Acquired Pelger-Huet anomaly associated with Mycoplasma pneumoniae pneumonia.

A case report of a healthy 33-year-old man with Mycoplasma pneumoniae pneumonia who concomitantly had the acquired Pelger-Huet anomaly develop is presented. Up to 31% of his total white blood cell count was comprised of Pelger-Huet cells at the height of his clinical illness. The Pelger-Huet cell count returned to 0% after doxycycline therapy and resolution of the pneumonia. No other explanation for the Pelger-Huet anomaly could be determined. A review of the pertinent hematologic literature is included.

Calcium-channel blockers and systemic hypertension.

Calcium-channel blockers selectively inhibit transmembrane flux of calcium in excitable tissues. Their ability to block calcium-mediated electromechanical coupling in contractile tissue produces peripheral vasodilation and has led to interest in their use for systemic hypertension. A postulated involvement of calcium in the development of the increased vascular tone of hypertension makes these agents appear particularly attractive for use as vasodilators. Clinical trials suggest a potentially important role for the calcium-channel blockers in the treatment of systemic hypertension.

Calcium antagonists. Clinical use in the treatment of systemic hypertension.

Increased peripheral vascular resistance is the cause of elevated systemic blood pressure in most patients with long standing hypertension. The desired haemodynamic effect in antihypertensive therapy is dilation of the constricted arterioles by a drug that acts directly on the vascular smooth muscle while not affecting the heart or the venous return. Hydralazine, diazoxide and minoxidil act directly on vascular smooth muscle to produce vasodilatation and have been used with variable degrees of success in the long term treatment of hypertension. Their cellular mechanism of dilation is not understood fully, but the ability to chelate certain trace metals required for smooth muscle contraction has been proposed as a possible mechanism of action for these drugs. The calcium antagonists (calcium entry blocking drugs) are a distinct group of compounds that interfere with the normal transmembrane flux of extracellular calcium ions on which vascular tissue depends for contraction or impulse generation. Thus, calcium anti-agonists can reduce the contractile activity of the heart, and promote coronary and systemic vasodilatation. These effects provide the clinical rationale for the use of calcium antagonists in the management of ischaemic heart disease and hypertrophic cardiomyopathy. Since systemic vasodilatation can be expected to reduce elevated arterial blood pressure, interest has focused recently on calcium antagonists in the medical management of systemic hypertension. All the calcium antagonists are able, in low concentrations, to relax the smooth muscle vasculature from coronary, cerebral, mesenteric, and renal arteries. The effects on the myocardium, cardiac impulse tissue, and vascular smooth muscle are different in magnitude, however, depending on the individual agent that is used. Clinical experience in the treatment of hypertension with this class of agents is confined to verapamil, nifedipine, and diltiazem. In this article, the scientific rationale for using calcium antagonists in the treatment of arterial hypertension is explored and the clinical experiences with the different calcium antagonists used in hypertension are reviewed.