SIADH Secretion With Castleman's Disease and Lymphoma
SIADH Secretion With Castleman's Disease and Lymphoma
In this case, the hyponatremia had existed for a long time and failed to gain proper attention until serious clinical manifestations developed. Her past history of MALT as well as the success of fluid restriction and failure of hydrocortisone infusion suggested the possibility of hyponatremia caused by SIADH. One limitation of our investigation was the failure to measure urine uric acid and urea levels. Fractional uric acid excretion (FE-UA) has been demonstrated as a useful criterion in the diagnosis of SIADH particularly when attempting to differentiate between SIADH and hypovolaemic hyponatremia.
The main therapeutic issue in SIADH is fluid excess, and hyponatremia is dilutional in essence. Fluid restriction is the primary treatment option for SIADH. The vasopressin V2 receptor antagonist is effective for assisting the SIADH treatment. Urea administration could be used in patients with chronic SIADH but also in acute SIADH like in critically ill patients.
Once a diagnosis of SIADH is established, determining its cause is most important. Castleman's disease is characterized by non-cancerous growths that may develop in the lymph node tissue throughout the body. Lesions often occur in the chest, abdomen, or neck, where the abnormal enlargement of lymph nodes could usually be found. Although SIADH is reported to be associated with Castleman's disease, the possibility of general lymphoma in this case could not be excluded. Several major points supported this conclusion including: (1) past history of MALT; (2) occurrence of itching (characteristic symptom of lymphoma); (3) CT scan findings suggested lymphoma; and (4) the manifestation of progressive anemia. Moreover, the patient had a long history of T2D treated with insulin. Recent studies suggest that insulin treatment may be associated with an higher risk of the developing certain types cancers including lymphoma.
Although Castleman's disease is inherently a nonneoplastic process, an association with concurrent or subsequent lymphoma has been well described. The hyaline-vascular type of Castleman's disease which contains numerous lymphoid follicles should be differentiated from Hodgkin lymphoma and low-grade B-cell lymphomas. Several B-cell lymphomas with prominent atrophic germinal centers and hyaline vascular penetration including follicular lymphoma, mantle cell lymphoma, and nodal marginal zone lymphoma tend to be misdiagnosed as Castleman's disease due to the similar clinicopathologic features. Furthermore, multicentric Castleman's disease could show similar FDG PET/CT appearance mimicking lymphoma, which reveals that Castleman's disease and lymphoma exhibit similar functions. After consulting the literaure and examining the presentation of SIADH caused by both diseases, we hypothesized that Castleman's disease can develop into lymphoma, and a variety of pathological lymphomas may result in the development of SIADH. One possible mechanism is the effect of hypercytokinemia. Some cytokines, such as interleukin (IL)-2, IL-6, IL-1β, and tumor necrosis factor (TNF)-α, have been reported to stimulate parvicellular and magnocellular neurons to secrete more ADH thus causing SIADH.
In our case, three separate biopsies showed differing results suggesting that this procedure is so imperative for certain conditions that several biopsies may be needed for a final diagnosis.
Discussion
In this case, the hyponatremia had existed for a long time and failed to gain proper attention until serious clinical manifestations developed. Her past history of MALT as well as the success of fluid restriction and failure of hydrocortisone infusion suggested the possibility of hyponatremia caused by SIADH. One limitation of our investigation was the failure to measure urine uric acid and urea levels. Fractional uric acid excretion (FE-UA) has been demonstrated as a useful criterion in the diagnosis of SIADH particularly when attempting to differentiate between SIADH and hypovolaemic hyponatremia.
The main therapeutic issue in SIADH is fluid excess, and hyponatremia is dilutional in essence. Fluid restriction is the primary treatment option for SIADH. The vasopressin V2 receptor antagonist is effective for assisting the SIADH treatment. Urea administration could be used in patients with chronic SIADH but also in acute SIADH like in critically ill patients.
Once a diagnosis of SIADH is established, determining its cause is most important. Castleman's disease is characterized by non-cancerous growths that may develop in the lymph node tissue throughout the body. Lesions often occur in the chest, abdomen, or neck, where the abnormal enlargement of lymph nodes could usually be found. Although SIADH is reported to be associated with Castleman's disease, the possibility of general lymphoma in this case could not be excluded. Several major points supported this conclusion including: (1) past history of MALT; (2) occurrence of itching (characteristic symptom of lymphoma); (3) CT scan findings suggested lymphoma; and (4) the manifestation of progressive anemia. Moreover, the patient had a long history of T2D treated with insulin. Recent studies suggest that insulin treatment may be associated with an higher risk of the developing certain types cancers including lymphoma.
Although Castleman's disease is inherently a nonneoplastic process, an association with concurrent or subsequent lymphoma has been well described. The hyaline-vascular type of Castleman's disease which contains numerous lymphoid follicles should be differentiated from Hodgkin lymphoma and low-grade B-cell lymphomas. Several B-cell lymphomas with prominent atrophic germinal centers and hyaline vascular penetration including follicular lymphoma, mantle cell lymphoma, and nodal marginal zone lymphoma tend to be misdiagnosed as Castleman's disease due to the similar clinicopathologic features. Furthermore, multicentric Castleman's disease could show similar FDG PET/CT appearance mimicking lymphoma, which reveals that Castleman's disease and lymphoma exhibit similar functions. After consulting the literaure and examining the presentation of SIADH caused by both diseases, we hypothesized that Castleman's disease can develop into lymphoma, and a variety of pathological lymphomas may result in the development of SIADH. One possible mechanism is the effect of hypercytokinemia. Some cytokines, such as interleukin (IL)-2, IL-6, IL-1β, and tumor necrosis factor (TNF)-α, have been reported to stimulate parvicellular and magnocellular neurons to secrete more ADH thus causing SIADH.
In our case, three separate biopsies showed differing results suggesting that this procedure is so imperative for certain conditions that several biopsies may be needed for a final diagnosis.