RESUMEN
Background: Activity-based costing is one of the main methods for operational budgeting which provides the ability to manage and control costs for managers. This study was conducted to estimate the cost price of Shafa hospital laboratory services in Kerman using activity-based costing technique and compared with services tariff.
Materials and Methods: This study is a cross-sectional and applied study was conducted in the clinical Laboratory of Shafa Hospital at Kerman University of Medical Sciences in 2011. The cost price of FBS, CPK and Cr tests calculated which had the highest frequency in the year as well as HBS, HIV and three times blood culture which had the higher tariffs than other tests. Initially, data were manually collected through interview with hospital officials and review of relevant documents. Then, in order to achieve the targets of the study, the cost price results were analyzed using Excel software.
Results: The results showed that the total annual costs of the departments were the sum of 5, 002, 917, 493 Rails that 94.9 percent and 5.1 percent of it were related to the direct and indirect costs respectively. Laboratory personnel cost by 74.2 percent and consumables cost by 21.1 percent had the largest share of the costing. The cost price of Cr and CPK tests calculated the sum of 10.019 and 21.517 Rails respectively that according to the public tariffs, had a suitable profit.
Conclusion: This study showed that there is a difference between the actual cost of the laboratory services and public tariffs that has led a loss to the laboratory. Therefore, by improving the performance management in the field of human resource and standardizing, can reduce the cost price of services and optimize resources consumption.
RESUMEN
Glycogen storage disease II [GSDII or Pompe disease, OMIM # 232300] is an autosomal recessive hereditary lysosomal disorder. Mutations in the GAA gene usually lead to reduced acid alpha-glucosidase [acid maltase, GAA, OMIM [asterisk] 606800, EC 3.1.26.2] activity, which results in impaired degradation and subsequent accumulation of glycogen within lysosomes. We present an Iranian boy, who was diagnosed with GSDII based upon clinical and biochemical findings. A single adenine insertion [insA] was detected at codon 693 that leads to a predicted premature stop codon at codon 736 in the GAA gene. The parents were heterozygous for the same change. According to the human genome mutation database [www.hgmd.org] and lecture reviews, the detected change is a novel mutation. We suppose that the discovered insertion in the GAA gene might lead to a reduced activity of the gene product. This assumption is in agreement with biochemical and clinical signs in the patient