Frank C B, Valentin S Y, Scott-Moncrieff J C R, Miller M A
Department of Comparative Pathobiology, Purdue University, West Lafayette, IN 47907, USA.
J Comp Pathol. 2013 Aug-Oct;149(2-3):268-79. doi: 10.1016/j.jcpa.2012.11.242. Epub 2013 Jan 21.
Hypoadrenocorticism or Addison's disease (AD) is a functional disorder in which insufficient mineralocorticoid and glucocorticoid hormones are produced by the adrenal cortex. Human AD is usually attributed to lymphoplasmacytic adrenalitis with autoimmune destruction of the adrenal cortex. Lymphoplasmacytic adrenalitis is also reported in some descriptions of canine AD; however, the histological aspects of adrenalitis or adrenocortical atrophy have not been well characterized because microscopical examination is not required for diagnosis of AD. In this study, sections of adrenal glands from 33 dogs with adrenalitis were compared with those of 37 dogs without adrenal lesions. The affected dogs were classified clinically as having AD (n = 3), being suspected of having AD (n = 17), not having AD (n = 11) or were unclassified (n = 2). The adrenal inflammation was lymphoplasmacytic in 17 dogs, lymphocytic in four, lymphohistiocytic in one, granulomatous in three and neutrophilic in eight cases. Adrenal glands from control dogs lacked leucocyte infiltration and had a cortical to medullary area ratio of 1.1-7.2. All three dogs with AD, 8/17 dogs with suspected AD and 1/11 dogs without AD had a cortical to medullary area ratio <1.1. Because the area ratio was correlated (r = 0.94) with a linear cortical to medullary thickness ratio, a thickness ratio <1.1 could also indicate severe adrenocortical atrophy. Severe adrenocortical atrophy was associated typically with lymphoplasmacytic infiltration and nearly complete loss of cortical cells; however, the zona glomerulosa was partially spared in three dogs with lymphoplasmacytic adrenalitis and severe cortical atrophy. In contrast, non-lymphoid inflammation was generally part of systemic disease, multifocal and was unaccompanied by severe adrenocortical atrophy.
肾上腺皮质功能减退症或艾迪生病（AD）是一种功能性疾病，其特征为肾上腺皮质产生的盐皮质激素和糖皮质激素不足。人类AD通常归因于淋巴细胞性肾上腺炎伴肾上腺皮质自身免疫性破坏。在一些犬类AD的描述中也报道了淋巴细胞性肾上腺炎；然而，由于AD的诊断不需要显微镜检查，肾上腺炎或肾上腺皮质萎缩的组织学特征尚未得到很好的描述。在本研究中，对33只患有肾上腺炎的犬的肾上腺切片与37只无肾上腺病变的犬的肾上腺切片进行了比较。受影响的犬在临床上被分类为患有AD（n = 3）、疑似患有AD（n = 17）、未患有AD（n = 11）或未分类（n = 2）。17只犬的肾上腺炎症为淋巴细胞性，4只为淋巴细胞性，1只为淋巴组织细胞性，3只为肉芽肿性，8只为中性粒细胞性。对照犬的肾上腺无白细胞浸润，皮质与髓质面积比为1.1 - 7.2。所有3只患有AD的犬、17只疑似患有AD的犬中的8只以及11只未患有AD的犬中的1只，其皮质与髓质面积比<1.1。由于面积比与皮质与髓质厚度的线性比值相关（r = 0.94），厚度比<1.1也可能表明严重的肾上腺皮质萎缩。严重的肾上腺皮质萎缩通常与淋巴细胞性浸润和皮质细胞几乎完全丧失有关；然而，在3只患有淋巴细胞性肾上腺炎和严重皮质萎缩的犬中，球状带部分未受影响。相比之下，非淋巴细胞性炎症通常是全身性疾病的一部分，多灶性，且不伴有严重的肾上腺皮质萎缩。
