Hepatic Calcification Research Articles

Dilemmas in the management of congenital cytomegalovirus (CMV)

<h3>Background</h3> Routine antenatal ultrasound screening revealed liver calcifications, and subsequent maternal serology (IgM and IgG) was shown to be positive for cytomegalovirus (CMV). Shortly after birth he was found to have hepatosplenomegaly, petechiae and visible jaundice. Bloods within the first few hours revealed marked conjugated jaundice, thrombocytopaenia and deranged coagulation. The baby was admitted to our neonatal unit for observation and treatment and congenital CMV infection was confirmed within 24 hours by positive CMV PCR from his urine. Further investigations revealed no intracranial abnormalities, no evidence of retinitis and normal newborn hearing. Abdominal ultrasound confirmed hepatic calcification and organomegaly. <h3>Management</h3> Following discussion between neonatal and paediatric infectious disease consultants, a decision was taken to treat the infant with IV ganciclovir for 2 weeks (necessitating insertion of a percutaneous long line), followed by oral valganciclovir for 4 weeks. Weekly Viral loads were checked, together with frequent monitoring for neutropaenia. <h3>Issues</h3> This case highlighted several dilemmas in the management of congenital CMV. CMV is the most frequent congenital infection and has a UK incidence of around 3-4/1000 live births. Around 10-15% of these infants will be symptomatic, of whom up to 90% will develop long term sequelae usually in the form of sensorineural hearing loss, visual impairment or developmental delay. Some 13% of asymptomatic infants also develop long term problems. In spite of such morbidity, decisions of whom to treat, and for how long, remain controversial. Whilst there is some support for treating infants with CNS symptoms, there is a paucity of high level evidence for treating infants with other organ involvement. In addition, the adverse effects of treatment - namely requirement of central venous access with its associated complications, and potential neutropaenia – are not inconsiderable. The controversies of treatment, and uncertainty regarding long term follow-up of symptomatic and asymptomatic babies, mean such cases provide difficult management problems.

Case of congenital varicella syndrome, presenting with antenatally detected hepatic calcification and ventriculomegaly

At 13+6 weeks gestation, a 37 year old para 1+2 woman presented after her daughter developed chickenpox. As booking bloods were IgG negative for varicella, varicella zoster immunoglobulin was administered....

Isolated fetal liver calcifications

Hepatic calcification in the fetus is considered an uncommon occurrence and the clinical significance is not fully known. We describe five cases with isolated hepatic calcification. The causes and postnatal outcome of the fetal liver calcifications detected by ultrasound imaging are discussed. Isolated fetal liver calcifications with no aneuploidy and infection have a good prognosis.

Diffuse Hepatic Calcification Following Ischemic Insult in the Setting of Impaired Renal Function

Diffuse Hepatic Calcification Following Ischemic Insult in the Setting of Impaired Renal Function

P22.09: Immunoglobulin fetal therapy in prenatal infection with Cytomegalovirus. Report of three cases

Cytomegalovirus (CMV) is a frequent infection that cause miscellaneous ultrasound findings and fetal well-being compromise. Sonographic markers, maternal serum (IgG, IgM, IgGavidity) and PCR are diagnostic. Treatment is antiviral medication or hypergammaglobulin and fetal support. We report three cases of prenatal CMV treated with gammaglobulin (total dose was 150 mg/kg each case) and fetal support. First patient sonogram showed polihydramnios, placentosis, ventriculomegaly, periventricular and liver calcifications, hydrops, hepatosplenomegaly and hyperechogenic spleen and IUGR with normal Doppler. Fetal treatment with globulin was given as described and hydrops and ventriculomegaly were solved. High resistance in umbilical artery (UA) and a week later brain sparing were observed and underwent to C-section. A 34 wks female was delivered to NICU, without sequelae in follow up. Second case was a 26wo pregnant woman with polihydramnios, fetal pleural effusion with mediastinal shift, and hydrops at ultrasound. Doppler showed high resistance in UA with high impedance in DV. Fetal therapy with globulin was ongoing and the fetus underwent to pleuroamniotic shunt. Mediastinal shift and hydrops were solved. Patient underwent to EXIT procedure. A 37 wks male was delivered. Neurological follow up was satisfactory. In last case, at 27wo pregnancy sonogram showed ventriculomegaly, brain and hepatic calcifications, hepatoesplenomegaly and ascites. IUGR with normal UA was seen. MCA-PSV was over 1.55 MoM and fetal anemia was diagnosed, patient underwent to globulin therapy and intrauterine transfusion was performed twice. Doppler showed central vasodilatation pattern at 31 wks and C-section was performed. Baby went to NICU. After critical condition, neurological follow up show left deafness. Congenital CMV is a common condition in underdeveloped countries. Fetal therapy consists on gammaglobulin as medical and invasive therapy support according with particular conditions.

Peripheral atrophy/central hypertrophy complex in chronic hepatic Schistosoma mansoni infection with histological correlation

Objective Peripheral atrophy/central hypertrophy (PACH) complex has been described in various chronic liver diseases but never in chronic hepatic Schistosoma mansoni infection. This study describes the imaging and anatomic features of PACH complex in four patients using high resolution cross-sectional imaging with 3D reconstructions and pathologic correlation. Materials and methods Two radiologists assessed imaging studies from four patients with proven chronic hepatic S. mansoni infections for presence of PACH complex, hepatic surface lobulations, capsular thickening, periportal fibrosis, hepatic calcification, gallbladder wall enhancement and thickening, and splenomegaly. 3D volume rendering and curved planar and oblique reformation in the planes of the hepatic veins were performed to better evaluate the 3D position of the hepatic veins relative to the liver parenchyma and capsule. Results All four patients had PACH complex and hepatic surface lobulations. 3D volume rendered images demonstrated severe peripheral atrophy with migration of hepatic veins on the capsular surface of the liver. Multiplanar reconstruction demonstrated coexisting hypertrophy about the central portal veins and atrophy of the peripheral liver parenchyma with thinned or no parenchyma between the hepatic veins and the liver capsule. All patients also had capsular thickening, splenomegaly, and no calcifications. While all patients had enhancement of the gallbladder wall in the arterial phase without thickening, three patients had dilated veins on the surface of the gallbladder wall. Three patients also had periportal fibrosis. Conclusion This study is the first to report PACH complex in chronic hepatic S. mansoni infection. Atrophy results in crowding of smaller hepatic veins in the periphery of the liver. Finally, hepatic capsular thickening on imaging is a further sign of this infection.

Hepatic Artery Calcification in a Liver Transplant Recipient

The abdominal aorta and the renal, mesenteric, and splenic arteries are frequently affected with arterial wall calcification upon increasing age; the hepatic artery is far less often found to be calcified. We report the case of a liver transplant recipient who presented with a calcified hepatic artery in the liver graft 13 years after transplantation for primary sclerosing cholangitis. Although the etiology of hepatic artery calcification was unknown, underlying causes for calcification may include chronic hemodialysis for renal insufficiency and subsequent secondary hyperparathyroidism, as well as a calcified aneurysms. However, it remained unclear whether hepatic artery calcification had to be considered an epiphenomenon or an original pathology of the liver. It thus seems unlikely that hepatic artery calcification as a single finding is to be considered a serious pathologic entity, even for a liver graft.

Sonographische Befunde bei materno-fetalen Infektionen

Infections acquired in utero or during the birth process are a significant cause of fetal and neonatal mortality and an important contributor to early and later childhood morbidity. Advances in ultrasound, invasive prenatal procedures and molecular diagnostics have allowed in utero evaluation and given rise to more timely and accurate diagnosis in infected fetuses. Transplacental transmission of the infectious agent, even in subclinical maternal infection, may result in a severe congenital syndrome. Prenatal detection of infection is based on fetal sonographic findings and polymerase chain reaction to identify the specific agent. Nevertheless, most affected fetuses appear sonographically normal, but serial scanning may reveal evolving findings. Sonographic fetal abnormalities may be indicative of fetal infections, although they are generally not sensitive or specific. These include growth restriction, hydrops, ventriculomegaly, hydrocephaly, microcephaly, intracranial or hepatic calcifications, ascites, hepatosplenomegaly, echogenic bowel, placentomegaly, and abnormal amniotic fluid volume. When abnormalities are detected on ultrasound, a thorough fetal evaluation is recommended because of potential multiorgan involvement. The sonologist should understand the limitations of ultrasound. Patients should be counseled that ultrasound is not a sensitive test for fetal infection and that a normal fetal anatomy survey cannot reliably predict a favorable outcome.

Diagnosis of Cystic Echinococcosis, Central Peruvian Highlands

We evaluated prevalence of cystic echinococcosis (CE) in a central Peruvian Highland district by using 4 diagnostic methods: ultrasonography for 949 persons, radiography for 829, and 2 serologic tests for 929 (2 immunoblot formats using bovine hydatid cyst fluid [IBCF] and recombinant EpC1 glutathione S-transferase [rEpC1-GST] antigens). For the IBCF and rEpC1-GST testing, prevalence of liver and pulmonary CE was 4.7% and 1.1% and seropositivity was 8.9% and 19.7%, respectively. Frequency of seropositive results for IBCF and rEpC1-GST testing was 35.7% and 16.7% (all hepatic cysts), 47.1% and 29.4% (hepatic calcifications excluded), and 22.2% and 33.3% (lung cysts), respectively. Weak immune response against lung cysts, calcified cysts, small cysts, and cysts in sites other than lung and liver might explain the poor performance of the serodiagnostic tests. We confirm that CE is highly endemic to Peru and emphasize the limited performance of available serologic assays in the field.

Diffuse Hepatocellular Calcification Developing in a Patient on Chronic Hemodialysis After Ischemic Hepatitis

Diffuse hepatic calcification is a rare condition. Previous reports have described patients with end-stage renal disease who developed diffuse hepatic calcification after ischemic hepatitis caused by shock. We herein present a similar case. A 41-year-old man on chronic hemodialysis developed ischemic hepatitis due to shock induced by ventricular tachycardia, followed by progressive hepatic failure. Necropsy of the liver revealed diffuse hepatocellular calcification. Given the similarity by which our case and previously reported cases developed this rare condition, we postulate that chronic renal failure is involved in the pathogenesis of diffuse hepatic calcification.

Thrombose portale calcifiée dans le suivi d’un shunt porto-cave: aspect échographique et diagnostic différentiel

The case of a patient with large hepatic calcifications along the portal vascular network caused by long-standing portal vein thrombosis is presented. These calcifications appeared in extended portal thrombosis and were confirmed in follow-up for a surgical portocaval shunt related to portal hypertension. The differential diagnosis should distinguish these from hyperechoic patterns observed along the periportal vascular network, including intraductal biliary stones, portal venous gas, gas in the biliary tract, biliary comet tail artifacts, periportal fibrosis in parasitosis, and calcifications of the hepatic arteries.

Post-survey follow-up for human cystic echinococcosis in northwest China

In Hobukesar, Xinjiang Uygur Autonomous Region, (China), a mass-screening programme for human cystic echinococcosis (CE) was performed during 1995 and 1996. After the survey 51 cases were followed-up using ultrasound scan and serology for 1–8 years (1996–2003). These included 20 CE cases treated by surgery (endocystectomy), four CE cases treated by percutanous drainage (PAIR), six untreated CE cases, five ultrasound ‘query’ cases, eight cases of isolated hepatic calcifications, four previous CE surgery cases whose ultrasound was now normal, and four seropositive cases who exhibited a normal hepatic ultrasound. Follow-up results indicated that in the untreated CE patients, one case exhibited a spontaneous cure within 4 years, another case changed from a hepatic hydatid cyst that contained a floating laminated membrane (type CE3) to a cyst that contained daughter cysts (type CE2) within 1 year of follow-up. In the 20 surgically treated cases, two recurrent CE cases occurred within 4 years, and five cases had had residual cavities for more than 4 or 8 years. Of the 4 PAIR treated cases, two recurrent cases of CE occurred within 4 or 8 years of follow-up. Serological follow-up data showed that specific IgG antibody levels were persistently positive in most CE cases, but exhibited a decreasing tendency in cases that were effectively treated by surgery; In contrast, serum IgG levels in the PAIR group or in the recurrent CE cases after surgery exhibited an increasing tendency. At least one persistant seropositive case with an isolated hepatic calcification was considered to be abortive CE.

Case Report

Case Report

First linezolid- and vancomycin-resistant Enterococcus faecium strain in Taiwan

To our knowledge, this is the firstreport of a linezolid-resistant Enterococcus faecium strainisolated in Taiwan.The 51-year-old woman developed disseminated Mycobacter-ium fortuitum infection and presented with fever, lymphadenopa-thy and bacteraemia in December 1999. During the 9 months oftreatment course in hospital and in outpatient clinic, she receivedamikacin, ciprofloxacin, doxycycline, clarithromycin, or rifabu-tin. Splenic abscess, granulomatous hepatitis, and generalizedlymphadenopathy developed in September 2000. Culture of liverbiopsy and bone marrow both yielded Mycobacterium aviumcomplex (MAC). She was treated with clarithromycin, ciproflox-acin and rifampicin for 6 months followed by ciprofloxacin andclarithromycin for 1 year.In December 2002, the patient was admitted due to fever andabdominal pain for 2 weeks. Abdominal sonography showedmultiple lymph nodes over the mesenteric and aortic areas.Blood cultures and bone marrow cultures carried out during theadmission all yielded MAC. During the following 20 months ofhospitalization, progressive osteomyelitis developed over the cer-vical and thoracic spine complicated with retropharyngeal andprevertebral abscess, quadriparesis, diffuse lymphadenopathy,granulomatous hepatitis with hepatic calcification, and empyemathoracis due to MAC. Several episodes of nosocomial pneumoniaalso occurred and necessitated ventilator support. Her conditionwas refractory to long-term treatment with many antimycobacter-ial agents, including ciprofloxacin (1000mg every day, 1030days), clarithromycin (1000mg every day, 1020 days), azithro-mycin (500mg every day, 188 days), imipenem (2g every day170 days), amikacin (500mg, every two days, 145 days), clofazi-mine (100mg every day, 175 days), mefloquine (500mg thriceweekly, 149 days), linezolid (600mg every 12h, 155 days), andinterferon-g (75mg thrice weekly) for 2 months (Figure 1).

Recurrent multiple hepatic abscesses, hepatic calcification and congenital hearing loss in a child with chronic granulomatous disease.

Chronic granulomatous disease (CGD) is a rare inherited primary immunodeficiency in which phagocytes cannot destroy catalase-positive bacteria and fungi. In this article, we describe a 6-year-old boy with CGD associated with recurrent multiple hepatic abscesses, hepatic calcification and congenital hearing loss because of rare presentation. To the best of our knowledge, congenital hearing loss in CGD has not been reported in the literature. In the treatment of our patient, a combination of antibiotherapy, percutaneous drainage and surgical intervention was used, but multiple hepatic abscesses recurred during the follow-up. On account of this case, we would like to reemphasize that recurrent hepatic abscesses are frequently observed and difficult to treat in patients with CGD. Additionally, we would like to state that congenital hearing loss may be a part of the disease, or it may be coincidental. To clarify the last point, we suggest that all patients with CGD should be tested for hearing impairment.

Massive hepatic artery atherosclerosis of an otherwise suitable donor liver: a case report

Most of the few reports about hepatic artery disease found in the literature describe hepatic artery aneurysms or hepatic artery calcifications. Atherosclerosis of the hepatic artery is not commonly evaluated during deceased donor liver procurement. Herein we present a case of a stable 47-year-old Caucasian female donor whose liver function tests were within normal limits and a liver biopsy showed less than 5% steatosis. The liver when received at our center appeared grossly unremarkable. Back-table evaluation showed a complete occlusion of the trunk of the proper hepatic artery. The pathology report revealed hepatic occlusion due to arterial atherosclerosis. Transplantation was canceled, and the liver was used for isolated hepatocyte perfusion, revealing <25% hepatocyte viability. Hepatic artery atherosclerosis and patency need to be evaluated at the time of procurement to prevent recipient morbidity due to anesthetic induction, or initiation of a recipient abdominal incision prior to declining the liver graft for this rare finding.

Sonographic Features of Hepatic Artery Calcification in Chronic Renal Failure

Little is known about radiological aspects of hepatic artery calcification. For this reason, the sonographic features of calcified hepatic arteries were studied in patients with chronic renal failure who frequently develop tissue calcification due to hyperparathyroidism. Ultrasound was performed in 314 patients on dialysis who underwent examination of the liver, spleen and kidney twice in the past 4 years and were reevaluated with particular attention to acoustic shadowing. Abdominal CT was carried out in 219 of these 314 patients, and ultrasound findings were reevaluated with reference to CT findings. A large acoustic shadow was seen in the hilum that corresponded to the calcified hepatic artery on CT in 8 patients, and in another 9, a similar large shadow was seen in the hilum without CT confirmation. Acoustic shadows of various sizes were definitely or most likely due to arterial calcification within the liver in 36 patients. The strength of shadow depended on the angle at which the ultrasound beam hit the artery. Probable calcification of small arteries accompanying portal veins was seen in 70 patients. These changes are different from those due to pneumobilia and biliary tract diseases. Calcification of the hepatic artery can be identified by its acoustic shadow.

Sonographic features of hepatic artery calcification in chronic renal failure.

Little is known about radiological aspects of hepatic artery calcification. For this reason, the sonographic features of calcified hepatic arteries were studied in patients with chronic renal failure who frequently develop tissue calcification due to hyperparathyroidism. Ultrasound was performed in 314 patients on dialysis who underwent examination of the liver, spleen and kidney twice in the past 4 years and were reevaluated with particular attention to acoustic shadowing. Abdominal CT was carried out in 219 of these 314 patients, and ultrasound findings were reevaluated with reference to CT findings. A large acoustic shadow was seen in the hilum that corresponded to the calcified hepatic artery on CT in 8 patients, and in another 9, a similar large shadow was seen in the hilum without CT confirmation. Acoustic shadows of various sizes were definitely or most likely due to arterial calcification within the liver in 36 patients. The strength of shadow depended on the angle at which the ultrasound beam hit the artery. Probable calcification of small arteries accompanying portal veins was seen in 70 patients. These changes are different from those due to pneumobilia and biliary tract diseases. Calcification of the hepatic artery can be identified by its acoustic shadow.

Fetal hepatic calcifications: Prenatal diagnosis and outcome

Objective: The purpose of this study was to provide information on the causes and postnatal outcomes of fetal liver calcifications that were detected by ultrasound imaging. Study Design: Cases with fetal liver calcifications that were encountered between 1992 and 2001 were evaluated. A detailed fetal ultrasound imaging for associated abnormalities, maternal STORCH (syphilis, cytomegalovirus, herpesvirus 1 and 2, rubella, and Toxoplasma ) analysis, parvovirus serologic condition, and parental cystic fibrosis mutations analysis were performed; amniocentesis was offered in all cases. All infants who were born alive were examined and followed up. Results: Sixty-one pregnant women with fetal liver calcifications were identified. Forty of 61 patients had additional fetal abnormalities; 21 of 61 cases of fetal liver calcifications were isolated; 11/61 patients (18%) had abnormal karyotypes (trisomy 13, 4 patients; trisomy 21, 2 patients; trisomy 18, 1 patient; monosomy X (45,X), 1 patient; 4p−, 22q+, and 8p+, 1 patient). Ten of 11 patients with abnormal karyotypes had other abnormalities that were found on ultrasound imaging. Two patients had intrauterine infection, one patient had cytomegalovirus, and one patient had parvovirus B19 infection. Eighteen of 40 patients underwent pregnancy termination, one fetus died in utero, one newborn infant died, and two infants had neurologic sequelae. Of 21 patients with isolated liver calcifications, one fetus had parvovirus B19 infection and one infant had trisomy 21. The remainder of the infants each had a good outcome. Conclusion: Fetal liver calcifications are relatively common. Isolated cases have a good prognosis after aneuploidy and infection have been ruled out. However, additional major abnormalities present a risk for chromosomal abnormalities, mainly trisomy 13. (Am J Obstet Gynecol 2002;187:1617-22.)

The effects of sevelamer hydrochloride and calcium carbonate on kidney calcification in uremic rats.

The control of serum phosphorus (P) and calcium-phosphate (Ca x P) product is critical to the prevention of ectopic calcification in chronic renal failure (CRF). Whereas calcium (Ca) salts, the most commonly used phosphate binders, markedly increase serum Ca and positive Ca balance, the new calcium- and aluminum-free phosphate binder, sevelamer hydrochloride (RenaGel), reduces serum P without altering serum Ca in hemodialysis patients. Using an experimental model of CRF, these studies compare sevelamer and calcium carbonate (CaCO(3)) in the control of serum P, secondary hyperparathyroidism (SH), and ectopic calcifications. 5/6 nephrectomized rats underwent one of the following treatments for 3 mo: uremic + high-P diet (U-HP); UHP + 3% CaCO(3) (U-HP+C); UHP + 3% sevelamer (U-HP+S). Sevelamer treatment controlled serum P independent of increases in serum Ca, thus reducing serum Ca x P product and further deterioration of renal function, as indicated by the highest creatinine clearances. Sevelamer was as effective as CaCO(3) in the control of high-P-induced SH, as shown by similar serum PTH levels, parathyroid (PT) gland weight, and markers of PT hyperplasia. Also, both P binders elicited similar efficacy in reducing the myocardial and hepatic calcifications induced by uremia. However, sevelamer caused a dramatic reduction of renal Ca deposition (29.8 +/- 8.6 micro g/g wet tissue) compared with both U-HP (175.5 +/- 45.7 micro g/g wet tissue, P < 0.01) and the U-HP+C (58.9 +/- 13.7 micro g/g wet tissue, P < 0.04). Histochemical analyses using Von Kossa and Alizarin red S staining of kidney sections confirmed these findings. The high number of foci of calcification in the kidney of uremic controls (108 +/- 25) was reduced to 33.0 +/- 11.3 by CaCO(3) and decreased even further with sevelamer (16.4 +/- 8.9, P < 0.02 versus CaCO(3)). Importantly, the degree of tubulointerstitial fibrosis was also markedly lower in U-HP+S (5%) compared with either U-HP+C (30%) or U-HP (50%). It is concluded that in experimental CRF in rats, despite a similar control of serum P and SH, sevelamer is more effective than CaCO(3) in preventing renal Ca deposition and tubulointerstitial fibrosis, including better preservation of renal function. These findings cannot be extrapolated to human disease, and further studies in patients are necessary to determine the benefits of either P binder.