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Extrapulmonary Tuberculosis
Published in Lloyd N. Friedman, Martin Dedicoat, Peter D. O. Davies, Clinical Tuberculosis, 2020
Patients with suspected gastrointestinal TB should undergo CT imaging and paracentesis to sample ascitic fluid, if present (Figure 14.6). Ultrasound may facilitate aspiration of loculated ascites. Ascitic fluid is usually exudative with typically 500–1000 cells/mm3 with a lymphocytic predominance (40%–92%).122 The serum-ascites albumin gradient (SAAG) is <1.1 g/dL and the peritoneal fluid protein concentration >3 g/dL in those without cirrhosis.117 The ascitic fluid/blood glucose ratio is below 1.0 in approximately 80% of patients.119 AFB smears of ascitic fluid are usually negative, but cultures are positive in approximately 45%–69% of cases123; the higher yield has been reported when 1 L of fluid was cultured.119 A meta-analysis of four studies estimated that the sensitivity and specificity of an elevated ADA level in peritoneal fluid was 100% and 97%, respectively, with a threshold to define an elevated level of 36–40 U/L.123 The sensitivity and specificity of IFN-γ levels is estimated to be 93% and 99%, respectively.124
Introduction to specialist investigations and procedures
Published in Louisa Baxter, Neel Sharma, Ian Mann, The Junior Doctor’s Guide to Gastroenterology, 2018
Louisa Baxter, Neel Sharma, Ian Mann, Ian Sanderson
Total protein and albumin. This is traditionally used to decide whether ascites is an exudate (> 25 g/1) or a transudate (< 25 g/1). The serum-ascites albumin gradient (SAAG) is a better measure (see below).
Gastroenterology and hepatology
Published in Fazal-I-Akbar Danish, Essential Lists of Differential Diagnoses for MRCP with diagnostic hints, 2017
Transudative ascites (protein <2.5 g/dL or serum-ascites albumin gradient >1.1):1 Liver disease (cirrhosis).2 Congestion (right heart failure; constrictive pericarditis; pericardial effusion; inferior vena cava obstruction; Budd–Chiari’s syndrome, i.e. hepatic veins obstruction).3 Hypoproteinaemia (nephrotic syndrome; starvation; protein-losing enteropathy, etc).4 Meigs’ syndrome.
Clinical presentation of peritoneal tuberculosis
Published in Baylor University Medical Center Proceedings, 2023
Nazli Begum Ozturk, Christos Tsagkaris, Naile Dolek, Raim Iliaz
Laboratory tests showed a mild anemia, with a hemoglobin of 13.0 g/dL (reference range, 13.1–17.2 g/dL), erythrocyte sedimentation rate of 34 mm/h (0–15 mm/h), and C-reactive protein of 34.46 mg/L (<5 mg/L). Abdominal ultrasound revealed the presence of free abdominal fluid and diffuse heterogeneous granular liver parenchyma, supporting the diagnosis of chronic liver disease. Liver tests were within normal limits, and tests for hepatitis A, B, and C and HIV were negative. A diagnostic paracentesis showed a serum ascites albumin gradient (SAAG) of 0.2 g/dL and ascitic fluid white blood cells of 1.70 × 103 cells/dL (91.8% lymphocytes). Ascitic fluid cytology was negative for malignant cells. An ascitic fluid acid-fast bacilli (AFB) test and mycobacterial culture were negative. The adenosine deaminase (ADA) level in ascitic fluid was elevated at 108.5 U/L (0–40 U/L). The Quantiferon test was positive.
Peritoneal carcinomatosis, unilateral malignant pleural effusion with bilateral hydronephrosis post-radical gastrectomy in a signet-ring gastric cancer patient: a case report
Published in Journal of Community Hospital Internal Medicine Perspectives, 2020
Yuting Huang, Moemen Eltelbany, R. Dobbin Chow, Aseem Sood
Chest tube placement and diagnostic paracentesis were performed. A large volume of yellowish serous pleural effusion and ascites with similar features were noted. Body fluid total protein 3.9 g/dL, albumin 1.8 g/dL, LDH 322 units/L, the serum LDH 316 units/L, and serum total protein 6.1 g/dL. These results met Light's Criteria for an exudative pleural effusion [3], suggesting an exudative pleural effusion. The serum-ascites albumin gradient (SAAG) is 0.7; indicating peritoneal fluid was not due to portal hypertension [4]. Cytology of peritoneal fluid was negative for malignant cells.
Successful treatment with tocilizumab for massive ascites due to secondary amyloidosis complicating rheumatoid arthritis: a case report
Published in Scandinavian Journal of Rheumatology, 2019
On admission, her abdomen was extremely dilated, but there was no abdominal tenderness or limb oedema. Laboratory data included white blood cells (WBCs) 6760 cells/μL, haemoglobin 9.6 g/dL, platelets 197 000 cells/μL, aspartate transaminase 25 U/L, alanine transaminase 15 U/L, alkaline phosphatase 244 U/L, albumin 2.8 g/dL, blood urea nitrogen 23.3 mg/dL, creatinine 1.75 mg/dL, C-reactive protein 2.71 mg/dL, amylase 179 U/L, free thyroxine 1.03 ng/dL, thyroid-stimulating hormone 27.3 μIU/mL, rheumatoid factor 141 IU/mL, anti-cyclic citrullinated peptide antibody 276 U/L, anti-nuclear antibody 40, anti-SSA antibody (–), myeloperoxidase–anti-neutrophil cytoplasmic antibody (ANCA) < 0.5 IU, proteinase-33–ANCA < 0.5 IU, matrix metalloproteinase-3 593 ng/mL, and SAA 28.4 μg/mL. Massive ascites was verified by computed tomography (Figure 1C). There was also a small amount of left-sided pleural effusion. The inferior vena cava and portal vein were slightly collapsed. Two litres of ascites was aspirated on day 2, and its examination revealed WBCs 203 cells/μL (neutrophils 1%, lymphocytes 52%, macrophages 44%), albumin 1.7 g/dL [thus, the serum ascites albumin gradient (SAAG) was 1.1 g/dL], total protein 4.6 g/dL, and adenosine deaminase activity 27.2 U/L. Bacterial culture and tuberculosis polymerase chain reaction assay were negative. No malignant cells were found. Echocardiography showed an ejection fraction of 62.8%, E/A ratio 0.59, E/E’ ratio 8.1, and tricuspid regurgitation pressure gradient 19.2 mmHg. As no common cause of ascites was noted, we presumed that secondary amyloidosis had resulted in these findings. On day 10, 320 mg of TCZ was injected. The RA activity decreased promptly. Her abdominal circumference gradually reduced without further aspiration of ascites. Five months after the first injection of TCZ, the massive ascites had completely disappeared (Figure 1D).