Hydrolases secreted into the blood stream cause little problem as they are inactivate at the near neutral pH of blood (7.4). It can be associated with N-acetylglucosamine-1-phosphate transferase (GNPTA). In a case report, I-cell disease was complicated by severe dilative cardiomyopathy (DCM).Though rare, a deficiency of phosphodiesterase which would cleave GlcNAc from the mannose-6-phosphate tag will also cause I-cell disease. The presence of lipids, glycosaminoglycans (GAGs) and carbohydrates in the blood provide for the distinguishing characteristic to separate I-cell from Hurler Syndrome. In Hurlers, only glycosaminoglycans would be present. Diagnosis
Diagnostic measures can include the following. Before birth:

Abnormally low concentrations of UDP-N-acetylglucosamine-1-phosphotransferase enzyme activity in amniotic fluid cells or chorionic villiIn infants:

Elevated plasma lysosomal enzyme concentrations 
Decreased concentration of lysosomal enzymes in cultured fibroblasts and increased in the surrounding medium 
Presence of inclusion bodies in peripheral blood lymphocytes
Low concentrations of UDP-N-acetylglucosamine-1-phosphotransferase enzyme activity as measured in white blood cells

Treatment
There is no cure  for I-Cell disease/Mucolipidosis II disease; treatment is limited to controlling or reducing symptoms. Nutritional supplements, particularly iron and vitamin B12, are often recommended. Physical therapy to improve motor delays and speech therapy to improve language acquisition are treatment options. Surgery can remove the thin layer of corneal clouding to temporarily improve the complication. It is possible that bone marrow transplant may be helpful in delaying or correcting the neurological deterioration that occurs with I-Cell disease.
Tumoral calcinosis is a rare condition in which there is calcium deposition in the soft tissue in periarticular location, around joints, outside the joint capsule. They are frequently (0.5–3%) seen in patients undergoing renal dialysis. Clinically also known as hyperphosphatemic familial tumoral calcinosis (HFTC), is often caused by genetic mutations in genes that regulate phosphate physiology in the body (leading to too much phosphate (hyperphosphatemia)). Best described genes that harbour mutations in humans are FGF-23, Klotho (KL), or GALNT3. A zebrafish animal model with reduced GALNT3 expression also showed HFTC-like phenotype, indicating an evolutionary conserved mechanism that is involved in developing tumoral calcinosis. Clinical features
The name indicates calcinosis (calcium deposition) which resembles tumor (like a new growth). They are not true neoplasms – they dont have dividing cells. They are just deposition of inorganic calcium with serum exudate. Children and adolescents (6 to 25 years) are the most commonly affected. The symptom that the accumulations cause is not pain but swelling around joints. They have propensity to enlarge progressively and ulcerate the overlying skin and extrude. They are most common around shoulders, hips and elbows. Laboratory evaluation reveal normal serum calcium levels and hyperphosphatemia. Rarely ALP (alkaline phosphatase – an enzyme active at sites of bone formation) may be elevated. Treatment is normalization of serum phosphate levels and resection of lesions. Surgical removal should be complete and if part of it is left, recurrence is likely to occur. Cutting through the excised calcium deposition reveals semifluid calcium suspension in albumin encapsulated by fibrous tissue.