Hepatic splenosis mimicking HCC in a patient with hepatitis C liver cirrhosis and mildly raised alpha feto protein; the important role of explorative laparoscopy.

BACKGROUND: Splenosis is a heterotropic implantation of splenic fragments onto exposed vascularised peritoneal and intrathoracic surfaces, following splenic injury or elective splenectomy. CASE PRESENTATION: A 60 year old cirrhotic patient was referred to us with a hepatic mass, suspected to be HCC in a cirrhotic liver. A computerized tomography scan (CT) demonstrated a cirrhotic liver with a 2 x 2.7 cm focal hypervascular nodule, lying peripherally at the junction of segment 7 and 8. Diagnostic laparoscopy demonstrated a 3 cm exofitic dark brown splenunculus attached to the diaphragm and indenting the surface of segment 7 of the liver. The lesion was easily resected laparoscopically and shaved from the live surface with no need for a liver resection. The histopathological assessment confirmed the diagnosis of splenunculus, with no evidence of neoplasia. CONCLUSION: Hepatic splenosis is not a rare event and should be suspected in patients with a history of splenic trauma or splenectomy. Correct diagnosis is essential and will determine subsequent management plans. In doubtful cases laparoscopic investigation can offere essential information and should be part of the standard protocol for investigating suspected splenosis.

Splenosis is regulated by a circulating factor.

Splenic rupture may result in splenosis, the growth of splenic fragments. We used a parabiotic model to test the hypothesis that splenotic growth is governed by a circulating mediator(s). Pairs of C57B1/6 mice underwent side-to-side anastomosis. After 2 weeks, each of four groups underwent a second operation in which one or both of the partners had a sham operation or a splenectomy, or had splenic fragments transplanted into their peritoneums, or some combination thereof. Six weeks later, splenotic fragments were excised and weighed. Spleen fragments involuted when inserted into the pairs that had two intact spleens. In contrast, in pairs with one intact spleen and one set of fragments, multiple splenules developed, whose aggregate mass was approximately half (ratio, 0.53 +/- 0.04 [mean +/- SE]) that of the original transplanted fragments. Significantly more splenosis (P < .01) developed in pairs with no intact spleens and one set of fragments (0.82 +/- 0.04). The pairs with no intact spleens and twice as many fragments had an intermediate amount of splenosis (0.66 +/- 0.08). The authors conclude that (1) splenosis is inhibited by a factor (or factors) that circulates across the capillary network in a parabiotic pair of mice, and (2) the level of inhibition of splenosis appears to be directly proportional to total splenic mass. The authors speculate that spleen-saving operations, even if partial, may decrease the incidence of splenosis in the patient with a shattered spleen.

Splenic autotransplantation after splenectomy: tuftsin activity correlates with residual splenic function.

This study set out to determine the relationship between splenic function (as assessed by the percentage of pitted red cells) and tuftsin activity, and to confirm the return of effective splenic function after splenectomy for trauma. Twenty-three patients (13 men) took part. Ten of mean age 48.5 (range 30-74) years had had the spleen removed for traumatic rupture and 13 of mean age 49.7 (range 23-66) years had undergone elective splenectomy. At the time of the study all patients had had the spleen removed a minimum of 1 year previously (mean 6.1 (range 1-15) years). Fifty healthy volunteers matched for sex and age were also studied. In each subject, residual splenic function was evaluated by counting the percentage of pitted red cells. Tuftsin activity was also determined. A highly significant negative correlation was found between pitted red cell percentage and tuftsin activity (rs = -0.80, P < 0.001). Compared with healthy controls (mean 21.6 (range 13-37) per cent), tuftsin activity was significantly reduced both in patients who had undergone splenectomy for trauma (mean 4.4 (range 0-9) per cent; P < 0.0001) and in those who had had elective splenectomy (mean 0; P < 0.0001). Tuftsin activity was significantly (P < 0.001) more depressed after elective than traumatic splenectomy. These data confirm a decrease in tuftsin activity following splenectomy and show that this deficit is significantly greater after elective than emergency removal. These observations confirm that residual splenic function is often present after traumatic splenectomy.