Soft plaque syndrome is a rare inflammatory disease first reported by Michaelis and Gutmann in 1902. In 1903, von Hansemann named the disease soft plaque in Greek, malaco (soft) and plakia (plaque). Stanton and Maxted (1981) reviewed 153 patients. Soft plaque syndrome occurs in the bladder in 40%, in the ureter in 11%, in the renal parenchyma in 16%, and in the retroperitoneal cavity in 16%. Soft plaque syndrome can also occur in other parts of the body such as the reproductive organs, gastrointestinal tract, skin, bones, mesenteric lymph nodes, etc. Patients with urinary system soft plaque syndrome often have chronic Escherichia coli bacteriuria.
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Urinary soft plaque syndrome
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1. What are the causes of urinary soft plaque syndrome?
2. What complications can urinary soft plaque syndrome lead to?
3. What are the typical symptoms of urinary soft plaque syndrome?
4. How should urinary soft plaque syndrome be prevented?
5. What kind of laboratory tests need to be done for urinary soft plaque syndrome?
6. Dietary taboos for patients with urinary soft plaque syndrome
7. Routine methods for the treatment of urinary soft plaque syndrome in Western medicine
1. What are the causes of urinary soft plaque syndrome?
1. Etiology
The etiology of this disease is complex, often accompanied by malnutrition and other diseases. The urinary soft plaque syndrome is closely related to Escherichia coli infection. Why only a few patients with Escherichia coli infection have concurrent soft plaque syndrome is currently believed to be related to host immune deficiency. However, abnormal humoral immunity has no significant effect on the onset of soft plaque syndrome. The main problem is the low cellular immune function, which reduces the phagocytic ability of phagocytes. Experimental evidence shows that the microtubule function (Microtubular function) controlled by cyclic nucleoside phosphate (cyclic nucleoside phosphate) is defective, leading to the loss of bactericidal ability within cells. Some scholars point out that the cyclic guanosine monophosphate (Cyclic-guanosine monophosphate, cGMP) level in some monocytes is low, thereby reducing the release of β-glucuronidase, causing changes in the intracellular digestive process. Wener and Curran found that the reduction in the cGMP/cAMP ratio in monocytes is more significant than the reduction in the level of cGMP alone. This defect causes changes in the lysosomal environment, resulting in the calcification of undigested bacterial fragments. Bacteria themselves can also produce endocytic membranes or toxins to resist phagocytosis, or cause the loss of intracellular phagocytic and digestive ability.
2. Pathogenesis
The mechanism is unknown. Stanto and Maxted (1981) reported that in 93 patients with this disease, urine, lesion tissue, and blood cultures confirmed the presence of Escherichia coli infection in 84 cases (89%), and 40 patients had immune deficiency syndrome, autoimmune disease, cancer, or other systemic diseases.
It is speculated that bacteria or bacterial fragments form calcium phosphate crystals, i.e., Michaelis-Gutmann bodies. The vast majority of observations support the theory that the defect in the digestion of bacteria within the phagosomes triggers an abnormal immune response, which is the etiology of nephrosclerosis.
The histological features include PAS-positive large eosinophilic histiocytes called von Hansemann cells, and small basophilic cytoplasmic extracellular and intracellular stone bodies called Michaelis-Gutmann bodies. Electron microscopy shows foamy softening plaque histiocytes phagocytizing intact Escherichia coli or bacterial fragments. Although the typical Michaelis-Gutmann bodies can confirm the diagnosis, they may not be present in the early stages of the lesion. Callea et al. (1982) reported that throughout the course of the disease, macrophages in renal and bladder softening plaque foci contain a large amount of α-antitrypsin, and immunohistochemical staining of it helps in the early diagnosis and differential diagnosis of the disease.
2. What complications can urinary tract nephrosclerosis easily lead to?
Bilateral renal nephrosclerosis is prone to renal failure. It is a rare histologically unique inflammatory reactive lesion, usually caused by intestinal bacteria, which can invade the mucosa of many organs, such as the prostate, ureter, pelvic mucosa, bone, lung, testis, gastrointestinal tract, skin, and kidney.
3. What are the typical symptoms of urinary tract nephrosclerosis?
Patients with weak physique, decreased immune function, or other chronic diseases often suffer from urinary tract infections. The most common bacteria isolated from urine cultures are Escherichia coli, followed by Proteus, Klebsiella, and mixed infections. Nephrosclerosis often presents with fever, lumbar pain, and lumbar masses. Cystosclerosis may cause symptoms of bladder irritation and hematuria. Cystoscopy shows that the lesions are often distributed on both sides of the bladder wall, appearing as scattered or clustered yellowish or grayish to brownish soft velvet-like or slightly elevated plaques, measuring 0.1 to 0.3 cm in size. The surface is generally covered by undamaged mucosa, and superficial ulcers may also be present. As the lesions progress, they become moldy, rigid, and form broad-based masses. Involvement of the ureters can lead to narrowing and cause renal function damage, even leading to dysfunction. Nephrosclerosis rarely spreads to the perinephric space, but can be complicated by renal vein and inferior vena cava thrombosis. Testicular involvement may lead to orchitis. Prostatic nephrosclerosis is rare, and when it occurs, it is easily confused with prostatic cancer.
4. How to prevent urinary soft plaque syndrome
The etiology of this disease is complex, often accompanied by malnutrition and other diseases. Urinary soft plaque syndrome is closely related to Escherichia coli infection. Why only a few patients with Escherichia coli infection develop soft plaque syndrome among many patients. It is currently believed that urinary soft plaque is related to host immune deficiency. However, abnormal humoral immunity has no significant impact on the onset of soft plaque syndrome. The main cause is low cellular immune function, which reduces the phagocytic function of phagocytes. Therefore, clinical prevention should be aimed at the etiology, avoid holding urine in the ordinary course, and actively treat patients with existing urinary system infection, which can reduce the occurrence of complications.
5. What laboratory tests need to be done for urinary soft plaque syndrome
1, Urine examination:Urine routine examination shows a small to large number of red blood cells and white blood cells; urine cytology examination, urine sediment smear or midstream urine bacterial culture can detect pathogenic bacteria, commonly Escherichia coli; urine exfoliated cell examination shows typical soft plaque tissue cells.
2, Renal soft plaque syndrome imaging:The manifestations are not specific and are difficult to differentiate from renal malignant tumors. In abdominal X-ray films, the outline of the kidney can be seen to be enlarged, intravenous urography shows compression of the renal pelvis and calyces, according to the degree of disease progression, renal excretion function can be weakened, even without function, the affected kidney does not show shadows, B-ultrasound examination shows enlargement of the kidney, unclear boundary between the cortex and medulla, multiple foci of strong echo in the renal area, occasionally there are diffused hyperechoic areas, which are difficult to differentiate from abscesses. Renal CT examination usually shows a non-uniform mass, due to frequent necrosis, CT enhancement scan shows low-density areas in the renal lesion sites, renal angiography shows compression and expansion of renal artery branches, sometimes new blood vessels can be seen, renal pelvis, ureter, bladder soft plaque syndrome urography shows filling defects, bladder soft plaque syndrome cystoscopy shows bladder masses and inflammatory changes.
6. Dietary taboos for patients with urinary soft plaque syndrome
1, Boil 30g of Job's tears and 30g of red bean into a thin porridge for consumption, it can prevent and treat cancer when taken regularly.
2, Boil 20g of silver ear in water and take it internally, once a day, it can prevent and treat cancer.
3, Boil 120g of fresh porophyllum, 250g of rabbit meat (cut into pieces) in water, season with salt, drink the soup and eat the meat, it can prevent and treat cancer when taken regularly.
4, Boil 100g of glutinous rice to make porridge, add 30-50g of arrowroot powder, and a suitable amount of brown sugar. Regular consumption can prevent cancer.
5, Boil 100g of luffa (clean, peel and cut into pieces) with 100g of duck blood, add seasonings and cook until done, it can clear heat, eliminate dampness, and detoxify, prevent and treat bladder cancer.
6, Squeeze 100g of fresh grape juice, 100g of fresh lotus root juice, and 60g of fresh rehmannia juice, mix them in an earthen pot and boil, add a suitable amount of honey and serve warm, it can be used for blood in urine and urinary pain due to bladder cancer.
7, Cut 100g of fresh radish into slices, marinate with white honey for a while, then dry it on an iron plate, dip it in honey again and repeat the process until 50g of white honey is used up. After cooling, chew slowly and drink a few sips of salt water, it can treat urinary pain due to bladder cancer.
8, Use 250g of sugarcane (cut into small pieces), 100g of white grass root cut into small sections, wrapped in a cloth bag together, boil with 100g of mung bean seeds in water until the beans are soft, remove the sugarcane and grass root, drink the soup and eat the beans. You can also add a suitable amount of rock sugar, suitable for patients with明显 blood in urine due to bladder cancer.
7. Conventional methods of Western medicine for the treatment of ureteral amyloidosis
1. Treatment
Ureteral amyloidosis is an inflammatory lesion that requires long-term antibiotic treatment, which can improve symptoms but is prone to recurrence. Some scholars have proposed the use of various antibacterial drugs, which can eliminate bacteria in urine, but cannot prevent the progression of the disease, because general antibiotics can only eliminate extracellular bacteria in amyloidosis patients, but cannot kill bacteria that enter the cells. Practice has proven that some antibacterial drugs such as rifampin and sulfonamide can enter phagocytes to help kill intracellular bacteria. In recent years, fluoroquinolones have been increasingly valued for their unique tissue penetration. The high concentration of fluoroquinolones in macrophages is very beneficial for clearing intracellular pathogens. Many studies have shown that the oral administration of ciprofloxacin 500mg, twice a day, alone in the treatment of renal amyloidosis is effective, with an efficacy rate of up to 90%. Sawamura found that bladder amyloidosis using enoxacin 600mg, once a day, orally for 8 weeks resulted in complete disappearance of pathological damage. For bladder amyloidosis, in addition to long-term application of antibacterial drugs, electrocoagulation of bladder lesions can also be performed through the urethra, which is beneficial for healing of the lesions. Due to the high recurrence rate of this disease, regular follow-up cystoscopy is required. For patients with renal amyloidosis, although some scholars suggest long-term application of antibacterial drugs, most scholars believe that unilateral renal lesions, once clinically diagnosed as amyloidosis, require nephrectomy on the affected side.
In recent years, some scholars have proven that cholinergic drugs and vitamin C can correct the functional defects of phagocytes in the body. Clinical application of carbamylcholine (carbamylmethylcholine, Bethanechol) 10-25mg, 4 times a day, and vitamin C treatment of amyloidosis has varying degrees of efficacy, but it is necessary to closely observe the condition. If there is no clinical relief and a trend of development, nephrectomy may be required.
2. Prognosis
The prognosis is related to the extent of the lesion. Stanton and Maxted (1981) reported that the mortality rate of the disease is over 50%, and patients with bilateral renal amyloidosis or transplant renal amyloidosis usually die within 6 months. Patients with unilateral renal amyloidosis can survive for a long time after nephrectomy.
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