Ménétrier-like disease in a Pointer with concurrent granulomatous gastritis, helicobacteriosis and leishmaniosis: a case report.

BACKGROUND: Ménétrier-like disease is a rare hypertrophic canine gastropathy, reported in only seven dogs. Clinical signs are vomiting, anorexia and weight loss. Macroscopically, giant cerebriform gastric mucosal folds are typically seen in the corpus and fundus of the stomach. Histopathologically, fundic mucous cell hyperplasia and loss of parietal and chief cells are typical. CASE PRESENTATION: A nine-year-old spayed female Pointer had a history of intermittent vomiting, marked weight loss and hypoalbuminaemia. A gastroduodenoscopy was performed three times within three months with macroscopic changes remaining the same. The gastric mucosa of the corpus, fundus and proximal antrum was markedly irregular, with cerebriform mucosal folds. In the first gastric biopsies, histopathology revealed a moderate granulomatous gastritis, with a severe manifestation of Helicobacter-like organisms. Treatment for Helicobacter spp. decreased the vomiting slightly. The dog was diagnosed with concurrent leishmaniosis; the conventional anti-Leishmania treatment decreased the vomiting moderately, the hypoalbuminaemia resolved and the dog gained weight back to a normal body condition. Granulomatous gastritis was not present in the gastric biopsies after these treatments. The dog increased vomiting when palliative treatment (maropitant citrate, ondansetron and esomeprazole) was discontinued, and thus, full-thickness biopsies of the stomach were taken and Ménétrier-like disease was diagnosed. The affected area was too large to be surgically removed; thus, palliative treatment was reinstated. The dog remained clinically well 39 months after the first clinical presentation. CONCLUSIONS: This is the first report of Ménétrier-like disease in a dog with a simultaneous manifestation of granulomatous gastritis, helicobacteriosis and leishmaniosis. The clinical signs decreased after treatment of helicobacteriosis and leishmaniosis, but vomiting remained probably as a sign of Ménétrier-like disease. Treatment options for dogs are surgical removal of the abnormal area or palliative treatment. In humans, promising results for a cure have been shown with cetuximab treatment, a human monoclonal antibody, but no canine antibody is commercially available yet. The dog here was doing well 39 months after first presentation, which is the longest reported survival time for Ménétrier-like disease with only palliative treatment in dogs. Full-thickness biopsies are preferred in macroscopic hypertrophic lesions of the stomach for better assessment of Ménétrier-like disease.

Urinary clusterin and cystatin B as biomarkers of tubular injury in dogs following envenomation by the European adder.

Diagnosing acute kidney injury remains a challenge since the established renal biomarkers, serum creatinine (sCr) and symmetric dimethylarginine (SDMA) reflect glomerular function and not tubular injury. Sensitive tubular markers such as urinary clusterin (uClust) and cystatin B (uCysB) have been proposed to detect AKI at an earlier stage. Since envenomation by the European adder (Vipera berus berus) could serve as a spontaneous disease model of AKI we investigated these new biomarkers in affected dogs. Concentrations of uClust and uCysB as well as sCr and SDMA were analyzed retrospectively in stored samples from 26 dogs with snake envenomation and 13 healthy controls. Higher concentrations of uClust (P < 0.012) and uCysB (P < 0.001) were observed in the snake-envenomed group. Normalization of uClust and uCysB to urinary creatinine did not alter the results. No differences were observed in sCr and SDMA between the snake-envenomed group and the healthy control group. Spearman rank correlation analysis revealed a strong association of uClust with uCysB in the snake-envenomed dogs (r = 0.75 P < 0.001) but not in the healthy controls. The high percentage of snake-envenomed dogs with increased uClust and uCysB concentrations in the absence of increased sCr and SDMA suggests renal tubular injury in the affected dogs. Larger prospective case-controlled studies are warranted to evaluate the clinical utility and prognostic value of these biomarkers.

Effects of oral versus parenteral cobalamin supplementation on methylmalonic acid and homocysteine concentrations in dogs with chronic enteropathies and low cobalamin concentrations.

The objective of this study was to compare the effects of parenteral (PE) versus oral (PO) cobalamin supplementation on serum methylmalonic acid (MMA) and homocysteine (HCY) concentrations in dogs with hypocobalaminaemia. Thirty-six dogs with serum cobalamin concentrations below 285ng/L (reference interval (RI): 244-959ng/L) were treated with PO (0.25-1.0mg daily) or PE cobalamin (0.25-1.2mg/injection) using a block-randomized schedule. Serum MMA and HCY concentrations were analysed at day 0, 28 and 90 after start of supplementation. There was no significant difference between the PO and PE group regarding serum MMA or HCY concentrations at any time point. Median (range, P comparing baseline and 28 days, P comparing 28days and 90 days) serum MMA concentrations (nmol/L; RI 415-1193) were 932 (566-2468) in the PO and 943 (508-1900) in the PE group at baseline, respectively, 705 (386-1465, P<0.0001) and 696 (377-932, P<0.0001) after 28 days, and 739 (450-1221, P=0.58) and 690 (349-1145, P=0.76) after 90 days. Serum HCY concentrations (median (range), P comparing baseline and 28 days, P comparing 28days and 90 days, µmol/L; RI 5.9-31.9) in the PO and PE groups were 12.2 (3.3-62.2) and 8.4 (3.7-34.8) at baseline, 12.5 (5.0-45.0, P=0.61) and 8.0 (3.8-18.3, P=0.28) after 28 days, and 17.7 (7.3-60.0 P=0.07) and 12.4 (6.3-33.1, P=0.0007) after 90 days, respectively. Oral and parenteral cobalamin supplementation had the same effect on serum MMA concentrations in this group of dogs.

Effects of dexmedetomidine and MK-467 on plasma glucose, insulin and glucagon in a glibenclamide-induced canine hypoglycaemia model.

The commonly used sedative α2-adrenoceptor agonist dexmedetomidine has adverse cardiovascular effects in dogs that can be prevented by concomitant administration of the peripherally acting α2-adrenoceptor antagonist MK-467. An ancillary effect of dexmedetomidine is to decrease insulin release from the pancreas, whereas MK-467 stimulates insulin release. This study assessed the effects of co-administered dexmedetomidine and MK-467 in a canine glibenclamide-induced hypoglycaemia model. In a randomised, cross-over experiment, eight beagle dogs received five intravenous treatments, comprising two administrations of saline, with dexmedetomidine or dexmedetomidine and MK-467, and three administrations of glibenclamide, with saline, dexmedetomidine or dexmedetomidine and MK-467. Plasma concentrations of glucose, lactate, insulin, glucagon and the test drugs were monitored. Administration of glibenclamide significantly increased insulin secretion and decreased blood glucose concentrations. Dexmedetomidine counteracted glibenclamide-evoked hypoglycaemia. This was opposed by the α2-adrenoceptor antagonist MK-467, but the glibenclamide-evoked hypoglycaemia was not potentiated by co-administration of dexmedetomidine and MK-467. None of the dogs developed uncontrolled hypoglycaemia. Thus, the combination of dexmedetomidine and MK-467 appeared to be safe in this canine hypoglycaemia model. Nevertheless, when MK-467 is used to alleviate the undesired cardiovascular effects of α2-adrenoceptor agonists in dogs, it should be used with caution in animals at risk for hypoglycaemia because of its insulin-releasing and hypoglycaemic effects.

Comparison of efficacy of oral and parenteral cobalamin supplementation in normalising low cobalamin concentrations in dogs: A randomised controlled study.

The aim of this study was to compare the efficacies of parenteral and oral cobalamin supplementation protocols in dogs with chronic enteropathies and low cobalamin concentrations. It was hypothesised that both treatments would increase serum cobalamin concentrations significantly. Fifty-three dogs with chronic enteropathies and serum cobalamin concentrations<285ng/L (reference interval 244-959ng/L) were enrolled. Dogs were randomised to treatment with either daily oral cobalamin tablets (0.25-1.0mg cyanocobalamin daily according to body weight) or parenteral cobalamin (0.4-1.2mg hydroxycobalamin according to body weight). Serum cobalamin concentrations were analysed 28±5days and 90±15days after initiation of supplementation. After 28 days, all dogs had serum cobalamin concentrations within the reference interval or above. In the parenteral group (n=26), median (range) cobalamin concentrations were 228 (150-285) ng/L at inclusion, 2107 (725-10,009) ng/L after 28days and 877 (188-1267) ng/L after 90 days. In the oral group (n=27), median (range) serum cobalamin concentrations were 245 (150-285) ng/L at inclusion, 975 (564-2385) ng/L after 28days and 1244 (738-4999) ng/L after 90 days. In both groups, there were significant differences in serum cobalamin concentrations between baseline and 28 days, and between 28days and 90days (P<0.001). In conclusion, both parenteral and oral cobalamin supplementation effectively increase serum cobalamin concentrations in dogs with chronic enteropathies and low cobalamin concentrations.

Antihistone Autoantibodies in Dobermans With Hepatitis.

BACKGROUND: Immune system involvement is suggested as an underlying cause for Doberman hepatitis (DH) based on female predisposition, lymphocyte infiltration, abnormal hepatocyte expression of major histocompatibility complex class II antigens, and homozygosity for dog leukocyte antigen DRB1*00601. OBJECTIVE: To measure serum antinuclear antibodies (ANA) and serum antihistone antibodies (AHA) in Dobermans with hepatitis. To determine whether increased serum ANA or serum AHA could be used to support the diagnosis of Doberman hepatitis (DH). ANIMALS: Privately owned 25 subclinically and 13 clinically affected DH Dobermans and 17 healthy control Dobermans. METHODS: Case-control study. Indirect immunofluorescence (IIF) microscopy and line blot tests were employed for the ANA pilot studies and an enzyme-linked immunosorbent assay (ELISA) assay for detection of IgG AHA. RESULTS: Indirect immunofluorescence revealed ANA-positive cases, and line blot showed AHA reactivity. In ELISA, importantly increased concentrations of AHA were found in 92% (23/25) of dogs in the subclinical stage and 84.6% (11 of 13) of dogs in the clinical stage of DH compared with no control dogs (0/17) (P < 0.0005). The mean AHA absorbance values of the blood samples obtained from the 25 subclinical DH dogs (1.36 ± 0.60, mean ± SD) and the 13 clinically affected dogs (1.46 ± 0.49) were significantly higher than in 17 control dogs (0.51 ± 0.18; P < 0.0001). CONCLUSIONS AND CLINICAL IMPORTANCE: As the presence of AHA indicates autoimmune activity, our results favor an autoimmune background as one cause for DH. Antihistone antibody could represent a novel means for screening Dobermans with increased serum alanine transaminase concentrations and suspicion of DH.

Identification of Glyceraldehyde-3-Phosphate and Alcohol Dehydrogenases as Autoantigens in Doberman Hepatitis.

An autoimmune background is suspected for Doberman hepatitis (DH). It is based on the finding of mononuclear cell infiltrates in the liver, strong female bias, association to the homozygous risk factor dog leucocyte antigen (DLA) allele DRB1*00601 and aberrant major histocompatibility complex (MHC) class II expression on hepatocytes that correlates with the degree of inflammation in the liver. The aim of this study was to search for autoantibodies against liver-related antigens associated with DH. Twenty-five Dobermans with subclinical DH (SDH), 13 that clinically manifest DH (CDH) and 17 healthy controls were studied. Immunoblotting analysis detected specific antibodies in the DH sera. By mass spectrometry the targets were identified as liver-related enzymes glyceraldehyde-3-phosphate dehydrogenase (GAPDH) and alcohol dehydrogenase (ADH). Using ELISA, anti-GAPDH IgG was detected in 36% (9/25) of SDH dogs and 69.2% (9/13) of the CDH dogs compared to healthy controls (0/17) (P < 0.0005). Anti-ADH IgG was detected in 72% (18/25) of SDH dogs and 76.9% (10/13) of CDH dogs and only in one (1/17) control (P < 0.0005). The finding of novel autoantigens, GAPDH and ADH strengthen the hypothesis that DH is an autoimmune disease of the liver. These findings suggest that DH could be diagnosed by screening for autoantibodies against the defined antigens.

Evaluation of a transcutaneous method to assess canine liver function by indocyanine green plasma disappearance rate in healthy adult Beagle dogs.

A non-invasive, transcutaneous method using near infrared spectroscopy to assess indocyanine green plasma disappearance rate (ICG-PDR) in healthy dogs subjected to different conditions was evaluated in eight healthy purpose-bred Beagles under isoflurane-anaesthesia (Trial 1) and when they had initially recovered from anaesthesia (Trial 2). Plasma ICG concentrations (0, 5, 10, 15, 30 min after rapid ICG injection (0.5 mg/kg) into a peripheral vein were determined by high-performance liquid chromatography in parallel with transcutaneous measurements. ICG clearance (mL/min/kg) and retention rate after 15 min (R15, %) were calculated from plasma concentrations to be 3.09 ± 0.83 (mean ± SD) and 30.6 ± 8.3 in anaesthetised dogs and 3.63 ± 0.88 and 28.1 ± 7.3 in recovering dogs, respectively. ICG-PDR (%/min) and R15 (%) obtained using the transcutaneous method were 7.11 ± 3.18 and 34.6 ± 12.4 (Trial 1) and 7.79 ± 3.33 and 32.3 ± 9.2 (Trial 2). The coefficients of determination (r(2)) for ICG clearance and ICG-PDR were 0.14 (Trial 1) and 0.81 (Trial 2) and 0.47 (Trial 1) and 0.29 (Trial 2) for R15, respectively. The mean bias (lower, upper limit of agreement) for R15 were 5.6 (-12.3, 23.5) (Trial 1) and 3.9 (-12.4, 20.1) (Trial 2). The results suggest good agreement between the two methods in dogs recovering from isoflurane-anaesthesia and the transcutaneous method might be useful in real-time assessment of liver function in conscious dogs.

Oral Cobalamin Supplementation in Dogs with Chronic Enteropathies and Hypocobalaminemia.

BACKGROUND: Cobalamin deficiency is commonly associated with chronic enteropathies (CE) in dogs and current treatment protocols recommend parenteral supplementation. In humans, several studies have reported equal efficacy of oral and parenteral cobalamin administration of cobalamin. OBJECTIVES: To retrospectively evaluate whether oral cobalamin supplementation can restore normocobalaminemia in dogs with CE and hypocobalaminemia. ANIMALS: Fifty-one client-owned dogs with various signs of CE and hypocobalaminemia. MATERIAL AND METHODS: Retrospective study based on a computerized database search for dogs treated at Evidensia Specialist Animal Hospital, Helsingborg, Sweden during January 2012-March 2014. Inclusion criteria were dogs with signs of CE, an initial serum cobalamin ≤270 ng/L (reference interval: 234-811 ng/L) and oral treatment with cobalamin tablets. Serum cobalamin for follow-up was analyzed 20-202 days after continuous oral cobalamin supplementation started. RESULTS: All dogs became normocobalaminemic with oral cobalamin supplementation. The mean increase in serum cobalamin concentration after treatment was 794 ± 462 ng/L. Serum cobalamin concentrations were significantly higher after supplementation (mean 1017 ± 460 ng/L; P < .0001) than at baseline (mean 223 ± 33 ng/L). CONCLUSION AND CLINICAL IMPORTANCE: Our results suggest that oral cobalamin supplementation is effective in normalizing serum cobalamin concentrations in dogs with CE. Prospective studies comparing cellular cobalamin status in dogs being treated with parenteral versus oral cobalamin supplementation are warranted before oral supplementation can be recommended for routine supplementation.

Evaluation of DLA promoters in Doberman hepatitis.

Doberman hepatitis (DH) is associated with homozygous DLA-DRB1*00601/DQA1*00401/DQB1*01303 indicating a role for the immune system in the development of the disease. The dog leucocyte antigen (DLA) class II expression is controlled at the transcriptional level with proximal promoters. Differential expression of DLA class II molecules of antigen-presenting cells is reported to affect susceptibility to or protection from different immune-mediated diseases. The aim of this study was to evaluate, whether the variation in promoter areas of homozygous DLA-DRB1*00601/DQA1*00401/DQB1*01303 Dobermans could explain why some dogs become afflicted with DH and others do not. Our findings suggest that promoter variants are not associated as risk modifiers in homozygous DLA-DRB1*00601/DQA1*00401/DQB1*01303 Dobermans, but additional factors are needed. Nevertheless, our study indicates that the whole DLA block is associated to the disease.

Association of Doberman hepatitis to canine major histocompatibility complex II.

Doberman hepatitis (DH) is a chronic and progressive inflammatory liver disease that mainly affects female dogs. The high incidence of chronic hepatitis in Dobermans is suggestive of a genetic predisposition. DH is characterized by mononuclear cell infiltration and copper accumulation in the liver and major histocompatibility complex (MHC) class II antigen expression in the hepatocytes. In dogs, the MHC is referred to as the dog leukocyte antigen (DLA) system. In this study, the potential role of DLA genes in DH was investigated by sequence-based typing in the exon 2 of DLA-DRB1, -DQA1 and -DQB1. The case group comprised 37 Dobermans with subclinical or clinical DH. The control group consisted of 37 healthy Dobermans, with normal liver enzyme values and without immunosuppressive medication. The control dogs were over 10 years old to include dogs with the lowest genetic risk of DH. Our results indicate that Dobermans with homozygous DLA-DRB1*00601/DQA1*00401/DQB1*01303 [odds ratio (OR) = 14.9, confidence limit (CL) = 3.1-71.7, P < 0.00005], especially with homozygosity for DLA-DRB1*00601 (P < 0.0005), are susceptible to DH. The DQ heterodimer DLA-DQA1*00901/DQB1*00101 and the allele DLA-DRB1*01501 appear to confer protection against DH (P < 0.001). Allele and haplotype frequencies were compared using chi-squared statistics. The disease shows a complex pattern of inheritance, but the observed DLA class II association with DH suggests a role for the immune system in the development of the disease.

Radioiodine treatment of feline hyperthyroidism in Germany.

AIM: Establishment of radioiodine treatment of feline hyperthyroidism in veterinary routine in accordance with German radiation protection regulations. PATIENTS AND METHODS: 35 cats with proven hyperthyroidism were treated with 131I in a special ward. Thyroid uptake and effective halflife were determined using gammacamera dosimetry. Patients were released when measured whole body activity was below the limit defined in the German "Strahlenschutzverordnung". RESULTS: 17/20 cats treated with 150 MBq radioiodine and 15/15 cats treated with 250 MBq had normal thyroid function after therapy, normal values for FT3 and FT4 were reached after two and normal TSH levels after three weeks. In 14 cats normal thyroid function was confirmed by controls 3-6 months later. Thyroidal iodine uptake was 24 +/- 10%, effective halflife 2.5 +/- 0.7 days. Whole body activity < 1 MBq was reached 13 +/- 4 days after application of 131I. Radiation exposure of cat owners was estimated as 1.97 microSv/MBq for adults. CONCLUSION: Radioiodine therapy of feline hyperthyroidism is highly effective and safe. It can easily be performed in accordance with German radiation protection regulations, although this requires hospitalisation for approximately two weeks. Practical considerations on radiation exposure of cat owners do not justify this long interval. Regulations for the veterinary use of radioactive substances similar to existing regulations for medical use in humans are highly desirable.

An immunoassay for canine pancreatic elastase 1 as an indicator for exocrine pancreatic insufficiency in dogs.

The detection of pancreatic elastase 1 in stool samples has become the noninvasive gold standard for the diagnosis of pancreatic insufficiency in humans. Accordingly, the development of a sandwich-ELISA specific for canine pancreatic elastase 1, based on monoclonal antibodies, is presented here. The test has a detection range of 4-240 microg canine pancreatic elastase l/g feces. The intraassay coefficient of variation is 7.4%, and the interassay coefficient of variation is 7.7%. Spiking experiments show that canine elastase 1 is quantitatively detectable in fecal samples. Interestingly, the range of the elastase 1 concentration in canine feces within several days is higher as compared with humans. As the proposed cutoff of 10 microg/g is below this variation range in 96.1% of the tested samples, the effect on the test specificity is negligible. Because the test detects neither human nor bovine and porcine elastase 1, pancreatic function can be monitored without interrupting an enzyme replacement therapy.

Zoonotic potential of Enterocytozoon bieneusi.

The reservoirs and the modes of transmission of the most frequent microsporidial species in humans, Enterocytozoon bieneusi, are still unknown. We have examined fecal samples of 26 humans and 350 animals from 37 species to find 18 samples containing this parasite from humans, cats, pigs, cattle, and a llama. Genotypic characterization of the internal transcribed spacer of the rRNA gene resulted in 14 different genotypes, 6 of them previously undescribed. Phylogenetic analysis revealed the lack of a transmission barrier between E. bieneusi from humans and animals (cats, pigs, and cattle). Thus, E. bieneusi appears to be a zoonotic pathogen.

Serum feline trypsin-like immunoreactivity following administration of ceruletide to healthy cats.

OBJECTIVE: To determine changes in serum feline trypsin-like immunoreactivity (fTLI) in response to administration of ceruletide to healthy cats. ANIMALS: 11 healthy cats. PROCEDURES: Serum fTLI was determined, using a radioimmunoassay, before and 10, 20, 30, 40, and 50 minutes after IM administration of ceruletide (0.3 mg/kg [0.14 mg/lb]). RESULTS: Mean +/- SD baseline serum fTLI was 23.1 +/- 4.1 mg/L. There was a statistically significant, but clinically unimportant, increase in serum fTLI 10 and 30 minutes after ceruletide administration. CONCLUSIONS AND CLINICAL RELEVANCE: In healthy cats, administration of ceruletide induced a statistically significant, but clinically unimportant, increase in serum fTLI. Whether responses in cats with exocrine pancreatic disorders would be different is unknown, but results suggest that a ceruletide stimulation test would likely not be useful for differentiating between healthy cats and cats with subclinical chronic exocrine pancreatic disorders.

A novel locus (DFNA23) for prelingual autosomal dominant nonsyndromic hearing loss maps to 14q21-q22 in a Swiss German kindred.

DFNA23, a novel locus for autosomal dominant nonsyndromic hearing loss, was identified in a Swiss German kindred. DNA samples were obtained from 22 family members in three generations: 10 with hearing impairment caused by the DFNA23 locus, 8 unaffected offspring, and 4 spouses of hearing-impaired pedigree members. In this kindred, the hearing-impaired family members have prelingual bilateral symmetrical hearing loss. All audiograms from hearing-impaired individuals displayed sloping curves, with hearing ability ranging from normal hearing to mild hearing loss in low frequencies, normal hearing to profound hearing loss in mid frequencies, and moderate to profound hearing loss in high frequencies. A conductive component existed for 50% of the hearing-impaired family members. The majority of the hearing-impaired family members did not display progression of hearing loss. The DFNA23 locus maps to 14q21-q22. Linkage analysis was carried out under a fully penetrant autosomal dominant mode of inheritance with no phenocopies. A maximum multipoint LOD score of 5.1 occurred at Marker D14S290. The 3.0-LOD unit support interval is 9.4 cM and ranged from marker D14S980 to marker D14S1046.

A novel locus (DFNA24) for prelingual nonprogressive autosomal dominant nonsyndromic hearing loss maps to 4q35-qter in a large Swiss German kindred.

Nonsyndromic hearing loss is one of the most genetically heterogeneous traits known. A total of 30 autosomal dominant nonsyndromic hearing-loss loci have been mapped, and 11 genes have been isolated. In the majority of cases, autosomal dominant nonsyndromic hearing loss is postlingual and progressive, with the exception of hearing impairment in families in which the impairment is linked to DFNA3, DFNA8/12, and DFNA24, the novel locus described in this report. DFNA24 was identified in a large Swiss German kindred with a history of autosomal dominant hearing loss that dates back to the middle of the 19th century. The hearing-impaired individuals in this kindred have prelingual, nonprogressive, bilateral sensorineural hearing loss affecting mainly mid and high frequencies. The DFNA24 locus maps to 4q35-qter. A maximum multipoint LOD score of 11.6 was obtained at 208.1 cM at marker D4S1652. The 3.0-unit support interval for the map position of this locus ranges from 205.8 cM to 211.7 cM (5.9 cM).

[Determination and clinical relevance of fecal pancreatic elastase in dogs]. / Die Bestimmung und klinische Relevanz der fäkalen pankreatischen Elastase beim Hund.

The determination of faecal pancreatic elastase 1 is a reliable test for the diagnosis of chronic pancreatic diseases in man due to its high sensitivity and specificity (93%). A clinical study was performed to investigate the detectability of canine faecal pancreatic elastase with polyclonal anti human pancreatic elastase 1 antibodies in 52 dogs with chronic diarrhoea and weight loss. To assess the diagnostic value of this parameter for the diagnosis of exocrine pancreatic insufficiency (EPI) in dogs faecal chymotrypsin activity was determined and serum trypsin-like immunoreactivity (TLI) concentration was measured within the Ceruletid test in all patients. The study revealed that canine faecal pancreatic elastase cross reacts with polyclonal anti human pancreatic elastase 1 antibodies. In comparison with the results of the other pancreas tests it was proved that the concentration of canine faecal pancreatic elastase determined by rocket immunoelectrophoresis is highly sensitive for EPI in dogs (sensitivity 100%) but there are species differences in specificity between man and dog (specificity 56.5%).

Genetic diseases of hearing.

The study of genetic hearing loss has always been hindered by the difficulty of separating sporadic genetic cases from cases affected by environmental influences. This is because audiologic methods are largely insensitive to causes, and the anatomical location of the affected structures in the middle and inner ear makes histopathologic verifications difficult. With recent progress in genetic investigation, eg, the mapping of the gene location for the Waardenburg and Usher syndromes, both syndromic and nonsyndromic genotypes have been elucidated in humans and in animal models. In the future, molecular genetics will play an increasingly important role in the genetic counseling of suspected carriers, as well as in the prevention of additional hearing loss from exogenic causes (noise, ototoxic drugs) in confirmed cases of genetically vulnerable ears.

[Hearing aid rehabilitation of hearing disorders in adults]. / Apparative Rehabilitation von Hörstörungen bei Erwachsenen.

Hearing-aid provision is still partly a medical task, in spite of technological progress and a confusing variety of types and models of devices. The diagnosis of the underlying disease, the appreciation of the consequences of hearing loss and the counseling of the hearing impaired person are prerequisites of the treatment. The physician should try to determine the etiology of the hearing loss. Also, a state-of-the-art otologic examination should be performed and the physician should be sensitive to the psychological and social consequences of the patient's hearing loss. For the assessment of fitted hearing aids, basic knowledge of the technical background is required. To measure hearing-aid benefit in the ENT office, suprathreshold and speech audiometry are indispensable tools.