Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0235108 (tense)
 2,176 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 42 year old heterosexual male with symptomatic human immunodeficiency virus infection presented with a 2-week history of tense blistering skin lesions following azidothymidine therapy. Urinary porphyrin excretion confirmed the diagnosis of porphyria cutanea tarda. The blisters resolved following the withdrawal of the drug but recurred when rechallenged. Three other cases of porphyria cutanea tarda, not associated with azidothymidine, who subsequently developed acquired immunodeficiency syndrome have recently been described. If azidothymidine is not the precipitating agent, it is possible that human immunodeficiency virus itself can impair porphyrin metabolism, leading to the clinical and biochemical features of porphyria cutanea tarda.
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PMID:Porphyria cutanea tarda in association with the human immunodeficiency virus infection. 325 16

A fatal case of cerebral mucormycosis occurring shortly after liver transplantation is described. The patient was a 32-yr-old male with advanced end-stage liver disease manifested by tense ascites, spontaneous bacterial peritonitis, deepening jaundice and anuria requiring hemodialysis. The 3rd day after successful liver transplantation the patient developed acute respiratory failure, then focal motor signs. Computed tomography showed fluid in the left maxillary sinus, partial opacification of the ethmoid and sphenoid sinuses, and diffuse low density lesions in both cerebral hemispheres. Despite treatment for cerebritis and cerebral edema, the patient's pupils became fixed and dilated, and brain death was declared. Autopsy revealed mucor sinusitis and cerebritis. Mucormycosis is an opportunistic fungal infection occurring in patients with diabetic ketoacidosis, malignancy, or immunodeficiency, and in those receiving wide-spectrum antibiotics, corticosteroids, or cytotoxic therapy. Mucor most frequently involves the face, rhinocerebral disease predominating. These infections are difficult to treat, but are curable with aggressive and frequent surgical debridement, discontinuation or reduction of immunosuppressive therapy and amphotericin. The diagnosis of mucormycosis is very difficult to make in cases such as the present one, in which the typical presentation and classical signs are not present. A high index of suspicion based on identified risk factors may assist in more rapid diagnosis of this life-threatening mycosis.
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PMID:Cerebral mucormycosis after liver transplantation: a case report. 985 Apr 59

A 39-yr-old male with hepatorenal syndrome type 1 and refractory ascites was treated with continuous renal replacement therapy (CRRT) resulting in clinical improvement. He was positive for antibodies to hepatitis B, C, and human immunodeficiency viruses, and had a history of chronic alcohol and iv drug abuse. The patient had 4 hospital admissions during a 12-wk period. He first presented with advanced liver disease including pedal edema and a serum ammonia level of 56 micromol/L (reference range: 11 - 35 micromol/L). In subsequent admissions, he had asterixis, nausea, vomiting, jaundice, and worsening pedal edema. On his 4th admission, there was lethargy, tense ascites, decreased urinary output, bilateral edema of the lower extremities and scrotum, serum creatinine of 6.2 mg/dl (reference range: 0.6 - 1.5 mg/dl), and weight gain of 16 kg during the prior 8 wk. During the first 3 hospitalizations, he was treated with lactulose with slight improvement. On the 4th admission, he was started on low-dose dopamine (3 microg/kg/min) and 25% salt-poor albumin without clinical improvement. A pulmonary artery catheter was placed and hemofiltration by CRRT was performed for 5 days, with removal of 26.7 L of fluid and a net reduction of 11 kg of body weight. Serum creatinine decreased to 4.2 mg/dl during CRRT and was 2.2 mg/dl at hospital discharge 2 weeks later. His PaO(2) improved from 66 to 78 mmHg and his systemic vascular resistance increased from 571 to 799 dyne.sec/cm(5). CRRT was effective in relieving severe fluid retention and producing marked clinical improvement. We suggest that CRRT should be considered for the treatment of refractory ascites including that caused by hepatorenal syndrome.
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PMID:Hepatorenal syndrome: resolution of ascites by continuous renal replacement therapy in an alcoholic coinfected with hepatitis B, C, and human immunodeficiency viruses. 1650 Dec 43

A 30-year-old man diagnosed with human immunodeficiency virus (HIV) infection 10 years earlier, presented with large tense blisters associated with minimal itching of 10 days' duration. He had no history of oral or genital erosions or ulcerations and showed no symptoms of HIV-related illnesses. Highly active antiretroviral therapy (HAART) had been started 6 weeks earlier when his CD4 count was 116/mL. He initially received nevirapine 200 mg once daily; after 2 weeks with no skin eruptions or other adverse reactions, the dose was increased to 200 mg twice daily. Other components of his HAART included lamivudine and stavudine. The patient was not taking any other prescription or alternative medicines. During the past year, he experienced 4 episodes of intensely itchy urticarial lesions that subsided with antihistamines. The present episode of bullous lesions was also preceded by urticarial lesions. On examination, he had multiple, large, tense bullae over relatively normal-looking skin involving all parts of the body (Figure 1). There were a few well-defined erosions. Nikolsky and bullae spread signs were negative, and no oral or genital erosions or ulcerations were noted. Results of a complete blood count, renal and liver function tests, and chest x-ray were within normal limits. Skin biopsy from one of the blisters showed a subepidermal bulla filled with eosinophils and polymorphonuclear leukocytes (Figure 2). The underlying dermis showed perivascular inflammatory infiltrate composed of polymorphonuclear and lymphomononuclear cells. The overall features were suggestive of bullous pemphigoid. A direct immunofluorescence test could not be done because of possible risk of cross-infection to the operator of the cryostat. Workup for herpes simplex virus and cytomegalovirus infection also could not be performed. HAART was discontinued temporarily with the suspicion that it was the causative factor. The patient was started on oral prednisolone 40 mg/d and topical clobetasol propionate (0.05%). Within 1 week of treatment, he had significant improvement with almost complete disappearance of the lesions. A few small, tense vesicles continued to appear between. Once the lesions completely disappeared, the prednisolone was gradually tapered off and all the components of HAART were resumed. The patient did well without any recurrence of lesions, thus virtually excluding HAART as the cause of the bullous pemphigoid-like eruptions. Subsequently, he did not return for follow-up.
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PMID:Bullous eruption in a patient infected with the human immunodeficiency virus. 1832 12

Infection with Mycobacterium tuberculosis and the human immunodeficiency virus has reached epidemic proportions in South Africa. Cardiac involvement occurs in approximately one per cent of patients suffering from active tuberculosis. This concerns predominantly pericardial involvement, resulting in chronic pericardial effusions, cardiac tamponade and constrictive pericarditis. Effusive-constrictive pericarditis is a clinical haemodynamic syndrome in which constriction by the visceral pericardium occurs in the presence of a tense effusion in a free pericardial space. We present a patient who was diagnosed with this condition, and highlight the value of contrast-enhanced magnetic resonance imaging in demonstrating the underlying structural and functional abnormalities.
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PMID:Tuberculous effusive-constrictive pericarditis. 1877 64

To define the likelihood of development of adverse reactions and complications due to vaccination, the authors conducted clinical and laboratory studies of 115 children aged 1 to 15 years with chronic pathology (allergic diseases, pyelonephritis, immunodeficiency states), vaccinated with diphtheria and tetanus toxoids and pertussis vaccine and diphtheria and tetanus-M anatoxin and revaccinated with diphtheria and tetanus-M anatoxin. The results of the study suggested the prognostic value of allergic reaction indicators (total IgE, DA- and CA-specific IgE, vaccine sensitization detected by the basophil degranulation test) against adverse events and complications of immunization. Vaccination in children with chronic pathology in the presence of higher parameters of allergic reactions, by using hyposensitization therapy, was followed by to the formation of tense antidiphtheria and antitetanus immunity. The given data support the immunological efficiency and safety of immunization of children with chronic diseases against diphtheria and tetanus provided that hyposensitization therapy is performed, by keeping in mind the results of prior clinical and laboratory studies.
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PMID:[Prognostic value of allergic reaction indicators in the vaccination of children with chronic diseases]. 2150 84

Porphyria cutanea tarda (PCT) is caused by inherited or acquired partial deficiency of the uroporphyrinogen-decarboxylase (Uro-D) enzyme activity. It is the most common form of porphyria. The main triggering factors to the development of porphyria cutanea tarda are alcohol, hepatitis C virus and human immunodeficiency virus. There are several reports of PCT associated with drugs, among them, antiretroviral therapy. We describe three HIV-positive patients, which showed photosensitivity as well as the emergence of tense blisters on sun-exposed areas during the use of highly active antiretroviral therapy (HAART) and discuss the possibility of PCT after the use of these drugs by those patients.
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PMID:HAART: a risk factor for development of porphyria cutanea tarda? 2329 85

Bullous lupus erythematosus is a rare variant of systemic lupus erythematosus (SLE) and is characterized by autoantibodies to type VII collagen. Co-existence of SLE and human immunodeficiency virus (HIV) infection is extremely rare; the development of bullous lupus in the setting of HIV has been, to our knowledge, reported in the literature only once. We describe a 26-year-old man with an 8-year history of HIV infection who developed bullous SLE. The patient presented with widespread, tense bullae as well as oral ulcerations. Clinical, laboratory, histological, and cutaneous immunofluorescence findings confirmed the diagnosis of bullous SLE. Given the immunological consequence of HIV infection, the co-occurrence of these two diseases would, theoretically, be unusual. Theories pertaining to the interplay of immunologic mechanisms of the seemingly paradoxical occurrence of autoimmunity in the setting of HIV infection are discussed.
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PMID:Bullous systemic lupus erythematosus in a patient with human immunodeficiency virus infection: a paradox of autoimmunity and immunodeficiency. 2524 71