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Renal Disease; Fluid and Electrolyte Disorders
Published in John S. Axford, Chris A. O'Callaghan, Medicine for Finals and Beyond, 2023
Calcium levels need to be corrected for the plasma albumin concentration (see Table 8.18). Renal function should be checked.A raised alkaline phosphatase level may indicate bone disease.Measure PTH to exclude hyperparathyroidism.A raised serum ACE level is non-specific but may indicate sarcoidosis.Blood and urine should be checked for the presence of a monoclonal antibody band to exclude myeloma.Imaging may identify cancer or other systemic diseases.ECG changes include a shortened QT interval.
Models of Toxicity Screening Using Cultured Cells
Published in John J. Lemasters, Constance Oliver, Cell Biology of Trauma, 2020
Roberta L. Grant, Daniel Acosta
The leakage of LDH into the culture medium, morphological observations, and a decline in alkaline phosphatase activity were used to assess cytotoxicity of cadmium chloride at concentrations of 50 to 400 μM. The loss of alkaline phosphatase activity was a more sensitive measure of toxicity than the leakage of LDH into the medium. This illustrates the importance of using several cytotoxicity assays to more thoroughly evaluate the toxicity of compounds. There was a time- and dose-dependent decline of alkaline phosphatase activity; a decrease in activity was evident as early as 2 h of treatment with 200 to 400 μM and with 50 to 400 μM after 4 h of treatment. Treatment of the cells with cadmium chloride resulted in cell shrinkage and plasma membrane irregularities. After 200 μM cadmium chloride exposure, the cells separated from one another and cell lysis was apparent in scattered areas, while 400 μM cadmium chloride treatment resulted in almost total cell lysis.
Hypophosphatasia
Published in William L. Nyhan, Georg F. Hoffmann, Aida I. Al-Aqeel, Bruce A. Barshop, Atlas of Inherited Metabolic Diseases, 2020
The major criterion for diagnosis of hypophosphatasia is an absent or extremely low activity of alkaline phosphatase in serum [39]. Alkaline phosphatase activity is also low in tissues, including bone [1]. Alkaline phosphatase activity is normal in intestine and placenta in these patients [40], indicating that the isozyme in these tissues is genetically different from that of plasma, bone, and other tissues. The defect can be demonstrated in leukocytes [41] and cultured fibroblasts [40]. There is no observable relationship between the degree of alkaline phosphatase abnormality and the clinical expression of the disease. Alkaline phosphatase is thought to be involved in the deposition of mineral crystals by the hydrolysis of pyrophosphate and other phosphate esters. Slices of rachitic cartilage from vitamin D deficient rats or patients calcify readily in normal serum or serum from patients with hypophosphatasia, but slices of cartilage from patients with hypophosphatasia do not calcify in normal serum, indicating that the defect is a local one at the site of mineralization [42].
Extracorporeal shock wave therapy to treat neurogenic heterotopic ossification in a patient with spinal cord injury: A case report
Published in The Journal of Spinal Cord Medicine, 2021
Hyun Min Jeon, Won Jae Lee, Hee Sup Chung, You Gyoung Yi, Seoyon Yang, Dae Hyun Kim, Kyung Hee Do
At the initial visit to the department of physical medicine and rehabilitation, the subject had suffered from severe right hip pain with a visual analog scale (VAS) score between 7 and 8 without definite heatness or swelling (Table 1). A radiograph of the right hip revealed NHO on the greater trochanter of the right hip (Fig. 1A). The maximum length of long axis for the NHO according to the radiograph was 13.63 mm and the maximum length of short axis for the NHO was 8.13 mm. The Computed Tomography (CT) scans also showed NHO on the greater trochanter of the right hip (Fig. 2). The NHO volume was measured using 3D slicer 4.10 and was found to be 818 mm3. The serum alkaline phosphatase level was 192 IU/L. Medications(aceclofenac 100 mg twice a day and disodium etidronate 600 mg once a day) and physical modalities for a minimum period of 3 weeks were used to treat the pain. However, he still complained of severe pain with a VAS of 7–8 after 3 weeks of conservative treatments (Table 1). In addition, because of his severe pain, the subject could not sit on the wheelchair for more than an hour and he could not transfer well.
Practical management of adverse events in patients with advanced systemic mastocytosis receiving midostaurin
Published in Expert Opinion on Biological Therapy, 2021
Jason Gotlib, Hanneke C. Kluin-Nelemans, Cem Akin, Karin Hartmann, Peter Valent, Andreas Reiter
A 65-year-old man presented with SM associated with CMML and KIT D816V and SRSF2 mutations (with mutant allele burdens of 42% and 36%, respectively). The patient experienced abdominal bloating and discomfort, with a weight loss of 4.5 kg over 3 months. In addition, he presented with diarrhea 2 to 3 times daily and paracentesis-dependent ascites (every 2 weeks). On physical examination, performed between episodes of paracentesis, splenomegaly of 8 cm below the left costal margin and hepatomegaly of 5 cm were evident. His complete blood count revealed a white blood cell count of 14.8 × 109/L, hemoglobin level of 10.4 g/dL, and platelet count of 108 × 109/L. His differential revealed 40% neutrophils, 20% lymphocytes, and 38% monocytes, for an absolute monocyte count of 5.62 × 109/L. A bone marrow core biopsy showed MC involvement of 40% as well as CMML-1 with a marrow blast count of 6%. The serum tryptase level was 220 ng/mL (normal, <11.4 ng/mL). An increase in serum alkaline phosphatase (AP) to 340 IU/L was noted [normal, <130 IU/L]. Liver biopsy as well as random biopsies via upper endoscopy and colonoscopy confirmed involvement by SM. Midostaurin therapy (100 mg twice daily) was initiated, with the patient reporting moderate nausea starting 30 minutes after the morning dose and lasting for 1 hour, resulting in 1 episode of vomiting.
Effects of verapamil on the pharmacokinetics of puerarin in rats
Published in Xenobiotica, 2019
Yun Zhou, Xiaoli Song, Gang Dong
The Caco-2 cell line was obtained from the American Type Culture Collection (Manassas, VA, USA). The Caco-2 cells were cultured in DMEM high glucose medium containing 15% FBS, 1% NEAA and 100 U/mL penicillin and streptomycin. The cells were cultured at 37 °C with 5% CO2. For transport studies, the cells at passage 40 were seeded on transwell polycarbonate insert filters (1.12 cm2 surface, 0.4 μm pore size, 12 mm diameter; Corning Costar Corporation, MA, USA) in 12-well plates at a density of 1 × 105 cells/cm2. Cells were allowed to grow for 21 days. For the first 7 days, the medium was replaced every 2 days, and daily thereafter. The transepithelial electrical resistance (TEER) of the monolayer cells was measured using Millicell ERS-2 (Millipore Corporation, Billerica, MA, USA), and TEER exceeding 400 Ω·cm2 was used for the flux experiment. The integrity of the Caco-2 monolayers was confirmed by the paracellular flux of Lucifer yellow, which was less than 1% per hour. The alkaline phosphatase activity was validated using an Alkaline Phosphatase Assay Kit. The qualified monolayers were used for transport studies.