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Attempt at electron microscopy was unsuccessful due to marked post mortem degenerative change of the Gaucher cells. Histopathological sections of the skin showed subcutaneous oedema.
The patient had been definitively diagnosed with GD at the age of 1 year based on the identification of Gaucher cells in her bone marrow and decreased leukocyte [sz]-glucosidase activity.
Some patients undergo splenectomy because of splenic enlargement that interferes with their life activity.5 Cytopenia develops in patients who have undergone splenectomy reflects advanced marrow infiltration by Gaucher cells.
As a result, the accumulation of Gaucher cells may cause spleen and liver enlargement, anemia, excessive bleeding and bruising, bone disease and a number of other signs and symptoms.
Lipid accumulation in macrophages results in engorged cells called "Gaucher cells." Rarely, a variant GD maybe secondarily caused by deficiency of the saposin C, the activator of the enzyme [23].
The decreased enzymatic activity leads to accumulation of glucocerebroside within characteristic "Gaucher cells" of mononuclear phagocyte origin identified in most tissues.
(29) Accumulation of immunoglobulin light chains within histiocytes may mimic the appearance of Gaucher cells or of the so-called pseudo-Gaucher cells seen in chronic myelogenous leukemia.
Microscopically, Spleen showed nodular & diffuse infiltrates of "Gaucher cells" in red pulp and these were PAS positive.
(1) This partial enzyme deficiency results in accumulation of glycosphingolipid-laden macrophages (Gaucher cells) throughout the liver, spleen, bone marrow, skeleton and occasionally the lung.
Pulmonary hypertension in Gaucher disease is not common but it is shown to be secondary to interstitial or perivascular infiltration of Gaucher cells or primary in patients exposed to enzyme replacement therapy (ERT).
As a result, lipid engorged cells (called Gaucher cells) amass in different parts of the body, primarily the spleen, liver and bone marrow.