Splenic purpura

Introduction Spleen purpura is one of the clinical symptoms of hepatic purpura. Most patients with hepatic purpura are asymptomatic, and a small number of hepatic enlargement and mild transaminase may occur, accompanied by spleen purpura.

Cause

(1) Causes of the disease

The cause is not clear, and may be associated with diseases such as severe tuberculosis, malignant tumors, acquired immunodeficiency syndrome (AIDS), taking certain drugs (such as steroids, azathioprine, tamoxifen), long-term hemodialysis, organs The application of immunosuppressive drugs after transplantation is related. It has been reported that a human or immunodeficiency virus (HIV)-positive population may have a liver or spleen of bacillary peliosis (BP), which is associated with the infection of the genus R. henselae and belongs to animal-borne parasitic diseases. Close contact with cats or infection with R. henselae and related pathogens.

(two) pathogenesis

The connection between the hepatic sinus and the central venous connection causes the hepatic sinus to dilate, or the hepatocytes are first necrotic or the sinusoidal barrier is destroyed, and the endothelial cells are damaged. The red blood cells enter the gap of the Disse from the hepatic sinus cavity to form a cystic cavity filled with red blood cells. It is also believed that hepatic purple spot disease, hepatic venular occlusive disease, hepatic sinus dilatation and perihepatic fibrosis are the same pathological process, which shows that endothelial cells in different parts are damaged. Various virulence factors can cause defects in the immune system, such as immunoglobulin IgA, IgG, IgM deficiency, complement system defects, T cell and B cell defects or combined immunodeficiency; secondary immunodeficiency disease, can be found in all age groups The incidence of the population is also higher than that of the original. These immunodeficiencies can be clinically manifested in a variety of manifestations, such as the spread, aggravation or recurrent episodes of infection; protein, calorie malnutrition; diarrhea and nutrient absorption disorders; diabetes, rapid deterioration of uremia; rapid spread and aggravation of malignant tumors The above manifestations may occur simultaneously or sequentially with hepatic purpura.

The liver is swollen and there are purple-blue or blue-black plaques on the surface. The lesions were randomly distributed and limited to one leaf or diffuse whole liver. The liver section is honeycomb-shaped, with pockets of varying sizes and filled with blood, ranging from a few millimeters to several centimeters. Under the microscope, the hepatic sinus is cystic dilatation, and the endothelial cells lining the cystic cavity are extensively damaged. The cavity is filled with red blood cells, which can communicate with the normal hepatic sinus or central vein. The Dicle's gap is dilated, and the endothelial cell barrier between the hepatic sinus is destroyed. Occasionally, red blood cells pass through. Endothelial cells and Kupffer cells proliferate. There is fibrosis around the hepatic sinus and hepatic venules, and hepatocyte atrophy is seen around the lesioned cyst. Liver, kidney, bone marrow, and lymph nodes can also be affected.

an examination

Related inspection

Blood routine liver, gallbladder, spleen CT examination

Stomach sputum burning pain, noisy pantothenic acid, mouth dry mouth bitter, thirsty do not want to drink, sweet and sticky mouth, sweet food is sour water, nausea, body weight, yellow urine, poor stool, yellow greasy tongue, The number of pulse slips.

Differential diagnosis

1. It needs to be differentiated from infectious purpura and drug-induced purpura. The latter is characterized by no certain predilection sites, asymmetric, and does not appear in batches.

2. It is still necessary to distinguish from thrombocytopenic purpura. The latter's purpura is characterized by scattered small spots or flakes, no tendency to fuse, no prominent in the skin surface, and asymmetric distribution.

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