LE cell

Possible adverse reactions include headache anorexia nausea vomiting diarrhea palpitations tachycardia angina pectoris toxic reactions (particularly the LE cell syndrome) lacrimation conjunctivitis dizziness tremors psychotic reactions rash urticaria pruritus fever chills arthralgia eosinophilia constipation paralytic ileus lymphadenopathy splenomegaly nasal congestion flushing edema muscle cramps hypotension paradoxical pressor response dyspnea urination difficulty ... 

Hydralazine and dihydralazine are predominantly arterial vasodilators which cause a reduction in peripheral vascular resistance but also reflex tachycardia and fluid retention. They were used in the treatment of hypertension, in combination with a -blocker and a diuretic. Long-term use of these compounds may cause a condition resembling lupus erythematodes with arthrosis, dermatitis and LE-cells in the blood. This risk is enhanced in women and in patients with a slow acetylator pattern. When combined with the venous vasodilator isosorbide (an organic nitrate) hydralazine was shown to be mildly beneficial in patients with congestive heart failure (V-HEFT I Study). Hydralazine and dihydralazine have been replaced by other therapeutics, both in hypertension treatment and in the management of heart failure. 

LE cells are neutrophil polymorphs, which have phagocytosed the basophilic nuclear material of leucocytes, which has been altered by interaction with antinuclear antibodies. The development of ANA requires a lower intake of hydralazine and occurs more quickly in slow acetylators than in rapid acetylators, and rapid acetylators have significantly lower titers of ANA than slow acetylators. There is also a significant correlation between the cumulative dose of hydralazine and the development of ANA, but as indicated above, patients who develop LE do not have a significantly different cumulative intake of hydralazine from those patients who do not develop the syndrome. 

H4. Hargraves, M. M., Production in vitro of the LE cell phenomenon Use of normal bone marrow elements and blood plasma from patients with acute disseminated lupus erythematosus. Proc. Staff Mayo Clin. 24, 234-237 (1949). 

All types of kidney damage were reported, ranging from a transitory fall in glomerular filtration rate and reversible renal insufficiency (part of multisystem disease with circulating LE cells) to the nephrotic syndrome. 

There may be positive LE cells and antinuclear factors. In exacerbation or triggering of lupus erythematosus, two pathogenetic mechanisms may be involved ... 

Chalmers [111] reported 6 rheumatoid arthritis patients with D-penidllamine-induced systemic lupus erythematosus syndrome. All patients had previous mucocutaneous reactions to chry so therapy. Manifestations included pleurisy in 5 of 6 patients, rashes in 3, and nephritis in 2. LE cells were present in 5 patients. 

When two different mAbs are used simultaneously in defining a cell subpopulation, controls should be included that define the four possible cell populations, Le. cells that are negative for both fluorochromes, cells which are positive for either FTTC or PE, and cells which are positive for both FTTC and PE. 

The patient, a 66-year-old man, was treated with 500 mg penicillamine daily for rheumatoid arthritis. After 6 months of treatment a bullous and crythcmatosquamous eruption developed on the trunk, scalp and arms. The Nikolsky phenomenon was positive. An erythematosquamous balanitis was present stomatitis did not develop. On cytological examination acantholytic cells were present. Histological examination revealed both aspects of toxicoderma and pemphigus. Intercellular immunofluorescence was positive in the superficial layers of both affected and apparently normal skin. Electron microscopic examination confirmed acantholysis. Anti-intercellular substances and anti-striational antibodies were detected in the serum ANF and LE cells were absent. The disorder rapidly disappeared after withdrawal of penicillamine, and a course of treatment with a corticosteroid. 

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