A quantitative analysis of lipocytes (fat-storing cells, Ito cells) has been conducted on needle liver biopsies of 8 subjects without hepatic impairment. The mean volume density of lipocytes was 1.88 ± 0.25% of parenchymal volume, and the number of lipocytes per 1,000 hepatocytes (Ito cell index) was 63.45 ± 19.18. A study of the zonal distribution showed that the values were significantly higher in the centrolobular than in the periportal areas. No correlation was evident between the volume density or the number of lipocytes and the volume density of parenchymal steatosis. The high coefficients of variation resulting from the present study are evidence that quantitative data are necessary to evaluate volumetrical or numerical variations of lipocytes.

A quantitative analysis of needle liver biopsies of patients with untreated, uncomplicated cholelithiasis has been performed to better evaluate eventual changes occurring under medical therapy of gallstones. With the light microscope, the intensity of parenchymal steatosis was variable among the patients but the mean volume density of lipid droplets was significantly increased as compared to normal subjects. In addition, there was a significant increase in the volume density of lipocytes (fat-storing cells) without an increase in the number per square area, suggesting a hypertrophy of individual cells. The data obtained by ultrastructural morphometry show a significant increase in the surface density of the rough endoplasmic reticulum in the hepatocytes, a significant increase of the mitochondrial volume density together with the presence of curled mitochondrial cristae and a slight, inconstant intracellular and intracanalicular bile retention. No qualitative or quantitative changes were observed at the level of the smooth endoplasmic reticulum. The activity of the microsomal enzyme NADPH-cytochrome c reductase as evaluated on liver biopsy material was in the normal range. Some of the features observed in this group of patients are reminiscent of alterations previously described in human or experimental cholestasis and suggest that they might depend on a common underlying disturbance in cholesterol and bile salt metabolism.

Objective The aim of this study was to assess the incidence of deep vein thrombosis (DVT) of the lower limbs, using serial compression ultrasound (CUS) surveillance, in acutely ill patients with COVID-19 pneumonia admitted to a non-ICU setting. Methods Multicenter, prospective study of patients with COVID-19 pneumonia admitted to Internal Medicine units. All patients were screened for DVT of the lower limbs with serial CUS. Anticoagulation was defined as: low dose (enoxaparin 20–40 mg/day or fondaparinux 1.5–2.5 mg/day); intermediate dose (enoxaparin 60–80 mg/day); high dose (enoxaparin 120–160 mg or fondaparinux 5–10 mg/day or oral anticoagulation). The primary end-point of the study was the diagnosis of DVT by CUS. Results Over a two-month period, 227 consecutive patients with moderate-severe COVID-19 pneumonia were enrolled. The incidence of DVT was 13.7% (6.2% proximal, 7.5% distal), mostly asymptomatic. All patients received anticoagulation (enoxaparin 95.6%) at the following doses: low 57.3%, intermediate 22.9%, high 19.8%. Patients with and without DVT had similar characteristics, and no difference in anticoagulant regimen was observed. DVT patients were older (mean 77±9.6 vs 71±13.1 years; p = 0.042) and had higher peak D-dimer levels (5403 vs 1723 ng/mL; p = 0.004). At ROC analysis peak D-dimer level >2000 ng/mL (AUC 0.703; 95% CI 0.572–0.834; p = 0.004) was the most accurate cut-off value able to predict DVT (RR 3.74; 95%CI 1.27–10, p = 0.016). Conclusions The incidence of DVT in acutely ill patients with COVID-19 pneumonia is relevant. A surveillance protocol by serial CUS of the lower limbs is useful to timely identify DVT that would go otherwise largely undetected.

Chenodeoxycholic acid (CDCA) is an effective treatment for dissolving gallstones but experimental studies have suggested that it might be hepatotoxic. The present study is concerned with a group of patients undergoing medical therapy for gallstones for periods of 30 days up to 14 months with CDCA (15 mg/kg/day). Routine functional tests, determination of some liver microsomal enzymes and stereological studies of the liver tissue have been performed and the data have been compared with those obtained before treatment. No significant changes were observed in the functional tests throughout the study. Also the microsomal mixed function oxidase system seemed unaffected by CDCA therapy. The histological features of the liver biopsies were not appreciably different from those observed prior to treatment. Although there were large interindividual variations, the volume density of parenchymal steatosis and of the lipocytes remained comparable in the same individual. The ultrastructural features noted in untreated subjects such as curled mitochondrial cristae, slight intracellular bile retention, increased surface density of the rough endoplasmic reticulum were still evident after 14 months of treatment. No additional changes were noted. These results show that no evidence of hepatotoxicity seems to develop in man under therapy with CDCA at the dose considered. But the structural abnormalities observed before treatment appear to persist even in subjects under long-term therapy.

It is known that a wild spectrum of hepatic manifestations can be common presentations of metastatic breast cancer. Pseudocirrhosis pattern has been often described as almost always secondary to systemic chemotherapy and it is defined by morphological liver changes that mimic cirrhosis including capsular retraction, nodularity, parenchyma atrophy and caudate lobe, radiologically identifiable. Acute liver injury is an occasional complication in oncologic patients, and it outlines an organ failure when there is evidence of encephalopathy and coagulopathy (international normalized ratio >1.5) in the absence of pre-existing liver disease, with an illness of <26 weeks duration. The two most common etiologies are leukemia/lymphoma followed by breast cancer but also in this case, liver is involved almost always after chemotherapy, hormonotherapy or radiotherapy. Here we present a case of rapid evolving acute liver failure presented as cryptogenic pseudocirrhosis without any evidence of primitive breast cancer but an incidental demonstration.