IGD & PNGD Flashcards
What does IGD and PNGD stand for ? Is tgere a unifying term ?
Palisaded neutrophilic and granulomatous dermatitis (PNGD)
and interstitial granulomatous dermatitis (IGD) with arthritis
represent two clinicopathologic patterns of granulomatous dermatitis that occur in patients with RA and other autoimmune disorders.
These entities may exist on a spectrum
some authors have proposed the overarching term reactive granulomatous dermatitists.
How do they differ in clinical presentation ?
PNGD typically presents as skin-colored to erythematous papules that appear symmetrically on extensor surfaces, particularly the elbows and fingers.
Central umbilication with crusts or perforation (with extrusion of necrobiotic collagen)
may be present (Rhematoud papules is an example , see Fig. 53 . I tg ), and ulceration occasionally occurs.
IGD with arthritis is characterized by erythematous plaques,
often with an annular configuration or linear cords (the “rope sign”) that favor the ]atera] trunk, axillae, buttocks, medial thighs, and groin. Large areas of involvement can be seen.
PGND is observed in which diseases ?
These lesions are observed most often in patients with RA, systemic LE or systemic vasculitis, particularly granulomatosis with polyangiitis.
IGD is observed in which diseases ?
It usually occurs in women with RA, seronegative arthritis, or polyarthralgias and it is often associated with autoimmune thyroiditis.
What histologic feature present in PNGD and not in IGD ?
neutrophil-rich small vessel vasculitis
With immune complex deposition in pathogenesis
Trigger by trauma that is why PNGD presents in extensor surfaces of trauma.
clinical differential for PNGD is
The clinical differential for PNGD includes
1) perforating disorders
2) early rheumatoid nodules
3) accelerated rheumatoid nodulosis
4) papular granuloma annulare (GA).
5)The interstitial granulomatous drug reaction, which is most often caused by calcium channel blockers or HMG-CoA reductase inhibitors (“statins”; Table 93.7 t@ ), can mimic PNGD and IGD,
both clinically and histologically.
The DD of IGD
The clinical presentation of IGD with plaques may resemble
1);patch-type GA,
2) the inflammatory stage of morphea
3) erythema migrans
4) mycosis fungoides.
5)The interstitial granulomatous drug reaction, which is most often caused by calcium channel blockers or HMG-CoA reductase inhibitors (“statins”; Table 93.7 t@ ), can mimic PNGD and IGD,
both clinically and histologically.
The interstitial granulomatous drug reaction
Most common drugs
Duration of drug intaje before lesiins
Histologic characteristics
most often caused by calcium channel blockers or HMG-CoA reductase inhibitors (“statins”; Table 93.7 ), can mimic PNGD and IGD, both clinically and histologically.
Also associated with TNF inhibitor therapy in patients with RAand psoriatic arthritis.
Onset typically occurs after months to years of therapy with the culprit medication.
Histologic features that favor an interstitial granulomatous drug reaction over IGD incude a vacuolar interface dermatitis atypical lymphocytes, prominent eosinophils, a lack of neutrophils, and minimal collagen degeneration.
How to differentiate GA from PNGD/IGD histologically ?
GA is more likely to have a patchy infiltrate concentrated in the upper dermis (“top heavy”) and
focal much deposition. A relative paucity of neutrophils and leukocytoclasis distinguishes GA from PNGD,
whereas the presence of either larger palisades or a lack of palisades (e.g. in the interstitial pattern seen in patch-type GA) differentiates GA from IGD.
How to differentiate from Rheumatoid nodules histologically ?
heumatoid nodules can be recognized by their central eosinophilia (rather than basophilia) and
predominant[y subcutaneous ]ocation (see Fig. 45.10 )
Additional diagnostic considerations for an interstitial granulomatous infiltrate with variable
neutrophils may include
dimorphic fungal or atypical mycobacterial infections, borreliosis, and leprosy.
