WEEKLY Clinicopathological Exercises: Adenocarcinoma of lung, left lower, with metastases to pleura, peritoneum, liver and vertebras.
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CASE REPORT: Peritoneal exposure to mercury has been rarely reported and long-term consequences of this type of exposure have not been documented. We report the clinical course of a patient who has survived almost eight years with a massive intraperitoneal load of mercury. She has suffered formication, pruritus, fatigue, irritiability, insomnia, alopecia, dizziness, a gait disturbance, loss of balance and multiple falls, abdominal pain, choking, and headaches. Two courses of chelation with dimercaptosuccinic acid using the standard protocol were undertaken, resulting in increased daily excretion, but without demonstrable objective or subjective benefit or lasting effect. She had multiple medical problems before the mercury intoxication, which complicates the attribution of all her problems to mercury intoxication. It is of particular interest that the patient survived and did not suffer any marked cognitive deterioration. She died in 2002 shortly after being diagnosed with lung cancer and declaring that she would fight it. Phasing out of mercury-weighted tubes is recommended.
The authors present five cases of an unusual inflammatory reaction in pelvic peritoneal tissues associated with oxidized regenerated cellulose, a topical hemostatic agent. The findings were observed in specimens from five women who had been treated with oxidized regenerated cellulose during abdominal surgery. Histologically, the lesion was characterized by collections of large cells beneath the mesothelial surface, with small bland nuclei and abundant granular basophilic cytoplasm that stained bright red with mucicarmine. Immunohistochemical studies demonstrated that these cells stained positive for KP1 (CD68) confirming their histiocytic nature, and negative for cytokeratin and S-100 protein excluding the diagnoses of carcinoma and granular cell tumor respectively. Although unlikely, the mucicarmine positivity may be misinterpreted, leading to a erroneous diagnosis of adenocarcinoma. To avoid misdiagnosis, pathologists need to be aware of this lesion.
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BACKGROUND: A recent survey puts the global dialysis population at 535100; of those on peritoneal dialysis, 85% are on continuous ambulatory peritoneal dialysis. Current hyperosmolar dialysis fluids are toxic to peritoneal cells and inhibit certain host-defence functions. An alternative preparation, glucose polymer, has recently been developed. METHODS: Mesothelial cell viability, interleukin-6 and prostacyclin synthesis, after exposure to 7.5% glucose polymer, 1.36% glucose or 3.86% glucose peritoneal dialysis effluent solution was assessed. RESULTS: In its neat form, at an original pH of 5.4, glucose polymer was as toxic as hyperosmolar solutions (P < 0.01). Synthesis of interleukin-6 and prostacyclin were significantly inhibited by neat dialysis fluid, (P < 0.01). However, after an in vivo intraperitoneal incubation of only 15 min the toxicity of all solutions tested in vitro was lost. CONCLUSIONS: Despite rapid in situ neutralization of dialysis fluid toxicity, mesothelial injury and inhibition of host-defence function, early in the dialysis cycle, may affect peritoneal physiology given the complex network of pathways to which these cells contribute. Although recent trials indicate improved ultrafiltration is achievable with glucose polymer, it is not a biocompatible dialysis fluid in its current manufactured form.
Serum concentrations of amikacin following operative wound irrigation were studied in 17 patients having laporatomy and in eight patients having thoracotomy. Irrigation was done with 500 mg of amikacin in 200 ml of saline. The irrigant was reaspirated after 3 minutes. Measurement of amikacin in the irrigant allowed calculation of the retained dose. Serum levels were measured before surgery, and at 30 minutes, 60 minutes, 6 hours, and 12 hours following irrigation. Amikacin was assayed by a microbiological technique. The retained dose after peritoneal irrigation was 350 +/- 128 mg, and after pleural irrigation was 100 +/- 79 mg. The average maximum serum level in the peritoneal irrigation group was 9.4 +/- 6.7 gm/ml; in the thoracotomy group it was 3.5 +/- 1.7. Fourteen of the 17 laparotomy patients but only one of the eight thoracotomy patients had measurable plasma levels at 6 hours. Plasma half-life in the laparotomy group was 2.81 +/- 1.34 hours, and in the thoracotomy group 1.53 +/- 0.83 hours. Interoperative amikacin irrigation, even with immediate aspiration, results in significant absorption in both thoracotomy and laporatomy patients. There was less absorption and a shorter serum half-life in the thoracotomy patients.
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The water channel aquaporin-1 (AQP1) is the molecular counterpart of the ultrasmall pore responsible for transcellular water permeability during peritoneal dialysis (PD). This water permeability accounts for up to 50% of ultrafiltration (UF) during a hypertonic dwell, and its loss can be a major clinical problem for PD patients. By analogy with the lung, the hypothesis was tested that corticosteroids may increase AQP1 expression in the peritoneal membrane (PM) and improve water permeability and UF in rats. First, the expression and distribution of the glucocorticoid receptor (GR) in the PM and capillary endothelium was documented. Time-course and dose-response analyses showed that a daily IM injection of dexamethasone (1 or 4 mg/kg) for 5 d induced an approximately twofold increase in the expression of AQP1 at the mRNA and protein levels. The GR antagonist RU-486 completely inhibited the dexamethasone effect. The functional counterpart of the increased AQP1 expression was a significant increase in sodium sieving and net UF across the PM, contrasting with a lack of effect on the osmotic gradient and permeability for small solutes. The latter observation reflected the lack of effect of corticosteroids on nitric oxide synthase (NOS) activity and endothelial NOS isoform expression in the PM. In conclusion, corticosteroids induce AQP1 expression in the capillary endothelium of the PM, which is reflected by increased transcellular water permeability and UF. These data emphasize the critical role of AQP1 during PD and suggest that pharmacologic regulation of AQP1 may provide a target for manipulating water permeability across the PM.
An unusual catalase-positive pleomorphic Gram-positive rod isolated from a human clinical specimen was subjected to a polyphasic taxonomic analysis. Comparative 16S rRNA gene sequence analysis revealed the unknown bacterium was a member of the high G+C branch of the Gram-positive bacteria (Actinobacteria), and was phylogenetically a member of the family Propionibacteriaceae, with Luteococcus japonicus as its nearest relative. Based on both phenotypic and phylogenetic evidence, it is proposed that the unknown bacterium be classified in the genus Luteococcus, as Luteococcus peritonei sp. nov. The type strain of Luteococcus peritonei is CCUG 38120T.
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