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Dirofilaria immitis is a mosquito-borne nematode-causing canine heartworm disease, with adult worms localized in the pulmonary arteries and right heart. In rare cases, ectopic migration might occur, and adults and blood circulating microfilariae can be found in unusual organs or fluids (e.g., eyes, abdominal cavity, bone marrow, and urine). A 17-year-old mixed-breed female dog was presented in a private veterinary clinic in Italy for hematuria and dysuria. Physical examination showed cardiac mitral murmur with marked respiratory distress and cyanotic mucous membranes after handling. Abdominal ultrasounds revealed a non-specific chronic cystopathy, while the echocardiography showed enlargement of the right heart associated with tricuspid insufficiency and mitral regurgitation, with the presence of an adult filariae in the right ventricular chamber. Circulating microfilariae were observed in the blood smear and molecularly identified as D. immitis. Unusual microfilaruria was detected in the urine sediment. Data presented raise awareness about the occurrence of microfilariae in unusual locations, such as the bladder, suggesting the need of a thorough clinical and laboratory assessment where D. immitis is endemic., (© 2024. The Author(s).)

Introduction: Alpha-1 antitrypsin deficiency (AATD) is still underdiagnosed, despite the recommendation to determine AAT in patients with chronic obstructive pulmonary disease (COPD)., Objective: To estimate the prevalence of AATD in COPD patients adjusted according to the population of the COPD prevalence study in Argentina (EPOC.AR)., Material and Methods: This was a multicenter prospective cross-sectional study of a population aged≥30 years of age diagnosed with COPD, involving AAT quantification in dry blood spot and subsequent genotyping in subjects with<1.5mg/dL AAT in dry blood spot (<80mg/dL in serum). AAT was defined as the detection of variants ZZ or SZ on genotyping. The EPOC.AR study population was used to calculate local adjusted prevalence., Results: We included 3,254 patients (544 with AAT<80mg/dL) with a spirometric diagnosis of COPD. The prevalence of AATD in the total study population was 1.29% (95% CI 0.93-1.74), of which 0.92% (95% CI 0.62-1.31) were Pi*ZZ and 0.37% (95% CI 0.19-0.64) Pi*SZ. The adjusted prevalence of AATD in COPD patients≥40 years of age was 0.83% (95% CI 0.23-2.08). We found that AATD was negatively associated with age (OR 0.94; 95% CI 0.90-0.98; P=.006), smoking habit (OR 0.98; 95% CI 0.96-0.99; P=.009), and FEV 1 % (OR 0.95; 95% CI 0.91-0.99; P=.015)., Conclusions: The prevalence of AATD in the adult population with COPD in Argentina is estimated to be 0.83%, which could represent 17,000 cases in our country., (Copyright © 2019. Publicado por Elsevier España, S.L.U.)

Alpha-1 antitrypsin (AAT) deficiency is one of the most common inherited disorders with a higher incidence in patients with chronic obstructive pulmonary disease (COPD). Its prevalence in patients with spontaneous pneumothorax is unknown. The objective was to estimate the prevalence of AAT deficiency in patients with spontaneous pneumothorax. This was a prospective cross-sectional study, in patients with spontaneous pneumothorax, where those with secondary pneumothorax were excluded. Quantification of serum AAT by nephelometry and subsequent rapid genotyping (real time PCR) was performed, in order to detect the most prevalent deficiency alleles (Z and S) in those subjects with serum AAT concentrations = 120 mg/dl. Fifty-eight patients with primary spontaneous pneumothorax were included. The average age was 34 ± 13 years with male predominance (72%) and high prevalence of current and past smoking (60%). Twenty six percent of them (95% CI: 15-39) presented AAT serum concentrations = 120mg/dl. We found 7 deficiency variants (12%; IC 95%: 5-23%). One patient presented a severe Pi•ZZ form (1.7%), 3 were heterozygotes Z (5.2%) and 3 heterozygotes S (5.2%). The prevalence of AAT deficient variants was high in patients with spontaneous pneumothorax.

Introduction: The magnitude of the secondary response to chronic respiratory acidosis, that is, change in plasma bicarbonate concentration ([HCO 3 - ]) per mm Hg change in arterial carbon dioxide tension (PaCO 2 ), remains uncertain. Retrospective observations yielded Δ[HCO 3 - ]/ΔPaCO 2 slopes of 0.35 to 0.51 mEq/l per mm Hg, but all studies have methodologic flaws., Methods: We studied prospectively 28 stable outpatients with steady-state chronic hypercapnia. Patients did not have other disorders and were not taking medications that could affect acid-base status. We obtained 2 measurements of arterial blood gases and plasma chemistries within a 10-day period., Results: Steady-state PaCO 2 ranged from 44.2 to 68.8 mm Hg. For the entire cohort, mean (± SD) steady-state plasma acid-base values were as follows: PaCO 2 , 52.8 ± 6.0 mm Hg; [HCO 3 - ], 29.9 ± 3.0 mEq/l, and pH, 7.37 ± 0.02. Least-squares regression for steady-state [HCO 3 - ] versus PaCO 2 had a slope of 0.476 mEq/l per mm Hg (95% CI = 0.414-0.538, P  < 0.01; r  = 0.95) and that for steady-state pH versus PaCO 2 had a slope of -0.0012 units per mm Hg (95% CI = -0.0021 to -0.0003, P  = 0.01; r  = -0.47). These data allowed estimation of the 95% prediction intervals for plasma [HCO 3 - ] and pH at different levels of PaCO 2 applicable to patients with steady-state chronic hypercapnia., Conclusion: In steady-state chronic hypercapnia up to 70 mm Hg, the Δ[HCO 3 - ]/ΔPaCO 2 slope equaled 0.48 mEq/l per mm Hg, sufficient to maintain systemic acidity between the mid-normal range and mild acidemia. The estimated 95% prediction intervals enable differentiation between simple chronic respiratory acidosis and hypercapnia coexisting with additional acid-base disorders.