular proteins. Despite these similarities with tacrolimus, sirolimus has a different side-effect profile and reportedly lacks documented specific renal toxicity. This is a case report of the isolated administration of sirolimus without a concomitant calcineurin inhibitor being associated with the development of renal transplant biopsy-proven thrombotic microangiopathy. The patient is a 47-year-old African-American woman whose primary cause of renal failure was not thrombotic micrangiopathy, and she received a 5-antigen mismatched cadaveric renal transplant. Because of preexisting nephrosclerosis in the renal transplant, this patient was never administered a calcineurin inhibitor but was always maintained on sirolimus. With recent animal data showing that sirolmus can be nephrotoxic in a renal ischemic-reperfusion model (similar to what happens with a renal transplant), the authors speculate on a mechanism for this adverse reaction.
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5/20. paraplegia and sensory deficit caused by angiotropic large cell lymphoma.

    We report a case of angiotropic large cell lymphoma (ALCL) with central system involvement in which there was initially an isolated spinal cord stroke with paraplegia. MR imaging of the spinal cord demonstrated increased signal intensity in the center of the cord on T2-weighted images and subsequently a cerebral lesion in the right temporal lobe. The diagnosis of ALCL was established by brain biopsy. An enlarged spinal cord with enhancement after administration of contrast material and increased signal intensity on T2-weighted images, while not specific for ALCL, may be the first imaging findings of that disease.
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6/20. Severe hypertension during postpartum haemorrhage after i.v. administration of prostaglandin E2.

    Severe hypertension with arterial spasm was observed after i.v. administration of prostaglandin E2 (PGE2) during uterine exploration under general anaesthesia for control of postpartum haemorrhage. This hypertension was exceptional because PGE2 is known to cause a decrease in systemic arterial pressure. Different hypotheses for this paradoxical hypertensive crisis after PGE2 administration are discussed.
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7/20. Fatal poisoning with intravenously injected methadone and no fresh injection marks found.

    Drugs addicts are commonly brought to casualty wards where they often pose a diagnostic problem. They are typically brought in unconscious with no signs of disease or trauma. The suspicion of poisoning arises by the finding of fresh injection marks. This paper describes a case in which a young male drug addict was dead on arrival in hospital without recognizable recent injection marks but with some old wounds or necroses in both groins. The autopsy and toxicological analyses revealed that death was caused by an overdose of methadone and that the necroses in the groins were fistulas facilitating administration of the drugs directly into larger veins.
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8/20. Postoperative vasospasm after antegrade mesenteric revascularization: a report of three cases.

    Vascular reconstruction for chronic intestinal ischemia can be accomplished by endarterectomy or aortomesenteric bypass. In our practice, antegrade bypasses from the supraceliac aorta to the celiac axis and superior mesenteric artery are currently the most frequently used techniques. Such reconstructions often use multiple or bifurcated large diameter vascular prostheses and have demonstrated excellent long-term patency. Despite these salutory results, we have noted an unusual perioperative response in three of these patients, which is the subject of this report. All three patients underwent uncomplicated elective mesenteric revascularization with grafts (diameter greater than or equal to 6 mm) originating in the supraceliac aorta. Indications for operation included (1) history of postprandial pain, (2) documentation of weight loss, and (3) angiographic evidence of advanced atherosclerotic disease with appropriate collateral development. Episodes of abdominal pain occurred 5 to 20 days after operation when normal food intake was reinstituted. In two patients immediate angiograms revealed patent grafts with diffuse mesenteric vasospasm. Treatment with intravenous hyperalimentation and nifedipine for 10 days resulted in complete resolution of symptoms. In the third patient, symptoms were totally relieved by temporary reduction in oral intake and administration of nifedipine. A later angiogram revealed a patent graft. All patients have remained asymptomatic and regained normal weight. This pattern of postrevascularization pain has not been seen in our patients undergoing revascularization with small (i.e., venous) conduits originating in the infrarenal aorta. The cause appears to be a heightened myogenic response of a "protected" vascular bed when suddenly exposed to the high perfusion pressure and blood flow of large caliber antegrade conduits. Prophylaxis with calcium channel blockers and use of smaller diameter grafts (5 mm) may avoid this disturbing syndrome.
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9/20. Claudication: an unusual side effect of DHE administration.

    DHE is effective in the treatment of acute and chronic migraine. The side effects most commonly observed are abdominal discomfort, muscle pain, diarrhea and anxiety. DHE is a dehydrogenated amino acid ergot alkaloid and, as such, causes only limited vasoconstriction; indeed, its overall effects include peripheral vasodilation. The literature is replete with reports of clinical vasospasm and claudication occurring with therapeutic doses of ergotamine. There has not been any previous description of claudication caused by DHE. This paper describes pulselessness in two patients during relatively short courses of DHE. Treatment consisted of calcium channel blockers and discontinuation of DHE. Recovery was complete.
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10/20. Bilateral upper extremity ischemia after administration of dihydroergotamine-heparin for prophylaxis of deep venous thrombosis.

    Prolonged arterial spasm as a complication of ergot-containing medications has been reported since antiquity. This article describes our experience with a patient who had severe bilateral arterial spasm in the upper extremities 6 days after the initiation of a regimen of dihydroergotamine and heparin for prophylaxis against deep venous thrombosis. The spasm was refractory to oral calcium channel blocking agents and direct intraarterial infusion of tolazoline (Priscoline). However, intraarterial nitroglycerin produced a prompt and dramatic improvement in symptoms and in physical and arteriographic findings. This experience suggests that intraarterial nitroglycerin may be an appropriate first choice for ergot-induced arterial spasm.
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