The Nyhus–Wantz lectureship: etiology, herniosis, diverticulosis coli, and cancer

Abstract

The Nyhus–Wantz Lectureship honors two giants who represent the few who formed a new surgical specialty: herniology. My topics are etiology, herniosis, diverticulosis coli, and cancer. Hippocrates blamed wear and tear for herniation. Russell’s (Lancet 1:1519–1523, 1902) explanation was congenital peritoneal “buds” extending down to the pelvis. Harrison (Arch Surg 4:680–689, 1922) attributed herniae to transversalis fascial degradation. Keith (Lancet 2(17):1398–1399, 1906) concluded that pathology was involved, even though Russell (Lancet 1:1519–1523, 1902) had denied it. Nevertheless, the congenital theory prevailed. According to McVay (Christopher’s textbook of surgery, W.B. Saunders, Philadelphia, 1960, p. 159), defects arise in normal musculo-aponeurotic structures. Research showed that atrophy was caused by damaged fibroblasts producing less collagen, which was abnormal (having a reduced I/III ratio). The disease was systemic, later named herniosis. Nicotine addiction increased the incidence of herniation by an inflammatory process named metastatic emphysema. In 1948, Saint’s Triad, an aggregation of hiatus hernia (later, any primary hernia), gallstones, and diverticulosis coli, was introduced. This association occurred eight times more often than expected, with herniosis appearing to be its cause, abetted by high blood cholesterol causing gallstones. In 2006, Krones et al. (Int J Colorectal Dis 21:18–24, 2006) provided evidence that colon cancer is accompanied by a reduction in diverticula. Klinge et al. (Hernia 8(4):300–301, 2004) showed that these entities require different extracellular matrices (ECMs). Ghajar and Bissell (Histochem Cell Biol 130:1105–1118, 2008) pointed out that the ECM, which comprises 80% of the breast, influences its epithelial genetic expression, likewise with other organs (kidney, skin, lung, colon, and ovaries). Recently, a fundamental change in our understanding of cancer growth and metastasis has taken place. Whereas the degradation of connective tissue was thought to encourage invasion, eliciting concern for the herniated, now, investigators report the reverse, a reactive vascularized stroma resembling wound healing with an increase in fibroblasts and collagen I. Words such as desmoplasia, fibrosis, and stiffening abound. In conclusion, degradation of the ECM may be why herniosis appears to be hostile to the development of cancer throughout the body. Studies are needed of patients with and without a history of hernia to determine their incidence of cancer. Data from smokers should be separated, since they carry their own high risk of malignancy.