Our study performed characteristics of thyroid gland and β-cell function in AL amyloidosis patients. Thyroid function showed that high level of hypothyroidism, euthyroid sick syndrome and subclinical hypothyroidism. Unexpectedly, the prevalence of thyroid nodule was as high as 75 percent. In addition, only two patients were diagnosed with diabetes via intravenous glucose tolerance test and the β-cell function revealed normal basic insulin secretion level and sufficient postprandial response.
AL amyloidosis has been reported to be involved in endocrine gland, such as pituitary gland [11], adrenal failure [12], thyroid gland [13,14]. The involvement of thyroid gland manifested as hypothyroidism and goiter [6,15-16]. As goiter can also be induced by hypothyroidism, it should be defined via thyroid gland biopsy to determine amyloidosis induced goiter. However, using fine needle aspiration biopsy gave a rather low positive amyloidosis deposition frequency which could be ameliorated by the pathology of subtotal thyroidectomy [17]. Therefore, few studies reported the amyloidosis induced goiter manifestation. Based on the above facts, abnormality of thyroid gland were often neglected in amyloidosis patients. Previous study [6] has shown a big prevalence of hypothyroidism which was similar to our study. However, our study revealed higher frequency of hypothyroidism than the result shown before which exhibited higher subclinical hypothyroidism [6]. In addition, we have previous indicated euthyroid sick syndrome is a common syndrome in CKD patients with more than 54% prevalence [18] which has been indicated similar frequency in amyloidosis in a review paper [19]. However, in amyloidosis patients of our study, the frequency revealed 30% which was lower than before attributed to more patients developed hypothyroidism. Although AL amyloidosis manifested as goiter, the previous studies were case reports. No data to date are available about the prevalence of thyroid nodule in our knowledge. In our study, we showed high frequency of thyroid nodule which was beyond our expectation. We speculated that hypothyroidism and amyloidosis both contributed to the phenomenon which should be verified via pathology. Nevertheless, our study gave an important remind of focusing on thyroid image in AL amyloidosis patients.
Apart from thyroid gland, we also explored whether islet function was involved. It is common that islet amyloid polypeptides deposit in islet which contributes to the pathogenesis of type 2 diabetes [20,21]. AL amyloidosis is rare to be reported to influence islet. There were only some case reports about the infiltration of amyloidosis stained with positive congo red and enlargement of islet [22,23]. Although islet was involved, no diabetes or hyperglycemia was presented which might be neglected clinically. In our study, we revealed only 2 patients diagnosed with diabetes which is similar to prevalence of type 2 diabetes in China. Additionally, islet function also exhibited no difference between amyloidosis patients and healthy populations suggesting normal glucose metabolism for this kind of patients.
There are some limitations in our study. First, there was only 20 patients in our study which may give a size bias. Because the study was focused in one hospital and the prevalence of Al amyloidosis is pretty low. Therefore, it is difficult to accumulate big size study to explore the metabolism status of AL amyloidosis patients which need further study to give more solid evidence. Second, lacking of pathology data will limit diagnosis of organ involvement. As the recruited patients reveled no significant organ related symptoms which may limit the biopsy of thyroid. Furthermore, islet biopsy is difficult to fulfill unless abnormality of nodule by radiography. Nevertheless, thyroid nodule biopsy in AL amyloidosis may be available in future to assess the involvement of the organ.