Endocrine Abstracts

Objective: To present a patient with long standing type 2 Diabetes complaining of chronic pelvic pain, due to an uncommon cause of bilateral vas calcification.

Methods: Clinical, laboratory and radiographic data are reported on a 62-year-old diabetic presenting with chronic pelvic pain.

Results: A 62-year-old man with a history of 17 years of diabetes presented with chronic dull aching, non radiating pain in the pelvis and in the region of sacal sulcus below 5th lumbar vertebra. There was no history of fever with chills and sweats, dysuria, urgency, frequency of urination. Pain was not aggravated during intercourse. There was no past history of sexually transmitted disease, frequent and extramarital sexual encounters, chronic kidney disease. Complete blood picture and routine urine examination did not reveal any evidence of infection or proteinuria. Fasting and post prandial blood sugars were 104 and 136 mg/dl with HbA1c at 6.7%. Other blood parameters including lipid profile, renal and liver function tests, serum calcium, phosphorous were all within normal limits. X ray showing anteroposterior view of pelvis revealed bilateral serpentine structures with symmetric and regular vas deferens calcification involving vas calcification.

Discussion: The causes of bilateral vas calcification include degenerative changes due to ageing, diabetes mellitus, end stage renal disease with secondary hyperparathyroidism. They give rise to regular calcifications within the muscular components of the vas with preservation of luminal patency. Causes of unilateral vas calcification include inflammatory conditions like tuberculosis, gonorrhea, syphilis, schistosomiasis, and chronic non-specific urinary tract infections. The calcifications are intraluminal and irregular leading to partial or complete occlusion of the lumen. Vasa differentia may calcify after relatively short duration of diabetes if the disease starts after the age of 40, whereas if the disease occurs before the age of 40, it has usually been present for at least 15 years before calcification is noted. Diabetes accelerates the process of senescent calcification of the vas deferens by augmented expression of several bone-associated proteins (e.g. osteopontin, bone sialoprotein, alkaline phosphatase, type one collagen, osteocalcin) that facilitate or regulate the calcification process. In addition uremic serum upregulates osteoblast transcription factor Cbfa 1 and osteopontin expression. Diabetic patients with vasal wall calcification may also develop failure of emission, where no sperm reach the posterior urethra due to aperistalsis of the vas deferens.

Conclusion: Type 2 diabetic subjects with long standing pelvic pain and without any elicitable cause should be evaluated for this uncommon etiology of vas calcification.