Risk factors for equine glandular and squamous gastric disease in show jumping Warmbloods.

BACKGROUND: Prevalence of, and risk factors for, equine squamous gastric disease (ESGD) are well established. Limited data exists on risk factors for equine glandular gastric disease (EGGD). OBJECTIVES: To identify management factors associated with EGGD in show jumping Warmbloods in training. A secondary objective was to identify management factors associated with ESGD. STUDY DESIGN: Cross-sectional. METHODS: Gastroscopies were performed in horses following a 12-16 h fast. Management questionnaires were collected for each horse. Risk factors were determined using multivariable logistic regression modelling. RESULTS: Eighty-three horses were included in the final analysis. Exercising ≥6 days per week increased the odds of EGGD grade ≥1/4 (odds ratio [OR] = 3.5; 95% confidence interval [CI] 1.2-10.7) compared to less frequent exercise. Currently showing increased the risk of EGGD grade ≥2/4 (OR = 10.2; 95% CI, 1.04-100), while competing at the international level decreased the odds of EGGD grade ≥2/4 (OR = 0.11; 95% CI, 0.01-0.97). Exercise intensity increased the odds of grade ≥1/4 ESGD (OR = 2.8; 95% CI, 1.03-7.8) and feeding beet pulp decreased odds (OR = 0.22; 95% CI, 0.07-0.7). Exercise intensity (OR = 3.8; 95% CI, 1.1-12.8) increased the likelihood of grade ≥2/4 ESGD and feeding beet pulp decreased the odds of grade ≥2/4 ESGD (OR = 0.1; 0.02-0.64) respectively. MAIN LIMITATIONS: This study used a convenience sample of horses within a relatively small (approximately 200 km) geographic radius. The sample size was relatively small, particularly within the international competition level group. CONCLUSIONS: Training and feeding strategies and competition level appear to influence the occurrence of EGGD and ESGD. Prospective studies evaluating the impact of training frequency, duration, and intensity on gastric physiology may clarify the role of exercise in gastric disease.

Phenylbutazone induces equine glandular gastric disease without decreasing prostaglandin E2 concentrations.

In equids, phenylbutazone at high doses induces gastric disease, primarily in the glandular portion of the stomach. However, the mechanism of nonsteroidal anti-inflammatory drug (NSAID)-induced gastric disease in horses has yet to be determined. While phenylbutazone-associated ulceration is often attributed to a decrease in basal gastric prostaglandins, this has not been demonstrated in the horse. Twelve horses were randomly assigned to treatment (n = 6; 4.4 mg/kg phenylbutazone PO in 20 ml molasses q 12 hr for 7 days) or placebo (n = 6; 20 ml molasses PO q 12 hr for 7 days) groups. Before treatment and 3 and 7 days after initiation of treatment, gastroscopy was performed and glandular gastric biopsies were collected and frozen at -80°C. Glandular disease was assessed on a scale of 0-4. Prostaglandin E2 concentrations in biopsies were measured using a commercially available enzyme-linked immunosorbent assay. All phenylbutazone-treated horses developed grade ≥2 glandular disease. Prostaglandin concentrations increased over time (p = .0017), but there was no effect of treatment (p = .49). These findings indicate that despite induction of glandular disease grade ≥2, phenylbutazone did not decrease basal glandular gastric prostaglandin E2 concentration.

Innovation in veterinary medical education: the concept of 'One World, One Health' in the curriculum of the Faculty of Veterinary Medicine at the University of Calgary.

'One World, One Health' is a foundation concept in veterinary medicine, much like comparative medicine. However, teachers of veterinary medicine often fail to identify it or speak of its importance within the veterinary curriculum. The resurgence of interest in the 'One World, One Health' concept aligns well with the underlying principles on which the University of Calgary Faculty of Veterinary Medicine (UCVM) has been newly founded. This concept is therefore a key component of the UCVM programme, and one that is well highlighted for those studying in the Doctor of Veterinary Medicine (DVM) course and graduate students.

The role of para-aminophenol in acetaminophen-induced methemoglobinemia in dogs and cats.

Acetaminophen (APAP) overdose in most species is associated with hepatotoxicity because of the metabolite N-acetyl-p-benzoquinoneimine (NAPQI). In dogs and cats, APAP overdose primarily causes methemoglobinemia and hemolysis. Although NAPQI has been proposed as the responsible intermediate in dogs and cats, it lacks chemical or pharmacokinetic characteristics that favor methemoglobin formation. We hypothesized that para-aminophenol (PAP) rather than NAPQI induces methemoglobinemia and that deficient arylamine N-acetyltransferase (NAT) activity in dogs and cats contributes to this species-dependent methemoglobinemia. Erythrocytes from dogs, cats, mice, and rats were exposed in vitro to APAP, NAPQI, and PAP. Only PAP induced methemoglobin and it induced more methemoglobin formation in dog and cat than rat and mouse erythrocytes. PAP also induced more methemoglobin in erythrocytes from Nat1/Nat2 knockout mice than wildtype (WT) mouse erythrocytes (P < 0.05), but less than in dog and cat erythrocytes (P < 0.01). APAP and PAP toxicity were compared in vivo in WT and Nat1/Nat2 knockout mice. APAP caused no hematotoxicity while PAP induced more methemoglobin in NAT1/NAT2 knockout mice than in WT mice (P < 0.05). These results support the hypothesis that PAP is the metabolite responsible for APAP-induced methemoglobinemia and that deficient NAT activity in dogs and cats contributes to this species-dependent toxicity.

Estrogen synthesis in the central nucleus of the amygdala following middle cerebral artery occlusion: role in modulating neurotransmission.

Stroke-induced lesions of the insular cortex in the brain have been linked to autonomic dysfunction (sympathoexcitation) leading to arrhythmogenesis and sudden cardiac death. In experimental models, systemic estrogen administration in male rats has been shown to reduce stroke-induced cell death in the insular cortex as well as prevent sympathoexcitation. The central nucleus of the amygdala has been postulated to mediate sympathoexcitatory output from the insular cortex. We therefore set out to determine if endogenous estrogen levels within the central nucleus of the amygdala are altered following stroke and if microinjection of estrogen into the central nucleus of the amygdala modulates autonomic tone. Plasma estrogen concentrations were not altered by middle cerebral artery occlusion (22.86+/-0.14 pg/ml vs. 21.24+/-0.33 pg/ml; P>0.05). In contrast, estrogen concentrations in the central nucleus of the amygdala increased significantly following middle cerebral artery occlusion (from 20.83+/-0.54 pg/ml to 76.67+/-1.59 pg/ml; P<0.05). Local infusion of an aromatase inhibitor, letrozole, into the central nucleus of the amygdala at the time of middle cerebral artery occlusion prevented the increase in estrogen concentration suggesting that this increase was dependent on aromatization from testosterone. Furthermore, bilateral microinjection of estrogen (0.5 microM in 200 nl) directly into the central nucleus of the amygdala significantly decreased arterial pressure and sympathetic tone and increased baroreflex sensitivity, and these effects were enhanced following co-injection with either an N-methyl-D-aspartate or non-N-methyl-D-aspartate receptor antagonist. Taken together, the results suggest that middle cerebral artery occlusion resulted in synthesis of estrogen within the central nucleus of the amygdala and that this enhanced estrogen level may act to attenuate overstimulation of central nucleus of the amygdala neurons to prevent middle cerebral artery occlusion-induced autonomic dysfunction.

Nitration and increased alpha-synuclein expression associated with dopaminergic neurodegeneration in equine pituitary pars intermedia dysfunction.

Equine pituitary pars intermedia dysfunction (PPID) is a spontaneously occurring progressive disease affecting aged horses and ponies. The pathogenesis of PPID is poorly understood, but the available evidence supports a loss of dopaminergic inhibition of the melanotropes of the pars intermedia. Horses with PPID have increased plasma concentrations of pars intermedia pro-opiomelanocortin-derived peptides that decrease in response to dopamine or dopamine agonist administration. Dopamine and dopamine metabolite concentrations are decreased in the pars intermedia of affected horses compared to age-matched control horses. Horses with disease that are treated with the dopamine agonist pergolide show improvement in clinical signs and normalisation of diagnostic test results. In the present study, immunohistochemical evaluation of pituitary and hypothalamic tissue demonstrated reduced tyrosine hydroxylase immunoreactivity in affected horses compared to age-matched and young controls, supporting the role of dopaminergic neurodegeneration in PPID. In addition, immunohistochemical evaluation revealed an increase in the oxidative stress marker, 3-nitrotyrosine and in nerve terminal protein, alpha-synuclein that colocalised in the pars intermedia of horses with disease. These findings suggest a role for nitration of overexpressed alpha-synuclein in the pathogenesis of neurodegeneration in PPID.

Liver histopathology and liver and serum alanine aminotransferase and alkaline phosphatase activities in epileptic dogs receiving phenobarbital.

Phenobarbital (PB) therapy is frequently associated with elevated serum alanine aminotransferase (ALT) and alkaline phosphatase (AP) activities in dogs without clinical signs of liver disease. The goal of this study was to determine if increased serum ALT and AP activities in clinically healthy PB-treated epileptic dogs are due to hepatic enzyme induction or to subclinical liver injury. Liver biopsies were obtained from 12 PB-treated dogs without clinical signs of liver disease but with elevated serum ALT and/or AP activities or both. Liver biopsies were obtained from eight healthy control dogs not receiving PB. Biopsies were evaluated histopathologically (all dogs) and liver homogenates were assayed for ALT (all dogs) and AP (six treated dogs, all controls) activities. As a positive control, liver cytochrome P4502B, an enzyme known to be induced by PB, was measured by benzyloxyresorufin-O-dealkylase activity and immunoblotting (five treated dogs, all controls). Serum AP isoenzyme analyses were performed. Results showed that ALT and AP activities in liver homogenates were not increased in treated dogs compared with controls, whereas the positive control for induction, CYP2B, was dramatically increased in treated dogs. Histopathological examination of liver biopsies revealed more severe and frequent abnormalities in treated dogs compared to controls, but similar types of abnormalities were found in both groups. Serum AP isoenzyme analyses in treated dogs demonstrated increased corticosteroid-induced and liver isoenzyme activities compared to controls. Results do not support induction of ALT or AP in the liver as the cause of elevated serum activities of these enzymes due to PB.

Reduction in infarct size by local estrogen does not prevent autonomic dysfunction after stroke.

Systemic estrogen administration in male rats has been shown to normalize the autonomic dysfunction and reduce the infarct size after permanent middle cerebral artery occlusion (MCAO). Therefore, the present investigation determined if local microinjection of estrogen at the site of the infarct also promoted recovery of autonomic function and reduction of the infarct size. Experiments were done in anesthetized (thiobutabarbitol sodium; 100 mg/kg) male Sprague-Dawley rats instrumented to record baseline and reflex changes in cardiovascular and autonomic parameters. The right middle cerebral artery was permanently occluded using bipolar coagulation. Local microinjection of estrogen into the insular cortex before MCAO significantly reduced the infarct size but did not attenuate the MCAO-induced autonomic dysfunction. Injection of ICI-182,780 alone significantly increased infarct area; however, the greater infarct area was not associated with enhanced autonomic dysfunction. These results suggest that within the insula, endogenous estrogen activity can affect the extent of MCAO-induced cell death, but extracortical central nervous system sites may be responsible for mediating the beneficial effects of estrogen on the autonomic disturbances.

Estrogen-induced recovery of autonomic function after middle cerebral artery occlusion in male rats.

Several studies have provided evidence to suggest that estrogen results in a significant reduction (approximately 50%) in the size of the ischemic zone in the middle cerebral artery occlusion (MCAO) model of stroke in a rat. The current study was done to demonstrate whether this estrogen-induced reduction in infarct size is associated with normalization of the autonomic dysfunction observed in an acute model of stroke in male rats. Experiments were done in anesthetized (thiobutabarbitol sodium; 100 mg/kg) male Sprague-Dawley rats instrumented to record baseline and reflex changes in cardiovascular and autonomic parameters. Estrogen was intravenously administered 30 min before, immediately before, or 30 min after MCAO. Estrogen administration resulted in a recovery of autonomic function and prevented the detrimental changes in autonomic tone observed following a stroke. In addition, infarct size was significantly increased in the presence of the estrogen antagonist ICI-182,780. These results suggest that both pre- or poststroke estrogen administration prevents or reverses acute stroke-induced autonomic dysfunction and that endogenous estrogen levels in males can contribute to this neuroprotection.

Effect of chronic exposure to excess dietary copper and dietary selenium supplementation on liver specimens from rats.

OBJECTIVE: To determine the effects of chronic exposure to excess dietary copper (Cu) on liver specimens from rats and the effects of dietary selenium (Se) supplementation in experimental Cu toxicosis. ANIMALS: 60 weanling male Fischer 344 rats. PROCEDURE: Rats were randomly assigned to 4 groups of 15 rats each and fed 1 of the following 4 diets: high Cu (500 microg/g)/adequate Se (0.2 microg/g); high Cu (500 microg/g)/supplemented Se (2 microg/g); adequate Cu (18 microg/g)/adequate Se (0.2 microg/g); or, adequate Cu (18 microg/g)/supplemented Se (2 microg/g). Five rats per group were euthanatized after 3, 6, and 12 months, and liver specimens were obtained for histologic examination, histochemistry, metal analysis by atomic absorption spectrophotometry, measurement of glutathione peroxidase activity, and assessment of lipid peroxidation, using quantification of malondialdehyde (MDA) by the thiobarbituric acid reaction. RESULTS: Hepatic Cu concentration was significantly higher in rats fed high Cu diets (range, 9 to 18 microg/g of tissue [wet weight]), compared with rats receiving adequate Cu diets (4.0 to 5.7 microg/g of tissue). Rats fed high-Cu diets for 3, 6, and 12 months had mild multifocal hepatitis often surrounding necrotic foci. However, an increase in hepatic MDA content, indicative of lipid peroxidation, was not detected in these rats. Development of morphologic changes was not prevented by use of dietary Se supplementation. CONCLUSION AND CLINICAL RELEVANCE: Long-term exposure to excess dietary Cu caused mild hepatic lesions in Fischer 344 rats. Dietary Se supplementation did not prevent hepatic damage in rats with Cu toxicosis.

Effect of lipopolysaccharide (LPS)-evoked host defense activation on hepatic microsomal formation and reduction of sulfamethoxazole hydroxylamine in the rat.

The incidence of adverse reactions to sulfamethoxazole-trimethoprim (SMX-TMP) combination products is higher in patients with AIDS than in the general population. Idiosyncratic adverse reactions to SMX are believed to be dependent upon the formation of the reactive intermediate, sulfamethoxazole hydroxylamine (SMX-HA), and its further oxidation product, nitroso-SMX. Changes in the disposition of SMX have been proposed to contribute to the increased risk of SMX adverse reactions in patients with AIDS. Activation of host defense mechanisms is known to alter drug metabolism and could decrease the enzymatic reduction of SMX-HA to the parent SMX, causing an imbalance in bioactivation and detoxification. We tested this hypothesis in a rat model of lipopolysaccharide (LPS)-evoked host defense activation. Rats were treated i.p. with 1 mg/kg of LPS, and hepatic microsomes were isolated 24 hr after treatment. The bioactivation of SMX to SMX-HA was reduced 50% by pretreatment with LPS (113 +/- 10 vs 65 +/- 4 pmol/min/mg; P < 0.05). However, the NADH-dependent reduction of SMX-HA to SMX was reduced by over 80% (454 +/- 90 vs 81 +/- 48 pmol/min/mg; P < 0.05). A decreased ability to reduce SMX-HA to SMX could predispose patients with systemic activation of host defense mechanisms, such as those with AIDS, to the occurrence of SMX-associated adverse reactions.

The failure of selenium supplementation to prevent copper-induced liver damage in Fischer 344 rats.

This study evaluates the ability of selenium (Se) supplementation to prevent experimental copper (Cu)-induced hepatocellular damage. Weanling male Fischer 344 rats were randomly assigned to groups of 15, 3 groups (A,B,C) were fed Cu-loaded diets (containing 2000 microg/g copper, added as CuSO4) and different levels of Se (added as Na2SeO3 x 5H2O) as follows: A) Cu-loaded/Se adequate diet (0.4 microg/g Se, fed basis); B) Cu-loaded/Se-supplemented diet (2 microg/g Se); and C) Cu-loaded/Se-deficient diet (< 0.2 microg/g). Three additional groups (D,E,F) were fed diets containing adequate levels of Cu (14 microg/g Cu, fed basis) and different levels of Se as follows: D) Cu-adequate/Se-adequate diet; E) Cu-adequate/Se-supplemented diet (2 microg/g Se); and F) Cu-adequate/Se-deficient (< 0.2 microg/g) diet. After 4, 8, and 12 weeks on the experimental diets, liver samples were processed for histology, histochemistry, metal analysis, glutathione peroxidase (GSH-Px) measurement, and quantification of malondialdehyde (MDA). Morphologic changes characteristic of Cu-associated hepatitis, without an increase in hepatic MDA levels, were seen in all Cu-loaded rats in each sampling. Similar changes occurred in rats fed Se-adequate, Se-supplemented and Se-deficient diets. This study demonstrates that Fischer 344 rats fed 2000 microg/g Cu develop morphologic changes due to Cu toxicity without evidence of lipid peroxidation. Furthermore, Se supplementation does not result in protection against Cu-induced liver injury.

Morphological and biochemical assessment of the liver response to excess dietary copper in Fischer 344 rats.

The aim of this study was to determine the amount of excess dietary copper (Cu) necessary to experimentally induce liver lesions characteristic of Cu-associated disease in Fischer 344 rats. Male weanling Fischer 344 rats of uniform age were divided into 6 groups (n = 5) and fed a rodent diet containing 18 (control), 750, 1000, 1250, 1500, and 2000 microg/g Cu added as CuSO4. Rats were euthanized after 3 months on the experimental diets and their livers processed for histology, histochemistry, Cu analysis (by atomic absorption spectrophotometry), and quantification of malondialdehyde (MDA) by the thiobarbituric acid reaction. Hepatic Cu levels were significantly higher (P < 0.01) in rats receiving over 1000 microg/g Cu compared to the controls (means for each diet: control = 4.8 microg/g, 750 microg/g Cu = 39.6 microg/g, 1000 microg/g Cu = 111.2 microg/g, 1250 microg/g Cu = 389 microg/g, 1500 microg/g Cu = 509.4 microg/g, and 2000 microg/g Cu = 766 microg/g). Histological lesions increased gradually according to the level of dietary Cu. Significant morphologic changes (necrosis, portal inflammation, hyaline remnants) and reduced growth rate occurred in rats receiving over 1250 microg/g Cu. However, no significant differences were found for MDA levels between groups. The present study demonstrates that compared to other species, very high levels of excess dietary Cu are needed to induce significant liver injury in Fischer 344 rats. Increased MDA content was not detected in rats with morphologic evidence of liver damage, suggesting that lipid peroxidation may not play a major role in this model of Cu toxicity.

Antigenicity and immunogenicity of sulphamethoxazole: demonstration of metabolism-dependent haptenation and T-cell proliferation in vivo.

Sulphamethoxazole has been associated with the occurrence of hypersensitivity reactions. There is controversy as to whether the immune response is metabolism-dependent or -independent. We have therefore investigated the site of antigen formation and the nature of the drug signal presented to the immune system in vivo. Male Wistar rats were dosed with sulphamethoxazole, sulphamethoxazole hydroxylamine or nitroso sulphamethoxazole. Antigen formation on cell surfaces was determined by flow cytometry using a specific anti-sulphamethoxazole antibody. Immunogenicity was determined by assessment of ex vivo T-cell proliferation. Administration of nitroso sulphamethoxazole, but not sulphamethoxazole or sulphamethoxazole hydroxylamine, resulted in antigen formation on the surface of lymphocytes, splenocytes and epidermal keratinocytes, and a strong proliferative response of splenocytes on re-stimulation with nitroso sulphamethoxazole. Rats dosed with sulphamethoxazole or sulphamethoxazole hydroxylamine did not respond to any of the test compounds. CD4+ or CD8+ depleted cells responded equally to nitroso sulphamethoxazole. The proliferative response to nitroso sulphamethoxazole was seen even after pulsing for only 5 min, and was not inhibited by glutathione. Responding cells produced IFN-gamma, but not IL-4. Haptenation of cells by sulphamethoxazole hydroxylamine was seen after depletion of glutathione by pre-treating the rats with diethyl maleate. Splenocytes from the glutathione-depleted sulphamethoxazole hydroxylamine-treated rats responded weakly to nitroso sulphamethoxazole, but not to sulphamethoxazole or sulphamethoxazole hydroxylamine. Dosing of rats with sulphamethoxazole produced a cellular response to nitroso sulphamethoxazole (but not to sulphamethoxazole or its hydroxylamine) when the animals were primed with complete Freund's adjuvant. These studies demonstrate the antigenicity of nitroso sulphamethoxazole in vivo and provide evidence for the role of drug metabolism and cell surface haptenation in the induction of a cellular immune response in the rat.

The diffusion of the health agenda and the fundamental need for partnership in medical education.

This paper explores the fundamental reasons for partnership in health care and medical education. It reviews the philosophical and policy contexts of health care trends and suggests that many of these trends can be summarized as a process of diffusion relating to: (a) what is on the health agenda, (b) who sets the health agenda and (c) the increasing indeterminacy of the health agenda. Various aspects of the 'social turn' in health care are introduced and offered as a partial explanation for the diffusion of the health agenda. Finally, some of the implications of these discussions for medical education are set out, in particular the need for partnerships within and beyond the academy.

Changes in serum thyroxine and thyroid-stimulating hormone concentrations in epileptic dogs receiving phenobarbital for one year.

A multicentric prospective study was conducted to monitor the effect of phenobarbital on serum total thyroxine (T4) and thyroid-stimulating hormone (TSH) concentrations in epileptic dogs. Serum T4 concentrations were determined for 22 epileptic dogs prior to initiation of phenobarbital therapy (time 0), and 3 weeks, 6 months, and 12 months after the start of phenobarbital. Median T4 concentration was significantly lower at 3 weeks and 6 months compared to time 0. Thirty-two percent of dogs had T4 concentrations below the reference range at 6 and 12 months. Nineteen of the 22 dogs had serum TSH concentrations determined at all sampling times. A significant upward trend in median TSH concentration was found. No associations were found between T4 concentration, dose of phenobarbital, or serum phenobarbital concentration. No signs of overt hypothyroidism were evident in dogs with low T4, with one exception. TSH stimulation tests were performed on six of seven dogs with low T4 concentrations at 12 months, and all but one had normal responses. In conclusion, phenobarbital therapy decreased serum T4 concentration but did not appear to cause clinical signs of hypothyroidism. Serum TSH concentrations and TSH stimulation tests suggest that the hypothalamic-pituitary-thyroid axis is functioning appropriately.

Pancreatitis associated with potassium bromide/phenobarbital combination therapy in epileptic dogs.

In a retrospective study, at least 10% of dogs receiving potassium bromide/phenobarbital combination therapy, compared with 0.3% of dogs receiving phenobarbital monotherapy, had probable pancreatitis. Pancreatitis may be a more frequent and more serious adverse effect of potassium bromide/phenobarbital combination therapy than has been reported previously.

The Long Evans Cinnamon (LEC) rat develops hepatocellular damage in the absence of antimicrosomal antibodies.

Long Evans Cinnamon (LEC) rats are an inbred strain with a mutation affecting a copper transporter. As a result, hepatic copper levels rise and the rats spontaneously develop hepatitis that is fatal in about 40% of the rats. The rats that die have been reported to develop anti-microsomal antibodies, most frequently against protein disulfide isomerase (PDI), prior to the onset of liver damage. The association between the presence of antibodies and death of the LEC rats, along with the detection of antibodies prior to the detection of liver damage suggested that the antibodies may have a role in the pathogenesis of liver damage. The objective of this study was to more clearly delineate the temporal relationship between antibody production and the onset of liver damage and copper accumulation. Serum was screened for the presence of anti-microsomal antibodies by immunoblotting. Liver damage was assessed by serum biochemistry and histological examination on rats between 6 and 12 weeks of age (four per group). Copper accumulation in the liver was determined by biochemistry and histological examination. Evidence of liver damage was detectable by serum biochemistry and histopathology by 11.5 weeks. Copper was rarely detected in hepatocytes, although it was detected in macrophages. Sera from only one of seven rats with evidence of liver damage had detectable anti-microsomal protein antibodies. The protein recognized was not PDI. The development of anti-microsomal autoantibodies did not precede the development of significant liver damage, suggesting that they play only a secondary role, if any, in the pathogenesis of hepatitis in this rat strain.

Sequential assessment of an antidrug antibody response in a patient with a systemic delayed-onset sulphonamide hypersensitivity syndrome reaction.

A 19-year-old man was treated with trimethoprim-sulphamethoxazole intermittently over 4 weeks. He developed a rash and fever. Despite treatment with low-dose methylprednisolone, his condition worsened. He developed a confluent erythematous macular eruption, elevated liver enzymes, lymphadenopathy, polyserositis and eosinophilia. A tentative diagnosis of sulphonamide hypersensitivity syndrome reaction (SHSR) was made and a serum sample (acute) was obtained to screen for antibodies associated with SHSR. Intravenous methylprednisolone sodium succinate (250 mg every 6 h for 48 h) was administered. The patient's condition improved, and he was discharged with oral prednisone. A convalescent serum sample was obtained 14 weeks later. By Western blotting and enzyme-linked immunosorbent assay (ELISA), antisulphamethoxazole IgG antibodies were detected in the acute serum sample, supporting the clinical diagnosis of SHSR. Contrary to expectations, antibodies were not detected in the convalescent serum sample by immunoblotting. Antisulphamethoxazole antibodies were detected by ELISA in the convalescent serum, but the titre was decreased approximately 45-fold. One possible explanation for the decrease in antibody concentration in the convalescent sample was the administration of high-dose glucocorticoids to the patient following collection of the acute serum sample.