The thyroid gland is a butterfly-shaped endocrine gland that is normally located in the lower front of the neck. Thyroid hormone helps the body use energy, stay warm and keep the brain, heart, muscles, and other organs working as they should. There are no symptoms unique to thyroiditis. If the thyroiditis causes slow and chronic thyroid cell damage and destruction, leading to a fall in thyroid hormone levels in the blood, patients experience the symptoms of hypothyroidism see Hypothyroidism brochure.
Typical hypothyroid symptoms include fatigue, weight gain, constipation, dry skin, depression and poor exercise tolerance. If the thyroiditis causes rapid thyroid cell damage and destruction, the thyroid hormone that is stored in the gland leaks out, increasing thyroid hormone levels in the blood.
These patients will experience the symptoms of thyrotoxicosis, which are similar to hyperthyroidism see Hyperthyroidism brochure. These symptoms often include anxiety, insomnia, palpitations fast heart rate , fatigue, weight loss, and irritability. This is seen in patients with the toxic phase of subacute, painless and post-partum thyroiditis. The symptoms of thyrotoxicosis and hyperthyroidism are both caused by elevated levels of thyroid hormone in the blood, but in thyrotoxicosis, the gland is not truly overactive.
In subacute, painless and post-partum thyroiditis, the thyroid gland often becomes depleted of thyroid hormone as the course of inflammation continues leading to a fall in thyroid hormone levels in the blood and symptoms of hypothyroidism.
Pain in the thyroid can be seen in patients with subacute thyroiditis. Thyroiditis is caused by an attack on the thyroid, causing inflammation and damage to the thyroid cells. Antibodies that attack the thyroid cause most types of thyroiditis. As such, thyroiditis is often an autoimmune disease, like juvenile type 1 diabetes and rheumatoid arthritis. It is not known why certain people make anti-thyroid antibodies, although this tends to run in families. In addition to close contact, the virus can also be transferred between two people through an organ transplant and through a blood transfusion 4.
There are some risk factors that individuals should be aware of — the presence of these risk factors means a particular individual is at a higher risk of contracting the virus. Women seem to be more commonly affected by the Epstein Barr Virus when compared to men.
Being Caucasian also causes a possible increased risk of contracting the virus. Other particular risk factors include having an impairment with the immune system, being a person who is regularly sexually active, and also those who reside within a tropical location.
The Epstein Barr Virus itself is not associated with any significant symptoms in most cases, and many people have this virus in their bodies without being aware of it. When the virus causes the common condition mononucleosis, then the patient may start to experience symptoms that are associated with mononucleosis. Particular symptoms that a patient should be wary of include a fever, combined with fatigue and an inflamed throat. Additional symptoms may include a rash, a liver that becomes inflamed, and an enlargement of the spleen 5.
There are some complications that need to be taken into account when diagnosed with an Epstein Barr Virus infection. Both acute and chronic complications may develop when a patient is infected with this virus, especially when no treatment protocol is implemented to suppress the activity of the virus.
Individuals who suffer from an impaired immune function should be especially concerned when they learn they have antibodies that suggest the presence of the Epstein Barr Virus. There are several complications that a patient may become a victim of should they fail to adequately suppress the virus, or should they suffer from a significant impairment in their immune function. One of the most worrisome complications that may be caused by an infection with the Epstein Barr Virus is viral meningitis, a condition where the tissue that covers the spinal cord and brain becomes inflamed 6.
While a weak immune system can lead to a higher risk of suffering from complications due to an infection with the Epstein Barr Virus, it should be noted that a possible complication of the virus can be a weakening of the immune system. Apart from the above-mentioned complications, we should also note that an association has also been made between the Epstein Barr Virus and the following conditions 7 :.
Once infected, the disease will stay contained in the human body and may become activated at some points, leading to the development of mononucleosis or another particular type of condition considered a possible complication of the virus. It is possible to suppress the activation of the virus, and possibly also avoid the development of mononucleosis, or other complications, in many patients. Antiviral drugs are often utilized in patients who have tested positive for the presence of the Epstein Barr Virus 8.
These drugs work by inhibiting the replication of the Epstein Barr Virus. DNA polymerase involved in viral infections, such as this particular pathogenic virus, is also targeted through the use of antiviral drugs.
When a complication develops, such as mononucleosis, a physician may also choose to provide adequate treatment to assist with relieving the symptoms and getting rid of the complication. Implementing certain strategies to help improve the efficiency of the immune system may also be useful in some cases. On the whole, the distinctive role of the virus itself or antiviral treatment remains to be clarified. Abnormalities in thyroid function should be included among the complications of HCV syndrome and patients should be periodically screened for thyroid involvement in order to identify patients in need of treatment as quoted in a recent review [ ].
A substantial number of patients with SARS have shown abnormalities in thyroid function. However, low serum triiodothyronine and thyroxine levels associated with decreased TSH concentration are in favor of central hypothyroidism induced by hypophysitis or by hypothalamic dysfunction [ ].
Enteroviruses play a role in immune-mediated pathological processes, such as chronic myositis and chronic dilated cardiomyopathy [ ]. Epidemiologic and prospective studies have provided a body of arguments that strongly suggest the role of enteroviruses in type-1 diabetes in which, interestingly, AITD is frequently observed [ , ].
Although the patients in our series are certainly different from patients with classic Hashimoto's thyroiditis, which are rarely treated surgically, our results suggest that the presence of EV-RNA in thyroid tissue is not associated with autoimmune thyroiditis.
Maternal enterovirus infection during pregnancy has been linked to thyroiditis in children. Sera taken at delivery from mothers whose children subsequently developed AITD was analyzed for antibodies against enterovirus, and compared with a control group.
However, the age at diagnosis of AITD was significantly lower in the group of children with IgM-positive mothers compared with children with IgM-negative mothers. Also hypothyroidism was significantly more frequent in the IgM-positive group, with no child in the IgM-negative group [ ].
Patients with recent onset of Graves' hyperthyroidism about two months before blood sample collection have been investigated in regard to enterovirus infection. A nested PCR reaction with primers of the enterovirus genome was employed on blood samples but all were negative for RNA of the enterovirus group [ ]. Reovirus infection of a neonatal mouse can induce thyroiditis and thyroid autoimmunity.
Mice infected with reovirus type 1 develop a thyroiditis characterized by focal destruction of acinar tissue, infiltration of the thyroid by inflammatory cells, and production of autoantibodies directed against thyroglobulin and thyroid microsomes [ ]. The segment of the reovirus type 1 genome responsible for the induction of autoantibodies to thyroglobulin encodes a polypeptide that binds to surface receptors and determines the tissue tropism of the virus [ ]. An endogenous retrovirus ev 22 was found to be expressed in obese-strain OS chickens but not in healthy normal strains.
Ev 22 is inherited autosomally in a dominant manner. The OS chickens develop a hereditary spontaneous autoimmune thyroiditis characterized histologically by lymphocytic infiltration of the thyroid gland. Thyroiditis is associated with obesity and hyperlipidemia. A similar thyroiditis has also been induced in normal chickens by retroviral infection [ ]. Lymphocytic choriomeningitis virus LCMV can persist in the thyroid gland of three strains of mice neonatally infected with the virus.
Furthermore, the virus that was shown to persist mainly in the thyroid epithelial cells in which thyroglobulin is synthesized induced a reduction in the level of thyroglobulin messenger RNA and circulating thyroid hormones, but there was no thyroid cell destruction. Then persistent, apparently benign virus infection with LCMV, can be induced in the thyroid of mice and this infection induces thyroid dysfunction.
This alteration in thyroid homeostasis is not caused to the thyroid by autoantibodies. Moreover, despite infection of the thyroid gland, neither necrosis nor inflammation occurs [ ]. Animals models show that a typical autoimmune thyroiditis can be induced by a direct viral infection but also by an inherited retrovirus infection. These models also show that thyroid dysfunction can occur without inflammation or antithyroid autoantibodies.
Further studies are then needed in humans to explore the role of viruses in the pathogenesis of thyroid dysfunctions. Lymphomas and Riedel's thyroiditis are rare disorders but both can occur in association with Hashimoto's thyroiditis.
Fibrous thyroiditis, also known as Riedel's thyroiditis, is characterized by extensive fibrosis and mononuclear infiltration that extends into adjacent tissues. It may consist in a primary fibrosing disorder or in the local involvement of a multifocal fibrosclerosis. The etiology of Riedel's thyroiditis is not known. It can occur in association with Hashimoto's thyroiditis [ ]. As this disease is rare, the literature is scarce.
Two cases of Riedel's thyroiditis onset have been reported after a subacute thyroiditis, which is thought, as already said, to be a viral induced disaese. Two women, first diagnosed with sub-acute thyroiditis, developed an enlargement of the thyroid gland and symptoms of compression eight months and three years later, respectively.
Post-operative histopathologic evaluation showed Riedel's thyroiditis characteristics associated with sub-acute thyroiditis [ , ]. Only one case report of infection has been reported in international literature. A year old woman had of long-term fever associated with a biologic inflammatory syndrome which was reported as due to EBV infection because of a positive EBV serology.
There was a dramatic improvement after thyroidectomy with normalization of inflammatory parameters. The role of EBV infection in the process of this unusual form of Riedel's thyroiditis was suspected [ ]. Thyroid lymphomas are nearly always of the non-Hodgkin's type. Hodgkin's lymphoma of the thyroid is exceedingly rare. Preexisting chronic autoimmune thyroiditis is the only known risk factor for primary thyroid lymphoma, and is present in about one-half of patients [ ].
Epstein-Barr virus EBV is found in many lymphomas. The clinicopathological characteristics in the Hong Kong Chinese population and the presence of EBV in thyroid lymphomas were analyzed by reviewing data collected over three decades. EBV gene expression by in-situ hybridization and immunohistochemistry were performed. Primary thyroid lymphomas were found in 23 patients and secondary lymphomas were found in 9 patients.
In-situ hybridization revealed positive signals in the nucleus of lymphoma cells, which also expressed latent membrane protein-1 [ ]. EBV-related mRNA presence was investigated in 32 cases of malignant lymphoma of the thyroid by in-situ hybridization and immunohistochemistry.
A patient with autoimmune thyroiditis had a transitory recurrence of her goiter during pregnancy with TPOAb becoming strongly positive. Six months post partum she had a subacute thyroiditis. Serology established the diagnosis of viral thyroiditis due to a Coxsackie-B virus. Two months later the goiter showed further growth, in association with cervical lymphadenopathy and an enlarged left parotid gland.
Histology revealed a primary thyroid lymphoma. A study was carried out to examine whether thyroid non-Hodgkin's lymphoma in an area in which ATL is endemic is also exclusively of B-cell type.
Eight cases with thyroid non-Hodgkin's lymphoma admitted to the hospital situated in an ATL-endemic area were studied. Immunophenotypic study revealed all but one case to be of B-cell nature The T-cell type lymphoma case also had antibodies against HTLV-1 in the serum [ ].
Lymphomas are frequent in HCV-infected patients but no thyroid lymphoma has been reported in these patients[ ]. Two cases of thyroid lymphoma have been described in HIV-infected patients.
The first is a year old woman with acquired immunodeficiency syndrome AIDS who presented a severe thyrotoxicosis and a markedly enlarged, diffuse, tender goiter. The patient died within days of her presentation. At autopsy, near-complete replacement of the thyroid gland with anaplastic large cell lymphoma was found, without coexisting infectious or autoimmune processes in the gland [ ].
The second case was a child with vertical transmission-acquired HIV, presenting with lymphomatous infiltration of the thyroid gland at diagnosis [ ]. Identifying etiological infections in human disease is difficult. Besides the fact that organ tissue is not always available for direct study, the interpretation of virological data must be cautious.
The presence of antibodies directed towards a virus does not prove that this pathogen is responsible for the disease, especially when the agent is common in the general population. On the other hand, the absence of viral markers at the onset of the disease does not refute the viral hypothesis.
Indeed the triggering infection can take place many years previously. A triggering virus can be cleared from the body without any virological trace except the presence of specific antibodies. It is relevant to look for viral agents in tissues in which they can persist without systemic manifestation.
A viral disease is the result of an interaction between a virus and the host, in which the genetic background plays a role. Therefore, it cannot be excluded that a virus plays a role in a disease even though most infected individuals do not show any sign of disease.
Eur J Endocrinol , Intern Med , PubMed Google Scholar. Pathol Res Pract , Volpe R: Thyroiditis: current views of pathogenesis.
Med Clin North Am , J Endocrinol Invest , J Clin Endocrinol Metab , Thyroid , Endocrinol Jpn , Arch Immunol Ther Exp Warsz , CAS Google Scholar. Faseb J , Pathol Biol Paris , Sato M: Virus-like particles in the follicular epithelium of the thyroid from a patient with subacute thyroiditis de Quervain's. Acta Pathol Jpn , Lancet , 2: Med Microbiol Immunol , Acta Virol , Int Arch Allergy Immunol , J Virol , Evidence of a causal association.
Lancet , A positive signal with a spumaretrovirus-specific genomic probe was found in DNA extracted from peripheral blood lymphocytes in 10 patients and spumaretrovirus related sequences were detected by PCR in the DNA of 19 patients. All 23 control subjects were negative.
These results strongly suggest the existence of an association between GD and the presence of spumaretrovirus related infection markers[ 81 ]. Other studies failed to detect the presence of antibodies by several immunodetection techniques and foamy virus DNA in peripheral blood lymphocytes [ 20 , 82 ] and the presence of the spumaretrovirus gag region sequence was not statistically significant in DNA extracted from the peripheral blood leukocytes and thyroid tissue of 81 patients with GD and of 66 controls [ 83 ].
Nevertheless, the nature of the HFV-related sequences identified in the genomes of healthy individuals and the GD patients appeared to be different. This suggests that these sequences may be used as a tool for screening for HFV in GD patients [ 84 ]. However, the data do represent the possibility that HFV-like sequences may be implicated and this is a possibility especially in some geographically distinct populations [ 21 ].
Simian virus 40 SV40 is a polyomavirus that is found in both monkeys and humans. Like other polyomaviruses, SV40 is a DNA virus that has the potential to cause tumors but most often persists as a latent infection.
In a study dedicated to thyroid tumors, SV40 sequences were also investigated in GD thyroid specimens, normal thyroid tissues, and peripheral blood mononuclear cells of healthy donors. Thyroid disorders in patients with congenital rubella were first reported in [ 86 ].
Infection of thyroid tissue by rubella was demonstrated in a case of congenital rubella with Hashimoto's thyroiditis: immunofluorescent studies of thyroid tissue demonstrated staining for rubella virus antigen [ 87 ].
Thyroid autoantibodies, anti-TPO or anti-Tg antibodies have been found more frequently in patients with congenital rubella syndrome than in controls [ 88 , 89 ]. These studies are old and a recent study has shown that humoral autoimmunity was not so frequent. In 37 subjects affected by or exposed to rubella during fetal life, one patient had diabetes, four patients had clinical hypothyroidism and five patients were positive for TPOAb at the time of the examination [ 90 ].
However, in an Australian study, the prevalence of thyroid disorders, as well as diabetes and early menopause, was higher in subjects with congenital rubella studied 60 years after their intrauterine infection than the general population. Since most reports have shown no evidence of active rubella infection at the time of thyroid dysfunction, the mechanisms proposed for thyroid dysfunction are destruction of thyroid cells by local persistent rubella virus infection, precipitation of an autoimmune reaction, or both [ 92 - 96 ].
The Herpesviridae are a large family of DNA viruses that share a common structure and a common characteristic which is latent and re-occurring infections. Herpesviridae can cause lytic infections. Thyroid tissue specimens were obtained postoperatively from four patients with multinodular goiter and 18 patients with AITD GD and Hashimoto thyroiditis.
EBV infection is known to be involved in tumoral diseases such as lymphoma but also in autoimmune diseases, such as multiple sclerosis, rheumatoid arthritis and systemic lupus erythematosus [ 98 ]. What is unusual is that EBV may induce anti-T3 antibodies. Acute EBV infection with severe primary hypothyroidism was described in a year old female patient.
Later, 34 patients with EBV infection were tested for thyroid hormone levels. Five patients with acute EBV and one with previous infection had total T3 values above the mean which was due to anti-T3 antibodies [ ]. HHV are ubiquitous, tissue tropism widespread. Both viruses infection increased the risk for Graves disease especially HHV7 that was significantly more frequent among patients Parvovirus B19 is known for causing a childhood exanthem but it has also been associated with autoimmune diseases: autoimmune neutropenia, thrombocytopenia, hemolytic anemia and rheumatoid arthritis [ ].
Recently, a few studies have suggested the association of parvovirus infection with thyroiditis. However, the possibility that thyroid epithelial cells harbor B19 DNA cannot be excluded [ ].
Serum samples from 73 children and adolescents with Hashimoto's thyroiditis and from 73 age-matched controls have been analyzed for the presence of specific antibodies. No differences are observed. But Parvovirus B19 DNA, indicating recent Binfection, is detectable more frequently in patients and a negative correlation exists with disease duration.
There is strong evidence that acute parvovirus B19 infections are involved in the pathogenesis of some cases of Hashimoto's thyroiditis[ ]. Parvovirus may also be present in the brain. Some authors hypothesize that parvovirus B19 is a common human pathogen which could explain the association between mental disorders and thyroid diseases because of its ability to infect the brain and to induce autoimmunity. This hypothesis is based on the fact that they found in patients with bipolar disorder both a thyroid disorder and brain B19 infection [ ].
A woman, whose son had an episode of exanthem two weeks previously, was infected with parvovirus and suffered successively GD, type-1 diabetes and rheumatic polyarthritis. Serological tests showed IgM antibodies to human parvovirus B19, but no IgM antibodies to cytomegalovirus, Epstein Barr virus, rubella, measles, or Coxsackie viruses. Anti-TSH receptor antibody was positive. Parvovirus viral protein 1 was detected in her bone marrow samples but no analysis was done on thyroid tissue [ ].
Discordant data are published about hepatitis. Thyroid involvement may be regarded as the most frequent alteration in HCV positive patients and is more frequent than in HVB.
In a retrospective cohort study which included , patients infected with HCV individuals with human immunodeficiency virus were excluded and , patients uninfected with HCV, thyroiditis risk was slightly increased, but there was no analysis of treatment [ ]. The prevalence of autoimmune thyroid disease in patients with HCV differs from that in patients with the hepatitis B virus HBV before, at the end of, and 6 months after stopping treatment with IFN-alpha.
Other authors don't find an association between hepatitis C virus and thyroid autoimmunity [ , ]. Thyroid autoimmunity may be a cytokine-induced disease in susceptible patients.
Indeed, the incidence is much greater in females and positive anti-TPOAb patients prior to the initiation of therapy. According Marazuela, thyroid dysfunction secondary to interferon is reversible after discontinuation of therapy [ ], which is discordant with Fernandez' data [ ]. Variable geographic distribution has also shown that genetic or environmental influences could be implicated [ ]. On the whole, the distinctive role of the virus itself or antiviral treatment remains to be clarified.
Abnormalities in thyroid function should be included among the complications of HCV syndrome and patients should be periodically screened for thyroid involvement in order to identify patients in need of treatment as quoted in a recent review [ ].
A substantial number of patients with SARS have shown abnormalities in thyroid function. However, low serum triiodothyronine and thyroxine levels associated with decreased TSH concentration are in favor of central hypothyroidism induced by hypophysitis or by hypothalamic dysfunction [ ].
Enteroviruses play a role in immune-mediated pathological processes, such as chronic myositis and chronic dilated cardiomyopathy [ ]. Epidemiologic and prospective studies have provided a body of arguments that strongly suggest the role of enteroviruses in type-1 diabetes in which, interestingly, AITD is frequently observed [ , ]. Although the patients in our series are certainly different from patients with classic Hashimoto's thyroiditis, which are rarely treated surgically, our results suggest that the presence of EV-RNA in thyroid tissue is not associated with autoimmune thyroiditis.
Maternal enterovirus infection during pregnancy has been linked to thyroiditis in children. Sera taken at delivery from mothers whose children subsequently developed AITD was analyzed for antibodies against enterovirus, and compared with a control group. However, the age at diagnosis of AITD was significantly lower in the group of children with IgM-positive mothers compared with children with IgM-negative mothers.
Also hypothyroidism was significantly more frequent in the IgM-positive group, with no child in the IgM-negative group [ ]. Patients with recent onset of Graves' hyperthyroidism about two months before blood sample collection have been investigated in regard to enterovirus infection. A nested PCR reaction with primers of the enterovirus genome was employed on blood samples but all were negative for RNA of the enterovirus group [ ]. Reovirus infection of a neonatal mouse can induce thyroiditis and thyroid autoimmunity.
Mice infected with reovirus type 1 develop a thyroiditis characterized by focal destruction of acinar tissue, infiltration of the thyroid by inflammatory cells, and production of autoantibodies directed against thyroglobulin and thyroid microsomes [ ]. The segment of the reovirus type 1 genome responsible for the induction of autoantibodies to thyroglobulin encodes a polypeptide that binds to surface receptors and determines the tissue tropism of the virus [ ].
An endogenous retrovirus ev 22 was found to be expressed in obese-strain OS chickens but not in healthy normal strains. Ev 22 is inherited autosomally in a dominant manner. The OS chickens develop a hereditary spontaneous autoimmune thyroiditis characterized histologically by lymphocytic infiltration of the thyroid gland. Thyroiditis is associated with obesity and hyperlipidemia. A similar thyroiditis has also been induced in normal chickens by retroviral infection [ ]. Lymphocytic choriomeningitis virus LCMV can persist in the thyroid gland of three strains of mice neonatally infected with the virus.
Furthermore, the virus that was shown to persist mainly in the thyroid epithelial cells in which thyroglobulin is synthesized induced a reduction in the level of thyroglobulin messenger RNA and circulating thyroid hormones, but there was no thyroid cell destruction. Then persistent, apparently benign virus infection with LCMV, can be induced in the thyroid of mice and this infection induces thyroid dysfunction. This alteration in thyroid homeostasis is not caused to the thyroid by autoantibodies.
Moreover, despite infection of the thyroid gland, neither necrosis nor inflammation occurs [ ]. Animals models show that a typical autoimmune thyroiditis can be induced by a direct viral infection but also by an inherited retrovirus infection. These models also show that thyroid dysfunction can occur without inflammation or antithyroid autoantibodies.
Further studies are then needed in humans to explore the role of viruses in the pathogenesis of thyroid dysfunctions.
Lymphomas and Riedel's thyroiditis are rare disorders but both can occur in association with Hashimoto's thyroiditis. Fibrous thyroiditis, also known as Riedel's thyroiditis, is characterized by extensive fibrosis and mononuclear infiltration that extends into adjacent tissues. It may consist in a primary fibrosing disorder or in the local involvement of a multifocal fibrosclerosis. The etiology of Riedel's thyroiditis is not known. It can occur in association with Hashimoto's thyroiditis [ ].
As this disease is rare, the literature is scarce. Two cases of Riedel's thyroiditis onset have been reported after a subacute thyroiditis, which is thought, as already said, to be a viral induced disaese. Two women, first diagnosed with sub-acute thyroiditis, developed an enlargement of the thyroid gland and symptoms of compression eight months and three years later, respectively.
Post-operative histopathologic evaluation showed Riedel's thyroiditis characteristics associated with sub-acute thyroiditis [ , ]. Only one case report of infection has been reported in international literature.
A year old woman had of long-term fever associated with a biologic inflammatory syndrome which was reported as due to EBV infection because of a positive EBV serology. There was a dramatic improvement after thyroidectomy with normalization of inflammatory parameters. The role of EBV infection in the process of this unusual form of Riedel's thyroiditis was suspected [ ]. Thyroid lymphomas are nearly always of the non-Hodgkin's type.
Hodgkin's lymphoma of the thyroid is exceedingly rare. Preexisting chronic autoimmune thyroiditis is the only known risk factor for primary thyroid lymphoma, and is present in about one-half of patients [ ].
Epstein-Barr virus EBV is found in many lymphomas. The clinicopathological characteristics in the Hong Kong Chinese population and the presence of EBV in thyroid lymphomas were analyzed by reviewing data collected over three decades. EBV gene expression by in-situ hybridization and immunohistochemistry were performed.
Primary thyroid lymphomas were found in 23 patients and secondary lymphomas were found in 9 patients. In-situ hybridization revealed positive signals in the nucleus of lymphoma cells, which also expressed latent membrane protein-1 [ ]. EBV-related mRNA presence was investigated in 32 cases of malignant lymphoma of the thyroid by in-situ hybridization and immunohistochemistry. A patient with autoimmune thyroiditis had a transitory recurrence of her goiter during pregnancy with TPOAb becoming strongly positive.
Six months post partum she had a subacute thyroiditis. Serology established the diagnosis of viral thyroiditis due to a Coxsackie-B virus. Two months later the goiter showed further growth, in association with cervical lymphadenopathy and an enlarged left parotid gland. Histology revealed a primary thyroid lymphoma. A study was carried out to examine whether thyroid non-Hodgkin's lymphoma in an area in which ATL is endemic is also exclusively of B-cell type. Eight cases with thyroid non-Hodgkin's lymphoma admitted to the hospital situated in an ATL-endemic area were studied.
Immunophenotypic study revealed all but one case to be of B-cell nature The T-cell type lymphoma case also had antibodies against HTLV-1 in the serum [ ].
Lymphomas are frequent in HCV-infected patients but no thyroid lymphoma has been reported in these patients[ ]. Two cases of thyroid lymphoma have been described in HIV-infected patients. The first is a year old woman with acquired immunodeficiency syndrome AIDS who presented a severe thyrotoxicosis and a markedly enlarged, diffuse, tender goiter.
0コメント