Biomedical subjects
Publications and source records attributed to M Karaayvaz.
In this report we describe a female patient with a history of heparin allergy and recurrent urticaria lesions at definite locations where the heparin injections were administered previously.
Additives and preservatives in commercial foods have been implicated in the etiology of chronic urticaria, but such foods have not been widely accepted. In some countries, as in ours, people prefer to use home-made foodstuffs to avoid potentially hazardous commercial additives. However, not all home-made foodstuffs are safe, especially regarding allergies. In this report, we describe a patient with chronic urticaria due to home-made canned tomato prepared using "tomato drug" as a "safe (!)" additive.
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The etiology of chronic urticaria and angioedema remains uncertain in most of the patients. There are several agents and factors including medications, foods and food additives, infections, contactants, inhalants, physical factors and autoimmunity that implicated in provoking urticaria symptoms. In addition, the possible role of house dust mites has been considered in a few reports. We investigated skin test positivity to house dust mites and other inhalants in 259 patients with chronic idiopathic urticaria and angioedema but without allergic rhinitis and/or asthma. Results were compared with both 300 healthy controls and 300 atopic patients. Immediate cutaneous reactivity to one or more allergens was detected in 71 patients in the study group (27.4%). The most common allergens were house dust mites (24.7%). Skin prick test sensitivity to other inhalant allergens including pollens, molds and cockroach were 7.7%, 0.4% and 0.8%, respectively. In the healthy control group 7% of patients were found as atopic with respect to skin prick test results. The most common allergens in healthy controls were pollens (6%), and house dust mites (4.7%). In atopic control group, pollens and mites are also the most common allergens detected in skin prick test (62% and 50.3%, respectively). The difference between study and healthy control group was statistically significant with respect to presence of atopy and mite sensitivity (p < 0.001). Similar differences were not established in other inhalant allergens. Significant mite sensitivity in the study group is not a coincidence. Because, ratio of skin test positivity to house dust mites in the study group was higher than the healthy controls, but was not as high as atopic patients. Furthermore, the rate of skin reactivity to other aeroallergens was not different from healthy controls. Urticaria as a sole clinical manifestation in mite sensitive patients was unusual.
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BACKGROUND: Although several medications have been reported to cause fixed drug eruption (FDE) reactions, triamcinolone acetonide has not been previously described as an offending agent. OBJECTIVE: To emphasize both an unprecedented causative agent and the extraordinary development of a FDE, we describe this response in a 42-year-old female patient. METHODS: Because her history included a questionable reaction to corticosteroid preparations, prick and intradermal testing with triamcinolone acetonide was done to determine whether she could safely receive a triamcinolone acetonide injection. RESULTS: Both skin test procedures and the intra-articular administration of triamcinolone acetonide caused FDEs on her right retroauricular area. CONCLUSIONS: Because any drug may induce a FDE by any administration route, physicians should be aware of this delayed skin reaction when skin testing drugs.
This study aims to investigate possible effects of aspirin treatment on cellular oxidant/antioxidant system. In the first part of the study, 15 guinea pigs were given aspirin at three different doses (2200, 440 and 10 mg/kg/day) for 30 days and five were fed on the same diet without aspirin. After a month, animals were killed and their hearts were removed for use in analyses. In the other part, after fasting blood samples were obtained from 11 volunteer subjects, they were given aspirin (approximately 10 mg/kg/day) for 30 days and second blood samples were obtained after 1 month. Five volunteer subjects also participated as placebo control. Oxidant/antioxidant parameters, namely superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), catalase (CAT), malondialdehyde (MDA), nonenzymatic superoxide scavenger activity (NSSA), susceptibility to oxidation (SO) and antioxidant potential (AOP) values, were assayed in the samples. Antioxidant system was found to be impaired in the heart tissue from guinea pigs and in the erythrocytes from volunteer subjects. AOP and NSSA values were lower and MDA higher after aspirin treatment in both heart tissues and erythrocytes. In guinea pig heart tissue, SO was lower, but GSH-Px and CAT were unchanged after aspirin treatment. In human erythrocytes, SO was unchanged, but GSH-Px and CAT activities were increased after aspirin treatment. Changes in guinea pig heart tissues from animals treated with higher aspirin doses were more drastic relative to those of human erythrocytes, but no meaningful differences were observed between analysis parameters of control and lower-dose (10 mg/kg/day) aspirin-treated animals. Our results suggest that high-dose aspirin exerts significant toxicity to guinea pig myocardium and normal dose aspirin may cause peroxidation in the human erythrocytes due to its oxidant potential. We suppose that antioxidant supplementation may be beneficial for the people using aspirin for longer periods in order to prevent peroxidation damages.
Antioxidant defense capacity was investigated in myocardial tissue from guinea pigs treated with 5-fluorouracil (5-FU) at a dose of 400 mg/kg/d daily for 5 d administered intraperitonally. Treatment with 5-FU lowered the activities of cardiac superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) accompanied by higher catalase (CAT) activity. Further, antioxidant potential (AOP) values were lower but oxidation resistance (OR) and malondialdehyde (MDA) levels were higher in the 5-FU-treated tissue. With regard to myocardial iron (Fe) and copper (Cu) levels, no significant differences were found between the groups. Results suggest that 5-FU treatment causes impairment in the myocardial antioxidant defense system and leads to cardiac peroxidation. It has been postulated that these changes might be responsible for the 5-FU cardiotoxicity seen in some patients, and antioxidant therapy might provide a therapeutic advantage.
We believe this case represents a clear example of drug fever, and it appears to be the first report to implicate ketotifen as the responsible agent, confirmed with double rechallenge. The recognition of drug fever is clinically important. Failure to recognize the etiologic relationship between the drug and fever has unnecessary consequences, including extra testing, empiric therapy, and longer hospital stays. We suggest that ketotifen should be considered as a possible cause of fever in allergic patients receiving this drug.
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Primary small cell carcinoma of the esophagus is a rare tumour. A primary composite tumour of the esophagus is even rarer and only four cases had been reported in the literature up to August 1998. The definitive histogenesis of this tumour remains controversial in spite of the additional information provided by electron microscopy and immunohistochemistry. In the presented case, histologically, the tumour tissue was composed of two malignant components: approximately 50% of a moderately differentiated squamous cell carcinoma, and approximately 50% of a small cell carcinoma. A lot of morphological transition zones were observed between the squamous cell carcinoma components and the small cell carcinoma components in some areas in the squamous cell carcinoma component. Histochemically and immunohistochemically, the small cell carcinoma cells demonstrated argyrophil granules, and Cytokeratin and Chromogranin A reactivity, but the squamous cell carcinoma cells demonstrated only Cytokeratin reactivity. Negative reactivity for argentaffin granules, neuron-specific enolase and S-100 were observed in both the small cell carcinoma and the squamous cell carcinoma components. Histological, histochemical and immunohistochemical findings suggest that a primary composite tumour of the esophagus may be derived from a totipotent primitive cell in the basal region of the squamous mucosa of the esophagus. The patient received chemotherapy preoperatively but died one month after the initial diagnosis.
It has been discussed in several studies that non-immunologic factors, such as renin angiotensin aldosterone system (RAAS) may play a role in the pathophysiology of anaphylaxis. This study aimed to determine whether RAAS plays a part in the fall in blood pressure during drug reactions or not. Twenty patients who experienced hypotension during drug reaction and 15 healthy volunteers were enrolled in this study. None of the patients in the study or control groups were under treatment with any drug that was capable of influencing to RAAS. Serum levels of angiotensin-I (A-I), angiotensin-II (A-II), angiotensin converting enzyme (ACE) and aldosterone were measured in both study and control groups. The Mann-Whitney U test was used to compare the results of the groups. There were no statistically significant differences between the groups with respect to A-I, A-II, ACE and aldosterone levels. It was concluded that a fall in blood pressure during drug reaction must be the result of mast cell mediator effects on the vascular wall rather than RAAS impairment.
This study was performed to investigate the effect of lymphatic blockage on the amount of endotoxin in portal venous blood, nitric oxide synthesis, the release of aspartate aminotransferase (AST) from the liver, hepatic damage, and survival in an experimental model of dogs with peritonitis. The dogs were divided into a control group (group 1), an unligated thoracic duct peritonitis group (group 2), and a ligated thoracic duct peritonitis group (group 3). Peritoneal fluid and blood from the portal vein and femoral artery were taken for peritoneal culture, endotoxin, and AST assay, respectively, and liver biopsies were performed to assess for hepatic damage and for nitric oxide assay. There was a higher bacteria count in the peritoneal fluid from group 3 than in that from group 2 (P < 0.0001). Bacteria grew in all of the blood cultures from the group 2 animals, but growth was seen only in blood cultures from four of the group 3 animals. The levels of endotoxin, nitrite, and AST levels in group 3 were significantly increased in comparison with those in group 2 (P < 0.0001). Extensive hepatocellular necrosis with hemorrhage was observed in the livers of the group 3 animals, and all of them died within 48 h. The results of this study suggest that the blockage of lymph flow has a negative effect on liver and survival in dogs with peritonitis, and that hepatic damage is directly related to the amount of endotoxin to which the liver is exposed.
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OBJECTIVES: To establish the antioxidant status of rat intestinal tissues after ischemia-reperfusion and to determine if pretreatment with an allopurinol and antioxidant vitamin combination gives any protection against mucosal injury. EXPERIMENTAL ANIMALS: Twenty rats were divided into 4 groups of 5 animals each. METHODS: Group 1 (control) rats were not subjected to ischemia-reperfusion and received no allopurinol plus vitamin combination; group 2 rats received vitamins C (200 mg/kg) and E (100 mg/kg) and allopurinol (50 mg/kg) combination daily for 3 days preoperatively; group 3 rats were subjected to ischemia-reperfusion only; and group 4 rats were subjected to ischemia-reperfusion and received the vitamin and allopurinol combination. MAIN OUTCOME MEASURES: Activities of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and catalase (CAT) enzymes, the level of thiobarbituric acid-reagent substances (TBARS) and histologic grading of tissue samples. RESULTS: SOD and GSH-Px activities were decreased, but the CAT activity and TBARS level increased. Pretreatment of the rats with the allopurinol-vitamin C-vitamin E combination did not have any significant effect on the enzyme activities. However, it resulted in important reductions in the TBARS tissue levels. Histologic investigation revealed significant mucosal injury in group 3 rats compared with group 4 rats (mean [and standard deviation] for grading, 4.6 [0.5] versus 1.8 [0.4]). CONCLUSIONS: The enzymatic antioxidant defence system was significantly changed after ischemia-reperfusion and intestinal tissue was exposed to increased oxidant stress, the results of which were peroxidation of some cellular structures and increased concentrations of oxidative products. Although antioxidant treatment did not drastically affect the enzyme activities or afford complete protection of cellular structures against deformation, it apparently could eliminate oxygen radicals and prevent peroxidative reactions.
Infiltration of antitumor agents into subcutaneous tissues may either result in a local area of self-resolving inflammation or progress to full-thickness loss of skin and underlying vital structures. Inadvertent extravasation of adriamycin can result in severe tissue necrosis. The mechanism of this tissue damage is believed to be release of oxygen free radicals into the tissue. After adriamycin extravasation, the treatment groups were made up according to drugs used, EGb 761, pentoxifylline, alpha-tocopherol acetate, and alpha-tocopherol succinate in rats. To prevent the necrosis and to decrease the tissue malondialdehyde levels, the most effective agent was found to be EGb 761, and pentoxifylline was also effective (P < 0.001). No difference was found between topical lanoline and saline (P > 0.05). The maximum ulcer diameter was obtained in 2 weeks. The maximum tissue malondialdehyde levels were obtained in 24 h, and in comparison to the control group the treatment groups showed lower levels. Our aim is to show the role of free radicals in the formation of skin necrosis as a cause of adriamycin extravasation and to prevent or decrease the skin necrosis using various free radical scavengers.
We investigated the effectiveness of using an autologous vein graft and stent in the repair of large defects of the common bile duct (CBD) in a canine model. A 3-cm segment of the vena cephalica antibrachii and a 2-cm segment of the CBD were removed from eight healthy mongrel dogs with normal blood biochemistry levels. A stent was passed through the vein segment, and one end was introduced into the proximal end of the CBD while the other end was introduced into the distal end. The venous graft was then sutured to the CBD. A liver biopsy was taken for histopathological examination during laparotomy and relaparotomy. Blood samples were obtained on postoperative days 7, 14, and 20 for biochemical examination. The defect was effectively repaired by the autologous vein graft and stent in 7 dogs, after the exclusion of 1 dog that died of hemorrhage 3 days after the operation. No change in blood biochemistry was observed postoperatively, and no histopathological change in the liver was found in the preoperative or postoperative periods. These findings indicate that the use of an autologous vein graft and stent to repair CBD injuries may be a feasible and alternative method of treatment.
BACKGROUND: Anaphylaxis to topical application of rifamycin SV, which is used topically in the fields of surgery and dermatology, is rare. METHODS: We report two cases of systemic reactions occurring after local administration of rifamycin (Rifocine, Gruppo Lepetit, Italy). Both of them needed repeated intermittent topical applications. Skin prick tests with Rifocine constituents were performed on our patients, and also on ten atopic and ten nonatopic subjects. Although an old investigative tool, Prausnitz-Küstner (P-K) test was also performed on one of the patient's spouses to show passive transfer and the IgE-mediated mechanism. RESULTS: Allergy assessment with skin tests on the patients were negative for aeroallergens, latex, and Rifocine constituents (except rifamycin SV). The patients' prick tests with rifamycin SV were positive, and the control subjects were negative. P-K testing was positive. CONCLUSION: Two case reports support the existence of IgE-mediated reactions to rifamycin SV. IgE-mediated anaphylactic reactions from rifamycin SV appear to be extremely rare.