Dense deposit disease (DDD) is a rare glomerular disease that typically affects children and young adults and much less commonly older patients. The pathophysiology underlying DDD is uncontrolled activation of the alternative pathway (AP) of complement cascade most frequently secondary to an autoantibody to C3 convertase called C3 nephritic factor, although mutations in factor H and auto-antibodies to this protein can impair its function and also cause DDD. Since 1995, we have diagnosed DDD in 14 patients 49 years of age or older; ten of these patients (71.4%) carry a concomitant diagnosis of monoclonal gammopathy of undetermined significance (MGUS). In one of ten, the index case described herein, we evaluated the AP and demonstrated low serum AP protein levels consistent with complement activity, heterozygosity for the H402 allele of factor H, and low levels of factor H autoantibodies, which can affect the ability of factor H to regulate AP activity. In aggregate, these findings suggest in some adults with MGUS, DDD may develop as a result of autoantibodies to factor H (or other complement proteins) that on a permissive genetic background (the H402 allele of factor H) lead to dysregulation of the AP with subsequent glomerular damage. Thus DDD in some older patients may be a distinct clinicopathologic entity that represents an uncommon complication of MGUS.

Ten cases of entomophthoromycosis encountered in a period of 4 years in Tamilnadu are reported. Basidiobolomycosis accounted for eight cases and was seen predominantly in children. Two cases of conidiobolomycosis were seen in elderly patients. Potassium iodide was the drug of choice in the treatment of entomophthoromycosis. All our patients, except one, responded with complete resolution of their lesions.

The occurrence of acanthomata in healed lesions of pemphigus is not uncommon; because histopathologic and immunofluorescence evidence of disease activity is present, cases of this sort require careful follow-up.