Microcirculation in white atrophy

There are two clinical phenomena which, owing to the French School, are still subject to violent criticism: the phenomenon described by M. Raynaud (1862) and the white atrophy termed Milian's (1929). Perhaps badly defined by the authors, the facts have been reviewed, but microcirculation - that of gauges less than 30 to 50 m - does not occupy the whole picture. The proof is that in direct capillaroscopy, functional explorations and biopsy are strikingly monotonous and lacking in exactitude. Capillaroscopy provides the usual aspects of cicatrization, "capillary" neogenesis and their histogenic disorders: central avascular zone, corona limited with loops in "club" formation, or in "clusters" owing to their confluence, "key" loops at the periphery near to the normal loops. These "neocapillaries" pose problems of the immaturity of the neovascular elements and of hydraulics in venous stasis. Of course, there are disorders of capillary permeability, and these are linked especially with vascular neogenesis, but it would not be reasonable to speak of "cutaneous infarctus", or "vascularitis", the necessary criteria being absent. On the contrary, we believe that it all comes down to a "histoangiopathy" by deterioration of the pericapillary sheath of proteoglycanes and of the interstitial conjunctiva. The anomalies are of the type of the deteriorations in plastic polymers and the apparatus of the endarterial bloc, which are included. A "trapping" of the leucocytes in the declivitous areas must also play a part.     

Clinical and experimental white atrophy

The author was, in 1952, the first to draw attention to the possibilities of revascularization of white atrophy. The data which he produced in 1952 have remained correct. Time has amply confirmed them and so, using these data, the author studies the nature of revascularization; he underlines the very important idea following the experiments carried out by Boersma, of rhythmical jarring in the return venous circulation, both superficial and deep, and shows how it is possible to counteract the ill-effects of these veritable battering-ram shocks by means of ambulatory compression perfectly applied. The more the compression offers resistance to the jarring during walking, the more limited the risk of relapse will be. A patient who carefully follows the prescribed treatment has a good chance that the development of the disease will not be crowned by relapse.     

Chlorpropamide-induced pure white cell aplasia

We investigated the mechanism for isolated agranulocytosis and marrow pure white cell aplasia in an elderly man receiving 0.5 to 1.0 g per day of chlorpropamide (Chl) without other toxic drug exposure or overt systemic illness. Patient marrow revealed an absence of recognizable granulocytic precursors; megakaryocytes and erythroid precursors were normal. The WBC count was 1800/mm3 on admission with only 2% neutrophils; the absolute neutrophil count first exceeded 500/mm3 on the 17th day following cessation of Chl. A serum Chl level on admission was 100 micrograms/mL (acute phase, AP); no Chl was detected in serum (convalescent phase, CP) assessed on the 22nd hospital day. Antineutrophil antibodies were not detected, and T cell depletion failed to augment patient in vitro granulopoiesis. Patient AP serum produced potent complement-mediated inhibition (87% +/- 7%) of autologous granulocyte progenitors (CFU-GM) with minimal inhibition of erythroid (11% +/- 5%) or multipotent (5% +/- 4%) progenitor cells. Selective inhibition by patient AP serum of CFU-GM (74% +/- 11%) was also seen against two allogeneic marrows. Patient CP serum no longer inhibited (6% +/- 4%) autologous CFU-GM. Addition of Chl (5 to 120 micrograms/mL) to CP serum but not to control serum resulted in potent drug concentration-dependent complement-mediated inhibition of autologous and allogeneic CFU-GM. Inhibition of CFU-GM in the presence of Chl was no longer demonstrable following immunoabsorbent removal of IgG from patient serum. Patient serum in the presence of Chl had limited activity against morphologically recognizable marrow granulocytic precursors in a microimmunofluorescence assay. These results are most consistent with the development of Chl-dependent, selective antibody-mediated immune inhibition of granulopoiesis.     

Treatment of white coat hypertension

White coat hypertension has been defined as the persistent elevation of blood pressure at the clinic or office only. It usually implies that daily ambulatory blood pressure is normal. The accepted cutoff for normal daytime ambulatory blood pressure is 135/85 mm Hg. The prevalence of white coat hypertension is high and varies from 20% to 45%. It appears to be more frequent in women, older patients, and persons with mild hypertension. White coat hypertension should not be confused with the white coat effect. The white coat effect signifies the difference in blood pressure between the office and daytime ambulatory blood pressure and occurs in patients with white coat hypertension as well as in patients with sustained hypertension that is treated or untreated. White coat hypertension is a benign condition, and the incidence of target-organ damage or cardiovascular morbidity and death is not significantly different from that in normotensive persons. Pharmacologic treatment should be withheld; instead, treatment should consist of lifestyle modification, moderate salt restriction, weight reduction, regular exercise, smoking cessation, and correction of glucose and lipid abnormalities. In addition, semiannual or annual follow-up with ambulatory blood pressure monitoring is advised.