scales is about to fall off or fall off the thin stratum corneum. Its size, shape, thickness, quantity, color varies, and some dry, some oily; mostly with skin erythema or papules damage secondary damage. erythema is the dermal papilla layer localized or systemic capillary network expansion to produce local or systemic red rash. Psoriasis, seborrheic dermatitis, pityriasis rosea, Vice psoriasis, discoid lupus erythematosus and other diseases can be manifested as erythematous scaly.[Cause]
hodgkin's disease is caused by what the?
1.EBV HL are few epidemiological tend to infection as the cause of malignant tumors. That may be associated with early onset HL EBV infection, which is due to a number of studies have shown that there is a history of mononucleosis syndrome patients with an increased risk of HL recurrence, and patients with EBV HL antigen titer increased. Despite its long-term epidemiological and serological data in doubt, but until 1987, Weiss and other applications southern blot method was confirmed Hodgkin's lymphoma, EBV genome exists to prove that the EBV and the more classical HL. Currently, the application of highly sensitive in situ hybridization, 18% to 50% of Hodgkin lymphoma is EBV (+). In addition, the application of direct anti-EBV probes revealed that some samples of hodgkin's lymphoma is very evident in the EBV episome DNA, prompted EBV infection occurs in tumor cells before clonal expansion. EBV (+) of malignant cells expressing viral latent membrane protein (LMP1), this protein prevents apoptosis in b cells (via induction of bcl-2 can mediate this effect occurs), this evidence is further evidence of EBV hodgkin's lymphoma of the play an active role in disease. Transgenic animal model experiments show that virus latent membrane protein has a carcinogenic effect. Again, LMP1 can up-regulate many cellular genes, including CD23, CD39, CD40 and MHC Ⅱ molecules and cell adhesion molecules such as LFA-1, LFA-3 and ICAM-1. EBV genome detection and mixed-cell Hodgkin's lymphoma. Studies have found that in mixed cell type in the proportion of EB virus-positive cases (58%) than nodular sclerosis (18%, P <0.001) were significantly higher. The cause of the doctrine of eb virus infection in isolated RS cells as eb virus genome further confirmed. Recently, it was reported that CD99 is down-RS cells in Hodgkin's basic requirements. The EBV latent membrane protein (LMP-1) can lead to high expression of CD99 reduced, the former in EBV-associated Hodgkin lymphoma Hodgkin-RS cells is highly expressed. That EBV LMP-1 protein in the transcriptional regulation of CD99 plays an important role in the reduction, leading to Hodgkin-RS cells occurred. eb virus but can not explain all cases, especially in developed countries, the most common type - nodular sclerosis. In the United States and Europe, most of the HL with EBV has nothing to do, especially young people, only 20% of EBV HRS +. Deleclue analysis of recurrence and other HL cases, the primary tumor is EBV HRS +, but the relapse specimen of EBV HRS-, speculated that the virus is lost during disease progression, but no formal evidence of primary tumor and recurrent tumor clone is the same. Moreover, the patient when the disease is only 5 years old, so can not represent the typical youth groups. HL cases are clearly some EBV seronegative, the EBV is not the cause of all cases.
2. other factors in the infection of non-EBV-associated cases are more likely to cause infection of other factors. herpes viruses are widely distributed in nature, may be related to the pathogenesis of HL. Recently, studies have shown that human herpes virus -6 (human herpesvinus-6, HHV-6) genome integrated into the host cell's DNA. HL patients and HHV-6 antibody titer increased, compared with older, higher antibody titers in young people, in EBV HRS-cases than in cases of high EBV HRS +. HHV-8 is a human herpes virus family, newly discovered viruses, EBV and HHV-8 although almost no homology between the sequences, but there are some features the same characteristics, EBV genes up-regulated in many cells, and these genes with HHV-8 genome homology. But there is no evidence that HHV-8 and HL pathogenesis.
polyomavirus JC has always been associated with acute lymphoblastic leukemia, whereas the HL-type disease in epidemiology and youth have many common features. It has been detected in the HL or SV40 virus long and short pro-lymphatic milk, did not get positive results. Application of PCR technology to detect 46 cases of HL JC and BK, did not find the virus genome. Other studies do not support 5 and 12 adenovirus, human T-cell lymphoma virus Ⅰ, Ⅱ or human retrovirus 5.
(B) the pathogenesis
1. the vast majority of genetic abnormalities in patients with classic Hodgkin lymphoma clone cytogenetic abnormalities, such as different cases and different abnormalities, and clones for heterogeneity within the exception, suggesting chromosomal instability. Many cases show 14q abnormalities, similar to the b-cell lymphoma, but rarely t (14; 18) exception. Two research groups using fluorescence in situ hybridization (with or without fluorescence immunophenotyping), found that all cases of hodgkin's lymphoma clone RS cells show abnormal values. Earlier reports, about 1 / 3 of the hodgkin's lymphoma found bcl-2 rearrangement, but other laboratories have not detected bcl-2 rearrangement. Moreover, high reactivity, such as reactive tonsil tissue was also found that bcl-2 rearrangement. Transformed with EBV-related protein in cultured cells can be increased Bcl-2, this evidence further showed that bcl-2 expression and the relationship between Hodgkin's lymphoma. Overexpression of bcl-2 immunohistochemical studies have concluded are not consistent. However, bcl-2 expression seems to histology, EBV (+) or t (14; 18) translocation independent, bcl-2 expression enhanced cell may exist in the background, and the incidence of hodgkin's lymphoma not play an important the role. But a research group application cytogenetic analysis, clearly confirms the presence of tumor cells, bcl-2 rearrangement, without the risk of t (14; 18). Most recently, in hodgkin's lymphoma in the discovery of new inhibitor of apoptosis Bcl-X (L), 94% of hodgkin's lymphoma in Bcl-X (L) is positive, and most of the RS cells express high-strength . In non-hodgkin's lymphoma expressed low (<20%), but except for mesh center lymphoma. It is speculated, Bcl-X (L) in the abnormal expression of the RS for the inhibition of apoptosis may be the etiology of Hodgkin's lymphoma. Found Bcl-X (L) expression correlated with EBV. By immunohistochemical analysis, in the Hodgkin and other lymphomas CD30 has been detected in p53 tumor suppressor gene expression. However, a recent study found that in eight cases of hodgkin's lymphoma non-Hodgkin and RS cells are p53 mutation.
recently, Humboldt and other reports, from HL lymph node biopsy samples, IκBα mrna is overexpressed in HRS cells, and to detect IκBα gene mutations, generate C-terminal truncated protein, suggesting that this protein could not inhibit NF-κB-DNA binding activity, and prevent apoptosis in HRS cells and lead to proliferation. So with HL pathogenesis.
NLPHL cytogenetic data are few and the findings of cytogenetic abnormalities is also inconsistent. tilly et al reported a large series of HL, only one case of NLPHL, NLPHL in this case has 46XY karyotype. Hansmann et al reported a case of high diploid NLPHL, 6q-, 21, and several are not clearly marked. The study found that originated in the NLPHL cell line DEV has the following abnormal karyotype: 48, XXY, t (3; 14) (3; 22), t (3; 7), del3, -2, 12, mar. Ploidy analysis of HL cases, 5 cases of NLPHL in 3 cases aneuploidy was not detected tetraploid, and tetraploid common in classical HL. bcl-2 gene rearrangement in only a small portion of cases detected by immunohistochemical detection of bcl-2 protein expression, the low number of positive cases. Inferred, bcl-2 translocation may not play an important role in pathogenesis of NLPHL.
2.HL the origin of tumor cells in patients with long believed that, HL representatives of different histological types of morphological variation of the same disease, in which HRS cells in a reactive background, and each have a characteristic histological subtype cells. In the past 20 years, people gradually found out that the concept is only partially true, such as nodular lymphocyte-predominant HL and HL of other types, different biological disease.
(1) HRS cells in classical HL Origins: The earliest expression of Ig HRS immunohistochemical studies such as the 1974 and subsequent Taylor Garvin, etc., etc., in their study confirmed HL biopsy specimens obtained igg results HRS expression, indicating that the HRS originated in b cells produce Ig, but other immunohistochemical studies have shown that HRS originated in non-lymphoid cells. Until then the application of monoclonal antibody technology, found the CD30 molecule. classical HL the HRS that the selective expression CD30, but only in some normal individuals activated lymphoblastoid cells. The data for the first time that the origin of HRS lymphocytes. Studies have shown that the genetic level, HRS occurrence of clonal Ig gene rearrangement, in Rajewsk series of 13 cases detected 12 cases of HL, stein also reported 25 cases to 24 cases of detected rearrangements, that 95% of b-cell origin of HLs . Sequence analysis showed that, in the rearrangement of the V region has a high load of somatic mutation. Because some of the classic HLs of HRS cells express one or more T-cell antigen and 40% of the cells in HL series with T cell phenotype and genotype, suggesting that the remaining 5% originated in HL into the classic T-cells. However, in the HRS cells has not been detected in the TCR gene rearrangement, this hypothesis can not be confirmed. Recent studies have found that classical HL originated in the germinal center b cells rather than germinal center B cells; B cell lines can occur two separate progeny into, a form HRS cells, another form NHL; produce a complete change in the conversion of HL a common progenitor cell morphology and immune phenotype (no expression of CD20, CDl0, Bcl-6 and igm and lower mutation mechanism, expression of CD30 and CDl5) and into the nhl cells more or less retained the B cell lineage ancestors characteristics. Cases of a particular group of HRS cells derived from single transformed cells completely, and clone proliferation. WHO (2001) classification that nodular lymphocyte-predominant hodgkin's lymphoma from the mother cell from the germinal center b-cell differentiation stage, and classical Hodgkin lymphoma from germinal centers from 98% in the mature stage of differentiation B cells.
(2) NLPHL in lymphocytes and (or) cells (H and L) of the cell origin: lymphocyte-predominant HL, is characteristic of tumor cells [ lymphocytes and (or) cells] of the subtypes, with the progressive transformation of germinal centers on the great tuberosity. immunohistochemical studies have shown that (H and L) cells are b-cell series. Because they express a large number of B cell markers including CD19, CD20, CD22, CD79a and J chain, and recent molecular studies also suggest: H and L. Cells are transformed into the center of the mother cell. Groups in the major clone, immunoglobulin heavy chain continuing high somatic mutations. In developed countries, EBV rarely associated with H and L cells, probably has nothing to do with this disease. H and L cells are often CD3, CD4, CD57, CD40, L-T-cells around, but this T-cell rosette significance is not clear. NLPHL may co-occur with large cell lymphoma to large b-cell lymphoma or. Numerous studies show that at least in some cases, B-DLCL and NLPHL correlation on the clone. NLPHL can have the cell-rich b-cell lymphoma (HRBCL) similar to nodules or large area, at least some HRBCL cases originated in NLPHL. T-cell-rich b-cell lymphoma (TCRBCL) may exist above. The NLPHL cell genes is scarce, and the study group reported cytogenetic abnormalities is also inconsistent.
3. Cytokine-Hodgkin's lymphoma of the main histological features are: a considerable amount of collagen sclerosis, inflammatory cells and malignant RS cells, while the RS cells and background cells cytokines led to the industry based on the difference. In the complex between these cells in a paracrine and autocrine role. RS cells and reactive cells produce various cytokines affect both the RS cells but also affect the surrounding cellular environment. For example, transforming growth factor-β1, (TGF-β1) mrna in nodular hodgkin's lymphoma of eosinophils has been tested to. Although the role of TGF-β1 determined by its relationship with other factors and the interaction of target cells, but it can stimulate fibroblast proliferation and production of collagen, collagen formation may play an important role, which is nodular Hodgkin lymphoma characteristics. The incidence of this disease play an important role in other cell factor is IL-5. IL-5 is eosinophil growth factor, and the number of eosinophils in Hodgkin lymphoma cells in the main background in the RS cells were also found in IL-5mRNA. In addition, RS is also secreted IL-1, IL-9, tumor necrosis factor-α, granulocyte - macrophage stimulating factor and clone macrophages-stimulating factor. IL-6 present in 10% to 60% of RS cells, which can induce proliferation of plasma cells and can stimulate lymphocyte proliferation and maturation. hodgkin's lymphoma of the different histological features may be RS and reactive background cells such as T lymphocytes, histiocytes and eosinophils secrete cytokines network results[Sign]
hodgkin's disease early symptoms?
1. symptoms onset and the first invasion of the tumor site is shown in table 1 with a single symptom onset in 504 patients (and there are 2 or 3 in the initial symptoms are not Statistics inside) to superficial lymph nodes as the first symptoms accounted for the vast majority (75%), of which the majority of cervical lymph nodes; abdominal symptoms abdominal pain, abdominal mass; chest symptoms of chest tightness, chest pain, cough, shortness of breath and the chest tumor; head and neck symptoms of sore throat, swollen tonsils and nasal congestion, etc.; whole body symptoms of fever. The first invasion of the tumor site in table 2, the vast majority of superficial lymph nodes, abdominal lymph nodes including mesenteric and retroperitoneal lymph nodes, and mediastinal lymph nodes. HD starting less extranodal involvement, mainly the small intestine, stomach, and Waldeyer's ring.
2. the whole body symptoms include fever, night sweats and weight loss, followed by pruritus and fatigue. treatment when symptoms are more associated with the whole body (55%), there is a whole body symptoms the prognosis is poor performance. HD fever is more common, and have certain characteristics. About 1 / 6 in HD patients, there may be such a cyclical fever. The fever is characterized by a gradual increase in the next few days, the temperature at 38 ~ 40 ℃, for several days. And then gradually decreased to normal. After 10 days to 6 weeks or longer interval, body temperature started to rise again, again and again, recurring, and gradually shorten the interval.
pruritus is a symptom of HD is more common, can be gradually developed from the local to the body, beginning with mild piyang enable the skin off, skin thickening, severe itching can scratch the skin, causing infection and skin pigmentation. Another special symptoms of alcohol pain, that caused the tumor site pain after drinking alcohol, drink a few minutes to several hours in the performance occurred.
3. lymph nodes is the most common clinical manifestations of HD, including the most common superficial lymph nodes, in the first invasion of the tumor in 86%, such as with abdominal and thoracic lymph nodes, accounted for 92% of the first part of the invasion, (Table 2). This result is similar to foreign data, HD violation of lymph nodes accounted for 9l%, 9% of extranodal by occupation. superficial lymph nodes easier to find and diagnose, but also initially misdiagnosed as lymphadenitis or lymph node tuberculosis. Mainly in the cervical lymph nodes, followed by axillary and inguinal lymph nodes, there are other lower jaw, ears, ears, chin, occipital, tackle and in[Aftertreat]
hodgkin's disease ate?[Prevent]
how to prevent scaly erythema ?
⒊ maintain adequate sleep, to eliminate trauma, lift the ideological concerns.
(2) Ⅰ B, Ⅱ B and Ⅲ A stage full of choice lymph node irradiation.
(5) Ⅳ of patients with chemotherapy, as most scholars now accept treatment (Figure 1).
① dose: every 4 to 6 weeks 40 ~ 44Gy.
② radiation field: subtotal lymph node (STLI) irradiation diaphragm disease and the use of full mantle field irradiation ribbed wild, wild Ah subphrenic lesions using inverted and the mantle field. All lymph nodes (TLI) that mantle field irradiation plus down Ah wild.
③ Because patients in the developmental stages of children: In order to prevent radiation-induced developmental disorders, should be appropriately reduced radiation dose, radiation field is also limited as appropriate, such as to expand the local field.
dose adjustment according to different age groups as follows: <5 years old 20Gy, 5 ~ 10 years old 25Gy, 11 ~ 15 years old 30Gy. Early HD by radical radiation can get a good result. Stanford University results are shown in table 12. In recent years, for early hodgkin's disease as a high cure rate and reduce the second primary cancer, the treatment tend to be conservative. Appropriate cases can be regional irradiation chemotherapy, long-term results and all the same lymph node irradiation.
2. chemical treatment with the drug increases, especially in the past 20 years combined experience in the development and chemotherapy accumulation, HD of chemotherapy has significantly improved. Commonly used chemotherapy regimens are shown in table 13.
about 75% to 80% of HD patients treated by MOPP reach complete remission, about 60% to 65 % of patients can have cured. ABVD and MOPP without cross-resistance as a complementary treatment to some extent to improve the efficacy of MOPP (Table 14, 15).
after many years of clinical research, ABVD program inhibition of male germ cells compared with MOPP light, as temporary; 2 primary acute leukemia, especially rare. Further research, scholars compare the half-Italian half-ABVD plus MOPP that MA / MA than in the whole entire MOPP plus ABVD, the MM / AA results, complete remission rates were 90%, the former 5-year disease-free survival rate was 78% , which is 72%, and no significant difference.
MOPP-ABV program canceled dacarbazine (en mi amine nitrogen), doxorubicin (adriamycin) dosage added to 35mg/m2, administration method there is a certain improvement, followed by 170 cases of 7 years Description: ① complete remission rate of 84%, ② 7-year survival rate of 80%, ③ 7-year disease-free survival rate was 65%, with no significant difference between MOPP-ABVD, but the patient tolerated well. Europe's new design CHLVPP / EVA solution: chlorambucil (tumor Ning) 6mg/m2 oral procarbazine (benzyl methyl hydrazine) 90mg/m2 oral prednisolone 50mg orally, 1 to 7 days; VP-16 75 ~ 100mg/m2, orally, 1 to 5 days; vincristine 1.4mg/m2 intravenously on day 1; vinblastine 6mg/m2 and doxorubicin (adriamycin) 50mg / m2 intravenously on day 8. 5-year follow-up by 701 cases Description: 5-year survival rate of 92%, 5-year disease-free survival rate was 85%, but patients with acute myeloid leukemia and MDS is relatively small.
(b) the prognosis
from the above discussion, it is easy to see that by proper treatment may cure the majority of HD. In addition to attention outside of the aforementioned principles of treatment, should note the following two aspects:
1. Recurrence of the initial treatment for patients with treatment failure or relapse after treatment, patients should be taken to strengthen the special deal with. Most of these patients with a certain drug-resistant tumor cells, even with multi-drug resistance gene (mdr) and p-glycoprotein expression. Therefore, the choice and do not cross-resistant chemotherapy such as ABVD program and high-dose chemotherapy plus autologous bone marrow transplantation and granulocyte - colony stimulating factor (G-CSF) can achieve better results. Armitage, etc., and Carella and other reports, such patients can be treated with 35% to 45% long-term survival. hematopoietic stem cell infusion has also achieved some results, but long-term efficacy remains to be seen. Now that the main treatment for this 1st remission period than 1 year of HD patients, unsuitable for elderly, poor general condition, and multiple lesions in patients resistant to conventional chemotherapy.
2. Long-term complications of treatment can make most effective treatment as long-term survival of patients, chemotherapy and (or) long-term complications of radiotherapy is noteworthy. The more important are:
(1) acute myeloid leukemia (AML): occurs in 2 to 10 years after treatment, may have a variety of molecular biology abnormalities, especially chromosomes 5 and 7. It is generally considered: ① single radiation rarely cause AML; ② MOPP 6 cycles of therapy occurred in patients in 10 years the risk of AML 1.5% ~ 3.0%; ③ ABVD alone rarely lead to AML; ④ some reports that the alkylating agent and synergistic effect of radiotherapy, the application of statistics in the U.S. NCI MOPP in the treatment of HD patients, 14 cases of AML, including 13 cases of combined radiotherapy patients. The risk of AML occurred in 3% 5 years 10 years 10%, the peak for the 6 years after treatment. This group of HD patients with AML, 96 times the normal incidence. Italy Milan's report card for patients treated with MOPP occurred 12 years of accumulated AML accounted for 1.4%; MOPP plus radiotherapy was 10.2%; do first and then after MOPP rescue radiation patients was 15.5%. However, a recent report indicates that synergy is not obvious. ⑤ HD patients 10 to 12 years after treatment, the occurrence of AML risk returned to normal. Consequent alkylating agent such as nitrogen mustard, chlorambucil (tumor Ning), nitrosourea, procarbazine is the main cause of AML drugs.
(2) NHL: long-term survival of HD patients developed nhl has been frequently reported. Most of the intermediate grade extranodal NHL, especially in the digestive tract of primary b-cell NHL. 1243 cases of HD in our hospital, 2 cases were in the rule 6 and 12 years after the occurrence of NHL.
(3) other solid tumors: there is a certain degree of increase, especially in areas such as thyroid cancer and other radiation.
scaly erythema which checks should be done?
erythematous scaly easy to confuse the symptoms with which?
(1) demarcated erythema of psoriasis, basal infiltration, patchy, thick scales covering the surface dry, silvery white , seen after curettage scales shiny translucent film, and then scrape the film can be seen spotting. This is a disease, psoriasis and other scaly erythema identify the main points.
(3) pityriasis rosea occur in the trunk and proximal extremities for the majority of small oval patch, its long axis along the direction of arrangement of ribs and striae, scales small and thin. Most patients heal after a few weeks, dissipated less recurrence. disease often have a mother first spot, then gradually increased.
(5) discoid lupus erythematosus occur in the face, cheeks and nose, especially the back, showing butterfly distribution. erythema state clearly visible on the surface telangiectasia. The scales for the adhesion of scales, strong adhesion with erythema, peeling scales, showing the expansion of the hair follicles under the mouth, scaly skin like the underside of a lot of barbed protuberances. Duration of the course of time, showing central atrophy depression damage, pigment changes.
(6) chronic eczema often manifested as erythema, overlying scales, especially those occurred in the calf. However, chronic eczema often accompanied by intense itching, skin lesions bilaterally symmetrical, the infiltration is more severe psoriasis, scaly surface, thin, not silvery white, red base color, may have seepage.
scaly erythema associated diseases
more skin symptoms
depressed depressed scar damaged scar after scar contraction depressed scars itching scars old age acne scars scar formation rash maculopapular rash of the skin lesions after exposure back zhangdou nasolabial red chapped skin lichen planus calcification full thickness skin epidermal keratinocytes necrosis and table exfoliative dermatitis pellagra-like rash
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