Hipertensión portal secundaria a sarcoidosis hepática

The etiology of hepatic granulomas varies depending on the epidemiology. In developed countries, primary biliary chol­angitis (PBC) is the main cause followed by sarcoidosis. In developing countries, it is tuberculosis. We present the case of a patient with chronic liver disease, whose anatomo­pathological diagnosis was compatible with sarcoidosis. It was a 55-year-old woman, with a history of type 2 diabe­tes (DBT), insulin-requiring and overweight. Her disease debuted with SAE, subsequently presenting HDA of vari­ceal origin. She was referred to our institution for study. Physical examination has hepatosplenomegaly and in the laboratory FAL and yGT augmented with non-reactive anti-LKM and AMA. Ultrasonography of the abdomen showed hepatosplenomegaly, without focal images. Hepatic biopsy puncture was performed, which reported numerous portal-site granulomas. The ECA dose was increased. The diagnosis of sarcoidosis was established and treatment with deflazacort was started. She presented an upper gastrointes­tinal bleeding causing her death.

Hepatic Silicone Granulomas Secondary to Ruptured Breast Implants: A Report of Two Cases

The differential diagnosis of hepatic granulomas is vast and includes infections, drugs, immunologic diseases, foreign material exposure, and neoplasia. Silicone, whether directly injected into tissues or used as a filler in breast implants, is known to cause localized granulomatous reactions. It can also migrate to other anatomic locations resulting in granulomatous inflammation at a distance. We report two cases of unsuspected hepatic silicone granulomas in patients undergoing liver biopsy for isolated elevated alkaline phosphatase levels, both with a history of ruptured breast implants. These cases highlight the need for awareness of hepatic silicone granulomas as an etiology of elevated liver enzymes in patients with a history of surgical interventions utilizing silica, such as cosmetic surgery.

Taurine Alleviates Schistosoma-Induced Liver Injury by Inhibiting the TXNIP/NLRP3 Inflammasome Signal Pathway and Pyroptosis

ABSTRACT Schistosomiasis is a parasitic helminth disease that can cause severe inflammatory pathology, leading to organ damage, in humans. During a schistosomal infection, the eggs are trapped in the host liver, and products derived from eggs induce a polarized Th2 cell response, resulting in granuloma formation and eventually fibrosis. Previous studies indicated that the nucleotide-binding oligomerization domain-, leucine-rich repeat-, and pyrin domain-containing protein 3 (NLRP3) inflammasome is involved in schistosomiasis-associated liver fibrosis and that taurine could ameliorate hepatic granulomas and fibrosis caused by Schistosoma japonicum infection. Nevertheless, the precise role and molecular mechanism of the NLRP3 inflammasome and the protective effects of taurine in S. japonicum infection have not been extensively studied. In this study, we investigated the role of the NLRP3 inflammasome and the hepatoprotective mechanism of taurine in schistosoma-induced liver injury in mice. NLRP3 deficiency ameliorated S. japonicum-infection-induced hepatosplenomegaly, liver dysfunction, and hepatic granulomas and fibrosis; it also reduced NLRP3-dependent liver pyroptosis. Furthermore, taurine suppressed hepatic thioredoxin-interacting protein (TXNIP)/NLRP3 inflammasome activation in mice with S. japonicum infections, thereby inhibiting the activation of downstream inflammatory mediators such as interleukin-1β and subsequent pyroptosis. Our results suggest that the TXNIP/NLRP3 inflammasome pathway and mediating pyroptosis are involved in S. japonicum-induced liver injury and may be a potential therapeutic target for schistosomiasis treatment. In addition, taurine may be useful to alleviate or to prevent the occurrence of schistosomiasis-associated liver fibrosis.

Multiorgan accelerated silicosis misdiagnosed as sarcoidosis in two workers exposed to quartz conglomerate dust

IntroductionClusters of silicosis cases have been reported in the fabrication of quartz conglomerate, a new high-silica-content artificial stone for kitchen and bathroom benchtops (countertops).AimWe describe two cases of accelerated-type silicosis with hepatic granulomas arising in workers exposed to artificial quartz conglomerates.MethodsA confident diagnosis of multiorgan silicosis was based on high level of respirable silica in the workplace, typical radiological alterations in chest high-resolution CT, histological findings in the lung and liver, and detection of silica crystals in both tissues by phase-contrast polarising light microscopy and scanning electron microscopy and energy dispersive spectroscopy.ResultsThe development of the disease <10 years after the first exposure is consistent with an accelerated-type of silicosis. Compared with other studies related to quartz conglomerate exposure, we determined that the levels of airborne crystalline silica during activity in the finishing area were between 0.260 and 0.744 mg/m3, that is, much higher than the threshold limit value according to American Conference of Governmental Industrial Hygienists (0.025 mg/m3). Moreover, liver granulomas were associated with accumulation of crystalline silica particles in the hepatic tissue.ConclusionsQuartz conglomerate fabrication is a potentially dangerous occupation. General practitioners and physicians should have awareness of this newly described occupational hazard. Accurate occupational history is critical in avoiding misdiagnosis, as silicosis caused by inhalation of dust from artificial quartz conglomerates may exhibit atypical presentation. These features seem to be related to the extremely high level of silica exposure and, possibly, to an increased toxicity of the dust generated in this process.