DOI: 10.1097/01.tp.0000178383.36187.43

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PMID: 16314811

Issn Print: 0041-1337

Publication Date: 2005/11/15


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Diabetic Mastopathy in a Patient with a Functioning Pancreas Transplant

Jason J. Klovning; William M.P. McKinnon; Odile David

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Diabetic mastopathy, also known as sclerosing lymphocytic lobulitis (1), is a rare benign entity that can be clinically confused with breast cancer. This entity makes up less than 1% of benign breast disease (2). First reported in 1984 (3), this condition is highly associated with Type 1 diabetes (4).
Diabetic mastopathy is presumed to be an autoimmune disorder. Lammie et al. found that five of seven patients studied were HLA DR3, DR4, or DR5 positive, either singly or in combination (5). Soler and Khardori (3) noticed high titers of antimicrosomal antibodies in most of the patients studied. The etiology is not perfectly clear as diabetic mastopathy can also be seen in type two diabetics (6). This leads some to believe that the disease results from exposure to hyperglycemia.
It has been reported that the observed incidence of benign breast disease after transplantation is higher than the general population (7, 8). One may expect to see higher rates of diabetic mastopathy in renal transplant patients because of the large number of diabetics, increased surveillance of these patients, and the reported higher incidence of benign disease. This does not appear to be the case as the literature provides no other case of diabetic mastopathy in any type of transplant patient.
E.J. is a 46-year-old African American female with a history of Type 1 insulin-dependent diabetes. She has several complications from diabetes including end-stage renal disease, neuropathy, and gastropathy. She received a combined kidney pancreas transplant in March of 1996. She is HLA DR 9,11. After transplant, from 1996 to 2003 she had normal blood sugars (86±14 gm/dl). She continues to be normoglycemic without the need for insulin. However, due to chronic rejection, her transplant kidney has failed.
She first presented to breast clinic in April of 2002 with a complaint of a left breast mass. This mass was eventually removed via an excisional biopsy that showed diabetic mastopathy. The patient presented again in November of 2002 and June of 2004 with complaints of new breast masses. Core and excisional biopsies again revealed diabetic mastopathy (Fig. 1).
This patient has been receiving tacrolimus, prednisone, and mycophenolate mofetil as immunosuppression for the last 8 years. Despite immunosuppression and good glucose control, she still developed diabetic mastopathy.
If the disease is due to hyperglycemia, the insult causing the lesions must have occurred prior to transplant and only recently manifested itself. Any palpable lesions should have been detected pretransplant as the patient received a thorough breast exam as part of her transplantation workup. This, along with recurrent disease after excision, makes hyperglycemia an unlikely cause.
If the disease is autoimmune in nature, the insult is ongoing. As immunosuppression does not always prevent progression of autoimmune diseases, it is still possible for her have a new presentation of the disease. It would be interesting to know if the transplanted kidney was HLA DR3, DR4, or DR5 positive and thereby exposed this patient to those antigens, possibly inciting her disease. Unfortunately this information is not available.
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