Gastric body diaphragm-like stricture as a rare complication of nonsteroidal anti-inflammatory drugs.

Increased risk due to nonsteroidal anti-inflammatory drugs (NSAIDs) therapy has been observed in patients. Although diaphragm-like stricture in the small bowel and colon induced by NSAIDs therapy has been rarely reported, gastric body diaphragm-like stricture has not been reported. We describe the first case of gastric body diaphragm-like stricture due to NSAIDs in a 44-year-old male patient who was successfully treated by an endoscopic approach to avoid complicated surgery. This case highlights new insight into the disadvantages of NSAIDs and provides new data for future clinical studies.

Influence of COX-inhibiting analgesics on the platelet function of patients with subarachnoid hemorrhage.

BACKGROUND: Platelet function of patients with subarachnoid hemorrhage (SAH) may play an important part in both rebleeding and delayed cerebral ischemia, but little is known about aggregation pathways during the acute phase of stroke. Analgesics are used regularly in the first days after bleeding, and some can potentially inhibit the cyclooxygenase (COX) enzyme. We examined the platelet function of patients with SAH in order to describe their basal situation and determine whether the administration of intravenous nonsteroidal antiinflammatory drugs (NSAIDs) affected platelet aggregation. METHODS: Arachidonic acid (AA)-induced aggregation and the platelet function analyzer (PFA)-100 test with collagen/epinephrine cartridges were used to study a group of SAH patients that was treated with dexketoprofen and dipyrone and to compare them to patients that had received no analgesia. RESULTS: Ninety-six consecutive SAH patients prospectively enrolled in platelet studies. Twenty-seven patients were taking NSAIDs (10 on dexketoprofen and 17 on dipyrone), and there were 15 cases in the control group. AA-induced aggregation was 10% ± 3.2% for NSAIDs (mean ± standard error), specifically 17.2% ± 7% for dexketoprofen and 5.7% ± 1% for dipyrone. Aggregation in the control group was 72.4% ± 6% (P = .001). Both analgesics slowed the platelet plug formation during the PFA-100 test, with closure times of 237.2 ± 25 seconds for dexketoprofen and 198.4 ± 22 seconds for dipyrone and 138.1 ± 21 seconds in controls (P = .02). CONCLUSIONS: The administration of COX-inhibiting analgesics leads to an hypoaggregability state in the first days of SAH. Further insight into their impact on complications such as rebleeding and delayed cerebral ischemia is needed in order to optimize the headache treatment of SAH.

A case of linear immunoglobulin A bullous dermatosis in a patient exposed to sun and an analgesic.

BACKGROUND: Medications are the most common triggers of linear immunoglobulin A bullous dermatosis (LABD). LABD induced by ultraviolet (UV) radiation has rarely been described. This article reports a case of LABD in a patient exposed simultaneously to an analgesic and UV radiation. CASE SUMMARY: A 45-year-old woman developed LABD lesions on sun-exposed skin after 3 days of sunbathing and consumption of a medication for headache containing propyphenazone, butalbital, and caffeine. The lesions spread to unexposed skin and, by day 5, the patient had vesicles and bullae on the palms and soles, face, trunk, and extremities. LABD was diagnosed with direct and indirect immunofluorescence microscopy and Western blot analysis. Treatment was successful with prednisone, started at a dosage of 1 mg/kg/d, for 5 months. Lesions located on sun-exposed areas, the absence of relapse for 5 years despite continuing sun exposure against medical advice, and subsequent avoidance of the suspected medication suggest that the bullous flare may have been due to the concomitant action of 2 triggers. That the analgesic had a role in this cutaneous manifestation is possible according to the Naranjo algorithm for adverse drug reactions. CONCLUSIONS: A case of LABD possibly associated with sun exposure and an analgesic is described. Treatment with prednisone successfully resolved the lesions in this patient.

Comparison of various doses of carbon 13-labeled aminopyrine for a carbon 13-labeled aminopyrine demethylation blood test in healthy dogs.

OBJECTIVE: To determine an optimal dose of carbon 13 ((13)C)-labeled aminopyrine for use in a (13)C-aminopyrine demethylation blood test in healthy dogs. ANIMALS: 9 adult dogs. PROCEDURES: Food was withheld from each dog for 12 hours. A 2-mL baseline blood sample was obtained from each dog and placed into an evacuated tube containing sodium heparin. Carbon 13-labeled aminopyrine was administered IV at doses of 1, 2, 5, or 10 mg/kg. Additional blood samples (2 mL) were obtained and placed into evacuated tubes containing sodium heparin 30, 45, 60, and 75 minutes after (13)C-aminopyrine administration. Hydrochloric acid was used to extract CO(2) from blood samples. The extracted gas was analyzed by fractional mass spectrometry to determine the percentage dose of (13)C administered as (13)C-aminopyrine and recovered in extracted gas (PCD). RESULTS: Gross evidence of clinical adverse effects was not detected in any dog after administration of (13)C-aminopyrine. The mean coefficient of variation (CV) for PCD was significantly lower than the mean CV for the summation of PCD values up to a given sampling time (CUMPCD). Mean PCD values among the 4 doses for each sample time were not significantly different. Administration of (13)C-aminopyrine at a dose of 2 mg/kg resulted in the lowest interindividual variability. CONCLUSIONS AND CLINICAL RELEVANCE: The PCD is superior to CUMPCD for the quantification of aminopyrine demethylation. Administration of (13)C-(13)C-aminopyrine at a dose of 2 mg/kg is appropriate for use in the (13)C-aminopyrine demethylation blood test in healthy dogs.

[The activity of enzymes and free radical oxidation in acute and chronic fetal hypoxia in general anesthesia during cesarean section]. / Aktivnostta na enzimite i svobodno-radikalnoto okislenie pri ostra i khronichna khipoksiia na ploda v usloviiata na obshta anesteziia pri tsezarovo sechenie.

The following study dwells on a basic problem in obstetrics anaesthesia. It shows a present view of the in NLA and ataractics having effect on free radical oxygenation process in mother-fetus system in Cesarean section. 101 pregnant women have been studied as the values of FROq serum antioxygenase activityq serum enzymes activity in women blood and in blood of umbilical cord have been compared.

Reactive metabolites and agranulocytosis.

Central to most hypotheses of the mechanism of idiosyncratic drug-induced blood dyscrasias is the involvement of reactive metabolites. In view of the reactive nature of the majority of such metabolites, it is likely that they are formed by, or in close proximity to the blood cells affected. The major oxidative system of neutrophils generates hypochlorous acid. We have demonstrated that the drugs associated with the highest incidence of agranulocytosis are oxidized to reactive metabolites by hypochlorous acid and/or activated neutrophils. There are many mechanisms by which such reactive metabolites could induce agranulocytosis. In the case of aminopyrine-induced agranulocytosis, most cases appear to involve drug-dependent anti-neutrophil antibodies, and these are likely to be induced by cell membrane antigens modified by the reactive metabolite of aminopyrine. The target of agranulocytosis associated with many other drugs is usually neutrophil precursors and may involve cytotoxicity or a cell-mediated immune reaction induced by a reactive metabolite. In the case of aplastic anaemia, there is evidence in some cases for involvement of cytotoxic T cells, which could either be induced by metabolites generated by neutrophils, or more likely, by reactive metabolites generated by stem cells.

[Amidazophen. Yes or no?]. / Amidazophen. Igen vagy nem?

The authors compare the side effects and hazards of the use of Paracetamol and Amidazophen on the basis of literary data. They draw the conclusion that in case of illnesses accompanied by fever, Amidazophen is preferable as an antifebrile, on both professional and cost-effectiveness grounds. This conclusion is supported by an acute tubularis necrosis case, where a direct link is suspected between the use of Paracetamol as an antifebrile and the development of kidney damage.

[Ergotamine-induced rectal stenosis in a patient with long-term migraine]. / Ergotamin-induzierte Rektumstenose bei einer Patientin mit langjähriger Migräne.

A 36 year old woman was admitted to our hospital for treatment of a high-grade rectal stenosis of unknown origin. She had a history of migraine going back 10 years. On intensive questioning she admitted using up to 5 ergotamine-containing suppositories a day. On the basis of history and clinical investigations the rectal stenosis must be connected with the abuse of ergotamine-containing suppositories. This case demonstrates that patients with an unexplained rectal syndrome should be asked for analgetics-containing suppositories specifically. Only discontinuation of treatment in time can preserve the patient from development of a rectal stenosis. In case of a rectal stenosis surgical treatment can be avoided by means of endoscopic controlled dilatation.

[A fatal thrombocytopenic hemorrhagiparous syndrome following aminophenazone in an infant]. / Sindrom hemoragipar trombocitopenic letal dupa aminofenazona la sugar.

A case of lethal thrombocytopenic purpura, with cutaneous and visceral haemorrhagic manifestations after the administration of aminophenazone suppositories in a suckling, without any intercurrent disease, is reported. General considerations regarding the action of some drugs, including aminophenazone, on blood platelets are made.

Drug-induced agranulocytosis. Peripheral destruction of polymorphonuclear leukocytes and their marrow precursors.

Drug-induced agranulocytosis is a highly individualized and unexpected reaction to specific drugs. It may be due to immunogenic or cytotoxic factors. Most instances are produced by a poorly understood immune response to immunogenic drugs. Others are associated with direct suppression of marrow committed stem cells by the direct action of the offending drug or its toxic metabolic end products. The early appearance of polymorphonuclear neutrophil (PMN) antibodies may offer an early warning to sensitized patients. Antibodies, if present, disappear shortly after the drug is discontinued. Agranulocytosis, due to direct action of the drug, is characterized by morphologic aplasia of marrow and is more likely to occur if the affected host has a concomitant defect in marrow cellular proliferation. Accumulation of toxic metabolic end products such as arene oxides may occur if the host is deficient in a microsomal system required to dispose of this material.