In particular, splenosis is differentiated from different forms of  lymphoma, metastisized cancers, cancer of the abdomen and pleural tissues, primary kidney or liver tumors, endometriosis or non-cancerous swollen lymph nodes. Treatment
Treatment of splenosis is often unnecessary, because it is benign and usually asymptomatic. For people experiencing symptoms, the splenic tissue can be removed by surgery. Epidemiology
Splenosis is slightly more common in males than females, probably due to the greater frequency of physical trauma experienced by men. == References ==
During periods of fasting, fatty acids are also an important energy source for the liver and other tissues.Mutations in the HADHA or HADHB genes that cause mitochondrial trifunctional protein deficiency disrupt all functions of this enzyme complex. Without enough of this enzyme complex, long-chain fatty acids cannot be metabolized. As a result, these fatty acids are not converted to energy, which can lead to some features of this disorder. Long-chain fatty acids may also build up and damage the liver, heart, and muscles. This abnormal buildup causes other symptoms of mitochondrial trifunctional protein deficiency.The mechanism of this condition indicates that the mitochondrial trifunction protein  catalyzes 3 steps in mitochondrial beta-oxidation of fatty acids: long-chain 3-hydroxyacyl-CoA dehydrogenase (LCHAD), long-chain enoyl-CoA hydratase, and long-chain thiolase activities. Trifunctional protein deficiency is characterized by decreased activity of all 3 enzymes. Clinically, trifunctional protein deficiency usually results in sudden unexplained infant death, cardiomyopathy, or skeletal myopathy. Diagnosis
Diagnosis of mitochondrial trifunctional protein deficiency is often confirmed using tandem mass spectrometry. Genetic counseling is available for this condition. Additionally the following exams are available:

CBC
Urine test

Treatment
Management for mitochondrial trifunctional protein deficiency entails the following:
Avoiding factors that might precipitate condition
Glucose
Low fat/high carbohydrate nutrition

See also
Long-chain acyl-CoA dehydrogenase

References
Further reading
Nyhan, William L.; Hoffman, Georg F.; Barshop, Bruce A.; Al-Aqeel, Aida I. (2012). Atlas of Inherited Metabolic Diseases 3E. CRC Press. ISBN 9781444149487. Thöny, Beat; Duran, Marinus; Gibson, K. Michael; Dionisi-Vici, Carlo (2013). Physicians Guide to the Diagnosis, Treatment, and Follow-Up of Inherited Metabolic Diseases. Springer. ISBN 9783642403378.