Massive ascites due to lupus peritonitis in a patient with pre-eclampsia and systemic lupus erythematosus: a case report
Shunya SugaiKazuaki SudaKana TamegaiKazufumi HainoTakeshi NakatsueIchiei NaritaTakayuki EnomotoKoji Nishijima
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Abstract Background Patients with systemic lupus erythematosus (SLE) are associated with pre-eclampsia. Pre-eclampsia can have systemic manifestations, such as ascites. Lupus peritonitis, a rare condition in patients with SLE, can also cause ascites. Case presentation A 31-year-old woman, primigravida, with SLE had a blood pressure of 170/110 mmHg and proteinuria at 29 weeks of gestation. She was diagnosed with pre-eclampsia. Her blood pressure was stabilized by an antihypertensive drug. At 30 weeks of gestation, a cesarean section was performed for maternal safety because of decreased urine output and massive ascites. Postoperatively, re-accumulation of ascites was observed. On the fourth postoperative day, ascites (approximately 3 L) was discharged from the cesarean section wound. A decrease in serum complement concentrations was observed, and she was diagnosed as having lupus peritonitis. The steroid dose was increased and she recovered well thereafter. Conclusions Ascites occurs in pre-eclampsia and SLE, but determining which of these conditions causes ascites can be difficult. However, careful observation is necessary because of the differences in treatment of these two conditions.Abstract Background Patients with systemic lupus erythematosus (SLE) are associated with pre-eclampsia. Pre-eclampsia can have systemic manifestations, such as ascites. Lupus peritonitis, a rare condition in patients with SLE, can also cause ascites. Case presentation A 31-year-old woman, primigravida, with SLE had a blood pressure of 170/110 mmHg and proteinuria at 29 weeks of gestation. She was diagnosed with pre-eclampsia. Her blood pressure was stabilized by an antihypertensive drug. At 30 weeks of gestation, a cesarean section was performed for maternal safety because of decreased urine output and massive ascites. Postoperatively, re-accumulation of ascites was observed. On the fourth postoperative day, ascites (approximately 3 L) was discharged from the cesarean section wound. A decrease in serum complement concentrations was observed, and she was diagnosed as having lupus peritonitis. The steroid dose was increased and she recovered well thereafter. Conclusions Ascites occurs in pre-eclampsia and SLE, but determining which of these conditions causes ascites can be difficult. However, careful observation is necessary because of the differences in treatment of these two conditions.
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A 52-year-old female patient with massive ascites due to lupus peritonitis is described. Skin biopsy specimens revealed typical features of systemic lupus erythematosus (SLE) in light microscopic and immunofluorescent examinations. Immune-complexes, antinuclear antibody and hypo-complementemia were detected in the peritoneal fluid. The massive ascites responded dramatically to steroid pulse therapy. The levels of circulating immune-complexes, anti-nuclear antibody and complement in sera were also improved after such therapy. It was suggested that steroid pulse therapy may be useful for massive ascites due to lupus peritonitis.
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Among 342 consecutive patients admitted to the hospital with cirrhosis of the liver 68 (17%) had ascites and had a diagnostic paracentesis performed. Fourteen episodes of peritonitis were diagnosed in 13 patients, which is an overall incidence of peritonitis of 19%. The incidence of peritonitis was 36% in patients with hepatic encephalopathy and 10% in patients without hepatic encephalopathy (P < 0.01). In all except one case the infecting organism was most likely of enteric origin–that is, gram-negative or anaerobic species. The infected patients had lower mean ascites pH and higher mean ascites leukocyte and polymorphonuclear cell counts than non-infected patients. However, there was a considerable overlap between the two groups, and the diagnostic sensitivity did not exceed 65% for any of these three features. The survival of infected patients without encephalopathy was 33%, which was significantly lower (P < 0.05) than that the 89% for non-infected patients. In patients with encephalopathy the survival was identical for infected and non-infected patients.
Spontaneous bacterial peritonitis
Hepatic Encephalopathy
Paracentesis
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Objective
To investigate the diagnostic value of serum procalcitonin (PCT) combined with C reactive protein (CRP) and interleukin-6 (IL-6) in spontaneous peritonitis of cirrhosis ascites.
Methods
A total of 136 patients who had post-hepatitis cirrhosis complicated with ascites who were treated in Shanxi Hospital of Integrated Traditional Chinese and Western Medicine from January 2016 to March 2018 were selected as research objects. Of them, 74 patients with spontaneous peritonitis were treated as peritonitis group, and 62 patients without spontaneous peritonitis were treated as non-peritonitis group. Another 74 healthy persons who underwent physical examination were selected as healthy group. The results of PCT, CRP and IL-6 in serum of three groups were analyzed retrospectively, and their application value was judged.
Results
The positive rates of PCT, CRP and IL-6 in peritonitis group were higher than those in healthy group and non-peritonitis group, the positive rates of PCT, CRP and IL-6 in non-peritonitis group were higher than those in healthy group (P<0.05). The area under the curve of PCT+ CRP+ IL-6 was 0.962 (95%CI: 0.928-0.995). The diagnostic value of PCT+ CRP+ IL-6 was better than that of PCT, CRP and IL-6 alone or in combination.
Conclusions
The combined detection of PCT, CRP and IL-6 has high sensitivity and specificity, which can effectively improve the diagnostic accuracy of spontaneous peritonitis in patients with post-hepatitis cirrhosis.
Key words:
Serum procalcitonin; C reactive protein; Interleukin-6; Diagnosis of spontaneous peritonitis
Procalcitonin
Spontaneous bacterial peritonitis
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The prevalence of spontaneous bacterial peritonitis (SBP) or its variants, bacterascites (BA), and culture-negative neutrocytic ascites (CNNA), may vary depending on the underlying liver disease and protein content of ascites. In this study, we compared the frequency of peritonitis (SBP, BA, CNNA) upon admission in alcoholic (ALD), cholestatic (CLD), and hepatocellular liver disease (HLD); determined the relationship between Child's class and prevalence of peritonitis; and assessed ascitic total protein as a risk factor for peritonitis. Between January 1989 and April 1991, 113 consecutive patients were admitted with chronic liver disease and ascites (49, ALD; 22, CLD; and 42, HLD). All had admission paracentesis. SBP was defined as polymorphonuclear cell count (PMN) > or = 250 mm3 with a positive culture, BA as PMN < 250/mm3 and positive culture, and CNNA as PMN > or = 250/mm3 with negative culture. No patients with obvious intraabdominal source for infection (i.e., secondary peritonitis) were included in the analysis. The prevalence of peritonitis was 8/113 (7%); four patients had SBP, one BA, and three CNNA. The occurrence of peritonitis was independent of the type of liver disease (ALD, 8%; CLD, 9%; HDL, 5%). Neither ascitic fluid total protein nor the severity of liver disease (Child's class) predicted the occurrence of peritonitis. We conclude that the occurrence of peritonitis is unrelated to the type of liver disease, and severity of liver disease did not predict the presence of peritonitis. Also, ascitic fluid total protein < 1.0 g/dl may not be a sensitive predictor of risk of peritonitis.
Spontaneous bacterial peritonitis
Liver disease
Chronic liver disease
Paracentesis
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Abstract Pre-eclampsia is a multifactorial and multisystemic disease specific to gestation. It is classically diagnosed by the presence of hypertension associated with proteinuria manifested in a previously normotensive pregnant woman after the 20th week of gestation. Pre-eclampsia is also considered in the absence of proteinuria if there is target organ damage. The present review takes a general approach focused on aspects of practical interest in the clinical and obstetric care of these women. Thus, it explores the still unknown etiology, current aspects of pathophysiology and of the diagnosis, the approach to disease prediction, its adverse outcomes and prevention. Management is based on general principles, on nonpharmacological and on pharmacological clinical treatment of severe or nonsevere situations with emphasis on the hypertensive crisis and eclampsia. Obstetric management is based on preeclampsia without or with signs of clinical and/or laboratory deterioration, stratification of gestational age in < 24 weeks, between 24 and less than 34 weeks, and ≥ 34 weeks of gestation, and guidance on route of delivery. An immediate puerperium approach and repercussions in the future life of pregnant women who develop preeclampsia is also presented.
Etiology
Hypertensive disease
Gestational hypertension
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To present a rare case of massive maternal ascites with severe pre-eclampsia at 35 weeks of gestation. A 35-year-old, gravida 3, para 2, woman presented with a 1-day history of headache, blurred vision, and abdominal pain with uterine contractions, at 35 weeks of gestation. Ultrasonography showed a fetus that was small for gestational age. A large amount of free fluid was noted intraperitoneally. This complication developed in association with a blood pressure of 202/107 mmHg, proteinuria, and abnormal laboratory values. More than 2 L of ascitic fluid was removed at the time of cesarean section. Massive ascites is an unusual complication of pre-eclampsia that can result in respiratory compromise. The rarity of this condition may be due to under-reporting. Careful clinical and ultrasonographic examinations are necessary to detect this condition.
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A 77-year-old Japanese woman with massive painless ascites caused by chronic lupus peritonitis is reported. Peritoneal effusion had been resistant to the administration of steroids during the whole treatment period. It was characteristic that the titers of anti-DNA antibodies and the level of immune complex were elevated in the peritoneal fluid with suppressed levels of complements in ascites, although serum immunological markers reflecting the activity of SLE presented improvement after initiation of the treatment. Fifteen patients with chronic lupus peritonitis were reported previously. We reviewed the literature and suggest that chronic lupus peritonitis at elderly onset may demonstrate a poor response to the glucocorticoid therapy because of persistent inflammation in the peritoneum and the presence of impaired vascular circulation in addition to immunological mechanisms.
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Systemic lupus erythematosus (SLE) is an autoimmune disease and can cause multi-organ damage. Peritoneal involvement, also called lupus peritonitis, is a rare but sometimes fatal manifestation. Deposition of immune complexes consisting of immunoglobulin G and complement is considered to be involved in the pathogenesis of lupus peritonitis; however, it remains unknown whether inflammatory cytokines contribute to the pathology of this manifestation. Here we present two patients with treatment-resistant lupus peritonitis: a 37-year-old woman with a 26-year history of SLE who had been treated with prednisolone and cyclophosphamide followed by azathioprine and a 65-year-old woman with a 33-year history of SLE who had been treated with prednisolone alone. Both patients were admitted to our department because of abdominal distention. Computed tomography scans showed massive ascites. Ascitic fluid examinations of both patients showed leukocytosis with no evidence of malignancy or infection. After eliminating other causes for ascites, they were diagnosed with lupus peritonitis. Despite the intensified immunosuppressive therapy, they died of uncontrolled peritonitis several months after admission. Examinations of the ascites at admission also revealed a large content of interleukin (IL)-6, compared with other inflammatory cytokines, IL-1β and tumor necrosis factor-α. In fact, the ascitic IL-6 levels of these two patients were 12,389 pg/mL and 5,486 pg/mL, much higher than their serum IL-6 levels of 36 pg/mL and 140 pg/mL, respectively. We therefore suggest that IL-6 may contribute to the pathogenesis of lupus peritonitis and that the inhibition of IL-6 signaling may provide a novel therapeutic strategy for lupus peritonitis.
Prednisolone
Pathogenesis
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Background/Aim: Ascites of tuberculous peritonitis (TBP) is an exudative type and may well be misdiagnosed as carcinomatous peritonitis, especially in the elderly. The aim of this study was to identify independent predictors that can differentiate TBP from peritonitis carcinomatosa without surgical intervention. Patients and Methods: This prospective cohort study was performed on 75 subjects in the following groups: TBP (n=27) (TBP group), ovarian cancer complicated with ascites (n=24) (Ov Ca group), and gastric cancer complicated with ascites (n=24) (Ga Ca group). The frequency of clinical symptoms, laboratory parameters, and serum tumor markers levels were compared. Results: In univariate analysis; fever, night sweats, and abdominal pain were significantly more frequent in the TBP group compared to those in the Ov Ca group (P < 0.001, P < 0.001, and P = 0.035, respectively) and the Ga Ca group (P < 0.001, P < 0.001, and P = 0.015, respectively). Serum CA 19-9 and carcino embryonic antigen (CEA) levels were significantly lower in the TBP and Ov Ca group compared to the Ga Ca group (P < 0.001 and P < 0.001, respectively). Elevated serum CA 125 level was found in all patients with TBP and Ov Ca and in 86.6% of patients with Ga Ca. In the multivariate analysis, presence of fever (P < 0.001), night sweats (P < 0.001), age under 40 years (P = 0.008), and normal serum CA 19-9 level (P = 0.044) were independent predictor of diagnosis of TBP. Conclusion: The presence of fever, elevated serum CA 125 level, normal serum CA 19-9, and CEA associated with lymphocyte predominant benign ascites may establish the diagnosis of TBP.
Univariate analysis
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