OBJECTIVE To perform a retrospective, multicenter observational study that compares the agreement of rectal temperature with the temperature measured with noncontact infrared thermometer (NCIT) in a population of dogs and cats. Animals 168 dogs and 61 cats. PROCEDURES NCIT readings were taken in triplicate from the medial pinna, then rectal temperature was taken with a standard digital rectal thermometer (RT). Ambient room temperature, signalment, presence of icterus, skin and coat color, reason for presentation, and final diagnosis were recorded. RESULTS In dogs, median (range) body temperature reflected by RT and NCIT measurements was 38.4 °C (33.4 to 40.3 °C) and 36.3 °C (30.8 to 40.0 °C), respectively. In cats, median (range) body temperature reflected by RT and NCIT measurements was 38.3 °C (36.2 to 40.0 °C) and 35.7 °C (31.8 to 38.0 °C), respectively. There was a weak positive correlation between body temperatures measured by NCIT and RT in dogs (Kendall tau = 0.154), but there was no correlation in cats (Kendall tau = –0.01). A significant, albeit weak, agreement was seen between temperature measured by NCIT and RT in dogs (Kappa value, 0.05), but not cats (Kappa value, –0.08). In both species, NCIT tended to underread body temperature, compared with RT (dogs: mean ± SD bias –2.2 ± 1.51 °C; cats: mean bias –2.7 ± 1.44 °C), with the degree of low measurements lessening as body temperature increased. CLINICAL RELEVANCE Given both poor correlation and agreement in body temperature measured by NCIT and rectal thermometer, NCIT measurements cannot be recommended at the current time as a means to determine body temperature in dogs and cats.
Objective: To describe the clinical presentation and management of a critically ill dog with profound renal tubular acidosis (RTA) with proximal and distal renal tubular dysfunction.Case Summary: A 3-year-old neutered female Border Terrier was presented with frequent regurgitation resulting from acute pancreatitis with severe ileus. Venous acidbase analysis and complete urinalysis confirmed the presence of normal anion gap metabolic acidosis with inappropriately alkaline urine (pH 8), consistent with distal RTA. Urinalysis, urine amino acids, and urinary fractional excretion of electrolytes revealed glycosuria (with normoglycemia), aminoaciduria, and increased fractional excretion of sodium, calcium, and phosphate consistent with generalized proximal renal tubulopathy or Fanconi syndrome. The dog responded well to supportive care and alkaline therapy and made a complete recovery.
We examined attitudes regarding genetic testing and psychosocial outcomes of HFE genotyping for hemochromatosis. A total of 87 persons with hemochromatosis (patients) (39 women, 48 men), who underwent HFE genotyping, and 50 persons with hypertension (controls) (22 women, 28 men), who had not undergone HFE genotyping, completed a structured interview in which they reported attitudes about benefits and disadvantages of genetic testing and their understanding of genetics and hemochromatosis. Among patients, adherence to treatment for hemochromatosis was assessed. Controls estimated the likelihood of experiencing several potential positive and negative psychosocial outcomes after a positive genetic test. Patients reported their experience pertinent to these outcomes. Patients received information about hemochromatosis when they were diagnosed, and controls read a brief description of hemochromatosis before answering questions. Patients correctly answered 65% of knowledge questions and controls correctly answered 59%. Most participants believed genetic testing is beneficial and described few negative aspects of testing. Controls expected to experience more anxiety, depression, and anger related to a positive genetic test than was reported by patients (p < 0.001). One patient reported discrimination related to the HFE genotype. Most patients were compliant with the iron depletion and maintenance phases of treatment for hemochromatosis. Race, sex, marital status, income, education, barriers to treatment, and knowledge were not significantly associated with adherence to maintenance phlebotomy. We conclude that HFE genotyping appears to be viewed positively and would be generally accepted were it offered as part of a screening program for hemochromatosis. Persons who have not undergone genetic testing may overestimate their emotional responses to a positive test result. In the present hemochromatosis patients, few reported that HFE genotyping was accompanied by negative psychosocial outcomes.
Hereditary hemochromatosis (HH) is a common iron overload (IO) disorder of people of western European descent. HH, defined using biochemical criteria, occurs in 0.2%–0.5% of US whites. Some HH patients absorb excessive dietary iron and develop consequent liver fibrosis and cirrhosis, hepatocellular carcinoma, diabetes mellitus, cardiomyopathy, and hypogonadotrophic hypogonadism. Most whites with HH have common mutations (C282Y and H63D) in HFE; this gene encodes HFE, which regulates iron absorption by modulating hepatic expression of hepcidin. The spectrum of HH phenotypes is broad, and mutations in known iron-related genes do not account for most phenotype variability. Thus, it is assumed that HH phenotypes are affected by other genetic and environmental factors. Gender and age are two important factors known to affect HH phenotypes. Putative genetic factors may influence dietary choices or modulate iron absorption or loss via mechanisms presently undefined. The Hemochromatosis and Iron Overload Screening (HEIRS) Study is a multi-center, multi-ethnic study in which transferrin saturation (TS), serum ferritin (SF), and HFE mutations were determined in 101,168 adults. We examined familial aggregation and genetic contributions to iron- and HH-related phenotypes in the HEIRS Family Study and hypothesized that both genetic and environmental factors influence serum iron measures after adjustment for gender, age, HFE C282Y and H63D genotype, and other clinical and demographic characteristics. Heritability (h2), defined as the proportion of total variation due to variability in genetic values, measures the fraction of variation between individuals in a population attributable to additive effects of their genotypes. We estimated heritability of TS, SF, and unbound iron-binding capacity (UIBC) in participants from the HEIRS Family Study (N=180 families, mean size 5.5). Eligible probands (aged >24 y) had both TS and SF values above gender-specific thresholds (TS>50% and SF >300 μg/L in men; TS >45% and SF >200 μg/L in women), or were C282Y homozygotes. Family members, 19 years of age or older, were eligible. There were 77% Caucasians, 3% African Americans, 8% Hispanics, and 10% Asians; average age (SD) was 49 (16) y; 56% were female. The distribution of HFE genotypes was 22% C282Y/C282Y, 7% C282Y/H63D, 2% H63D/H63D, 34% C282Y/+, 8% H63D/+, and 26% +/+. A variance component approach using SOLAR software estimated residual heritability, adjusting for age, gender, their interaction (age × gender), race/ethnicity, and HFE genotype (model 1). In another model, study site, body mass index, menopausal status, phlebotomy treatment, hepatitis, average daily intake of alcohol, and level of C-reactive protein were added to the core set of covariates (model 2). Log transformation of serum ferritin was performed prior to analysis. In model 1 (N=938 individuals), h2 was 0.40 (SE 0.060) for UIBC, 0.26 (0.055) for log SF, and 0.25 (0.056) for TS; P < 0.0001 for each test of h2=0. Age, gender, race/ethnicity, and HFE genotype accounted for 38%, 38%, and 36% of the variability in UIBC, log SF, and TS, respectively. In model 2, based on complete data from N=828 individuals, adjusted for the full set of covariates, h2 was 0.31 (0.067) for UIBC, 0.26 (0.067) for log SF, and 0.16 (0.061) for TS; P < 0.0013 for each. The proportion of variance due to age, gender, HFE gene and all measured environmental factors was 0.43 for UIBC, 0.44 for log SF, and 0.41 for TS. We conclude that quantitative serum iron measures in HEIRS Family Study participants have significant heritability components, even after accounting for effects of HFE C282Y and H63D genotypes. This suggests that other genetic variants contribute to the variability in TS, SF, and UIBC, and indicates the need for gene discovery studies to provide insight into clinical disorders in which morbidity and mortality are affected by perturbations of iron metabolism.
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