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PubMed2005

Calcium antagonists in dermatology: a review of the evidence and research-based studies.

Calcium antagonists (CAs) or calcium-channel blockers are a common group of antihypertensive medications. These drugs have the property of blocking the calcium channels of vascular and cardiac smooth muscle fibers. Some of these drugs may inhibit the growth and proliferation of vascular smooth muscle cells and fibroblasts, and inhibit the synthesis of extracellular-matrix proteins (collagen, fibronectin, proteoglycans). Other CAs also have immunomodulatory or dysregulatory effects on lymphocytes and can suppress superoxide generation and phagocytic action of neutrophils. Moreover mast cell degranulation and platelet aggregation may also be impaired. On account of these properties, calcium antagonists have also been used for the prevention and treatment of various dermatologic diseases such as erythromelalgia, idiopathic- or CREST-related calcinosis cutis, primary and secondary Raynaud phenomenon, chilblains, chronic anal fissures, keloids, and burn scars. They are also used for prevention of skin flap necrosis in experimental models. Calcium antagonists, apart from their well known and established antihypertensive action, should also be considered as possible therapy for several dermatologic diseases.

Animals↗

PubMed1994

What clinical and laboratory data are indicative of polycythemia and when are blood volume studies needed?

An increased hematocrit can be caused by primary proliferative polycythemia (PPP), by secondary polycythemia, by relative polycythemia (reduced plasma volume with a normal red cell mass), or by modifications of the red cell mass and the plasma volume within their normal ranges. As an increased hematocrit by itself is a risk factor for thrombosis, it is important to diagnose not only polycythemia, but also its possible cause, in order to offer optimal therapy. Smoking is the most frequent cause of an increased hematocrit. Splenomegaly, aquagenic pruritus, and erythromelalgia often exist in PPP, whereas other symptoms such as dyspnea are more likely to be associated with secondary polycythemia. Smokers with an increased hematocrit will be asked to stop smoking before ordering blood volume studies. These studies are not indicated in patients with obvious pulmonary disease. Male patients with an hematocrit over 60% and female patients with an hematocrit over 55% always have absolute polycythemia. The associations of an increased hematocrit with splenomegaly, a raised white blood cell count or thrombocytosis are indicators for PPP. The necessity for blood volume studies is questionable in these patients. However, blood volume studies are useful in patients with an increased hematocrit and no other clinical or biological signs suggestive of any form of polycythemia.

Blood Cell Count↗

PubMedDate not supplied

Is ticlopidine a safe alternative to aspirin for management of myeloproliferative disorders?

BACKGROUND: Bleeding and thrombosis are frequent complications in patients with chronic myeloproliferative disorders (cMPD). Antiplatelet therapy is extensively used by many physicians for primary prophylaxis of thrombotic events, even though there have been no prospective trials that demonstrate clinical benefit. The use of aspirin has been associated with a heavy incidence of serious hemorrhages, particularly of gastrointestinal origin. This evidence is mainly based on data from patients treated with dosages far higher than those presently recommended. Moreover, patients with bleeding symptoms or prolonged bleeding time (BT) had not usually been excluded from treatment. METHODS: In this study 58 patients with cMPD and thrombocytosis were treated with aspirin (325-500 mg/day, 31 patients) or with ticlopidine (500 mg/day 27 patients). Only patients with negative bleeding histories and normal BT were considered. Ticlopidine, a drug not extensively investigated in cMPD, was reserved only for patients with histories of gastritis, gastric discomfort, peptic ulcer and/or intolerance to aspirin. All other patients were given aspirin combined with antacids in a buffered preparation. RESULTS AND CONCLUSIONS: Average follow-up was 2 years. Aspirin was associated with a high incidence of gastrointestinal hemorrhages (5/31). Ticlopidine was tolerated better and no bleeding complications were recorded. Both drugs were similarly effective in relieving erythromelalgia and painful paresthesia in almost all cases with these symptoms within 24-48 hours.

Adult↗

PubMed1993

[Essential thrombocythemia. Apropos a case of cerebrovascular stroke].

The authors report the case of a 60-year-old white man with a previous history of pulmonary tuberculosis, smoking habits, hypertension, intermittent claudication and erythromelalgia, admitted to our ward with an ischemic cerebral event. Initial laboratory evaluation documented thrombocytosis (platelet-950000/mm3) and discrete anemia. Additional studies confirmed the diagnosis of essential thrombocythemia, meeting all the criteria proposed by the Polycythemia Vera Study Group in 1986, after exclusion of the possible causes of reactive thrombocytosis. Therapy was initiated with alpha-2b interferon (3 MU/m2 subcutaneously three times a week) and aspirin. Platelet count control was obtained and the patient remained asymptomatic. Nine months later cutaneous toxicity obliged the discontinuance of alpha-interferon. Due to a continuous increase of platelet count, hydroxyurea was introduced. The patient is asymptomatic, with platelet counts < 500000/mm3, without toxicity manifestations, two years after diagnosis. The contribution of cardiovascular risk factors versus thrombocythemia in the pathogenesis of the ischemic cerebral event and the benefit of platelet count control are discussed.

Aspirin↗

PubMed1978

[Paroxystic vasomotor skin manifestations (author's transl)].

Paroxystic vasomotor skin manifestations are provoked by various etiologies. Widespread or generalized vasomotor skin manifestations may be induced by a physiological reaction (emotinal flushing), by a drug (vasodilator drugs, antabuse, antidiabetic, sulfonamides), by a discharge of histamine (urticaria, mastocytosis) or by an hypersecretion of serotonin (dumping-syndrome, carcinoid syndrome). They may be caused by an endocrinopathy (menopause, hyperthyroidism, hypoglycaemia, medullary thyroid carcinoma, pheochromocytoma, endocrine pancreas, carcinoma). More rarely vasomotor troubles happen in homocystinuria, inhalation of a toxic (trichlorethylen, calcic cyanamid) and exceptionally in some immunohaematologic diseases. Main localized vasomotor skin manifestations observed are dermographism, facial flushing (Sluder's syndrome, cluster headaches, Frey's syndrome, Riley-Day's syndrome) and acral syndromes (Raynaud's phenomenon, erythromelalgia).

Amidohydrolases↗

PubMed1996

[Dysmegakaryocytopoiesis and dysthrombopoiesis in myeloproliferative syndromes].

Megakaryocyte proliferation in bone marrow is a feature common to the three Philadelphia negative chromosome myeloproliferative disorders (MPD)--essential thrombocythemia (ET), polycythemia vera, and myelofibrosis with splenic myeloid metaplasia--and chronic myelocytic leukemia. Enlarged megakaryocytes, clustering in close neighbouring with multilobulated nuclei are the hallmark of all the Philadelphia negative chromosome MPD. Clonality of hematopoietic cells, based on X-chromosome inactivation can now be studied in a majority of female patients in all nucleated cell fractions as well as in platelets. A significant increase in circulating CFU-MK has been repeatedly observed in MPD as well as a spontaneous megakaryocyte colony formation in a majority of ET patients. Hypersensitivity to thrombopoietin (TPO) in relation with a functional defect of the TPO-MPL pathway may play a major role in spontaneous megakaryocyte growth. There is presently no currently available test of platelet functions able to predict the risk of occurrence of thrombotic or haemorrhagic complications in MPD patients. However the role of platelets activation in the pathogenesis of ischemic erythromelalgia has been established.

Blood Platelets↗

PubMed1963