The increased use of immunosuppressants in the treatment of malignant and non-malignant diseases in today's medicine has significantly contributed to the increased interest in infections caused by opportunistic microorganisms and rare parasites. A fifty-eight-year old male patient, professor, born in Bosnia, was admitted to the Institute due to poor general condition and decompensated steroid diabetes. He had been under immunosuppressant therapy for the previous 5 weeks. Six months before, he noticed squamous and crusted changes on capilli, and afterwards on his body too. As these changes did not respond to local therapy he was admitted to the Department of Dermatovenereology, Zagreb University School of Medicine. Histologic analysis indicated pemphigus erythematosus. He was treated with immunosuppressants (methylprednisolone + azathioprine). Endoscopic examinations revealed duodenal ulcer, in addition to diabetes which could not be regulated by oral hypoglycemics. He received antiulcerative therapy for ulcer treatment. Several hours upon admission the patient became highly febrile, and vomited a sanguinolent content. In spite of intensive therapy, he became comatose and died 20 hours later. On autopsy, generalized strongyloidosis of the lungs, liver, duodenum and small intestine, and a bleeding duodenal ulcer due to strongyloidosis were found. This review should remind us that hyperinfestation with strongyloides is a rare and severe complication, and could be expected in immunocompromised patients.

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PubMedDate not supplied

The neural cell adhesion molecule (NCAM) provides clues to the development of testicular Leydig cells.

As previously shown, Leydig cells in culture dramatically up-regulate the expression of the neural cell adhesion molecule (NCAM) gene and express alternatively spliced forms. Because the family of NCAM adhesion molecules is known to be involved in cell migration and differentiation, we examined the potential involvement of NCAMs in Leydig cell differentiation in the developing testis. We detected NCAM-immunoreactive cells in the rat and mouse at embryonic day (ED) 13-14 in epithelia of mesonephric tubules and cell clusters between the mesonephros and testis. At about ED 17-18, strongly NCAM-immunoreactive cells were demonstrated extending from the mesonephros/mesonephric tubules into the region occupied by the forming rete testis and spreading into the testis itself. Within the testis, interstitial fetal Leydig cells, identified with an antiserum directed against P450-side-chain cleavage enzyme, were also NCAM immunoreactive, although to a lesser degree, and in part expressed NCAM-associated polysialic acid. In situ hybridization histochemistry demonstrated the presence of NCAM mRNA, mainly in the cell population corresponding to the strongly immunoreactive cells. NCAM forms with molecular weights of 140 and 180 kDa, the latter polysialylated, predominate in immunoblots of fetal testes. Because testicular development occurs along the mesonephros, from which precursor cells are thought to migrate into the developing gonad and then differentiate into the various testicular cell types, our results may suggest that the expression of NCAMs and NCAM modification are associated with cells that appear to migrate into the developing testis. Although it remains to be proven whether these cells could be precursor cells of Leydig cells, this assumption is supported by the fact that within the developing testis, NCAMs and NCAM modifications are expressed during differentiation of testicular P450-side-chain cleavage enzyme-positive Leydig cells. Thus, the adhesion molecule NCAM and its variants and modifications are expressed in the developing testis and may be of functional, "morphogenic" importance. Because Leydig cells in vitro and during fetal development express NCAMs, these molecules may prove to be a suitable specific marker for the study of Leydig cell development and differentiation.

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