In a study of cutaneous leishmaniasis (CL) caused by Leishmania major in Saudi Arabia, 10% of the patients were found to have subcutaneous nodules (SCN). The SCNs were usually inconspicuous, painless, and proximal to the primary skin lesions; when multiple, they showed a "sporotrichoid" configuration or appeared as "beaded cords." Their number ranged from 1-16 (average 3 25 +/- 2.50; mean +/- 1 SD). In some patients, the SCNs seemed to be triggered by antileishmanial treatment. The clinical picture and pathologic findings suggest that SCNs in patients with CL represent lymphatic dissemination, a phenomenon not widely recognized.
In a study of zoonotic cutaneous leishmaniasis (CL) due to leishmania major in an endemic focus in Saudi Arabia, lymph node enlargement was observed in 66 of 643 patients (10.26%). The epitrochlear lymph nodes were most commonly involved (68%), but cervical (11%), axillary (15%), and inguinal (18%) lymph nodes were also involved. In eight patients (12%), two lymph node areas were involved. The affected lymph nodes were typically solitary, firm, mobile, nontender, only moderately enlarged, and appeared to persist beyond the clinical healing of the associated skin lesions. The results of pathologic and immunopathologic studies carried out on eight lymph nodes obtained from this group of patients supported the leishmanial etiology. Although amastigotes were only demonstrated in two lymph nodes, the leishmanial antigen was found in all eight specimens. The lymph node involvement is another manifestation of dissemination in infection with a dermotropic leishmania. It appears that in some cases, instead of the parasite, it may be the leishmanial antigen that disseminates and produces lymphadenitis.
Sickle-cell disease (SCD) is a wide-spread inherited hemolytic anemia that is due to a point mutation, leading to the substitution of valine for glutamic acid, causing a spectrum of clinical manifestations in addition to hemolysis and anemia. Acute painful crisis is a common sequela that can cause significant morbidity and negatively impact the patient's quality of life. Remarkable improvements in the understanding of the pathogenesis of this clinical syndrome and the role of cell adhesion, inflammation, and coagulation in acute painful crisis have led to changes in the management of pain. Due to the endemic nature of SCD in various parts of the Middle East, a group of physicians and scientists from the United States and Middle East recently met to draw up a set of suggested guidelines for the management of acute painful crisis that are reflective of local and international experience. This review brings together a detailed etiology, the pathophysiology, and clinical presentation of SCD, including the differential diagnoses of pain associated with the disease, with evidence-based recommendations for pain management and the potential impact of low-molecular-weight heparin (LMWH), from the perspective of physicians and scientists with long-term experience in the management of a large number of patients with SCD.
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