ABSTRACT
Joint involvement occurs in about half the patients with hereditary hemochromatosis and may constitute the presenting manifestation. Joint damage is now the main cause of quality-of-life alterations in patients with hereditary hemochromatosis. The most common sites of involvement are the metacarpophalangeal joints and the hip. We report a case that illustrates the clinical, imaging-study, and pathological characteristics of hip disease in hereditary hemochromatosis.
Subject(s)
Hemochromatosis/complications , Hemochromatosis/genetics , Hip Joint/physiopathology , Aged , Arthroplasty, Replacement, Hip , Cartilage, Articular/metabolism , Cartilage, Articular/pathology , Ferritins/blood , Hemochromatosis/diagnosis , Hip Joint/pathology , Hip Joint/surgery , Humans , Male , Osteoarthritis, Hip/pathology , Osteoarthritis, Hip/physiopathology , Osteoarthritis, Hip/surgery , Transferrin/metabolismABSTRACT
The evolutionary process leading to the emergence of viviparity in Squamata consists of lengthening the period of egg retention in utero coupled with marked reduction in the thickness of the eggshell. We used light microscopy and scanning electron microscopy to study uterine structure during the reproductive cycle of oviparous and viviparous females of the reproductively bimodal Lacerta vivipara. We compared the structure of the uterine shell glands, which secrete components of the eggshell, during preovulatory and early gestation phases of the reproductive cycle and also compared histochemistry of the eggshells. The uterine glands of both reproductive forms undergo considerable growth within a period of a few weeks during folliculogenesis and vitellogenesis preceding ovulation. The majority of the proteinaceous fibers of the shell membrane are secreted early in embryonic development and the uterine glands regress shortly thereafter. This supports previous observations indicating that, in Squamata, secretion of the shell membrane occurs very rapidly after ovulation. The most striking differences between reproductive modes were larger uterine glands at late vitellogenesis in oviparous females, 101 microm compared to 60 microm in viviparous females, and greater thickness of the shell membrane during early gestation in oviparous females (52-73 microm) compared to viviparous females (4-8 microm). Our intraspecific comparison supports the conclusions of previous studies that, prior to ovulation, the uterine glandular layer is less developed in viviparous than in oviparous species, and that this is the main factor accounting for differences in the thickness of the shell membrane of the two reproductive forms of squamates.