To the editor: The letter from Drs. Buckley and Tolnai will serve to remind physicians of this serious complication associated with IUCDs. We believe that genital actinomycosis is seriously underdiagnosed in its early stages, mainly because of the poor rate of recovery of Actinomyces israelii on culture, but also, no doubt, because of a lack of awareness of this hazard of the use of IUCDs. Study of published reports indicates that diagnosis has usually been made late in the course of the disease when severe pelvic complications are already established. The suggestion that yearly Pap smears might serve to alert physicians to this potential complication before the onset of serious disease is useful. It remains to be seen if this approach will prove effective in prevention. We wish to draw attention to a further variant of mycetomatous endometritis associated with use of IUCDs. We have found "sulfur granules" (Fig. 2) on histologic examination of tissue adherent to the IUCD in three women with a variety of gynecologic complaints. Gram-staining of these granules demonstrated eumycotic fungal hyphae approximately 5 /L in diameter (Fig. 3). The exact nature of these fungal organisms remains to be established by cultural methods, which so far have yielded negative results. Two of the women had had a Dalkon Shield in situ for more than 2½ years. The third had had a Cu-7 device inserted 10 months prior to discovery of disease. These cases will be recorded in detail later. In view of the differing antibiotic sensitivities of actinomycotic and fungal organisms it is essential that special stains be carried out on all such IUCD-
.
-.
64
1i4,
. FIG. 2-Sulfur granule (hematoxylin..eosin; x200, reduced 30%).
U,
'I
associated granules to establish the morphology of the organism pending more accurate identification by microbiologic methods. Plastic IUCDs should probably be changed at least every 2 years and copper-containing devices perhaps more often. At the time of changing, the removed device should undergo labo.ratory examination. P.K. O'BluEN, MB, FRcP[c]
L. Rom-Movo, MD, FRcP[c]
Department of pathology Etobicoke General Hospital 101 Humber College lllvd. Rexdale, Ont.
Thrombotic thrombocytopenic purpura To the editor: I read with interest the recent excellent review by Dr. P.B. Neame and his colleagues (Can Med Assoc J 114: 1108, 1976) of their experience and that of others with the treatment of thrombotic thrombocytopenic purpura (TTP). As Dr. Neame mentioned, therapy in TTP has been mainly empirical and has included exchange transfusion, heparin, steroids, splenectomy alone, steroids and splenectomy, fibrinolytic agents and hemodialysis. He also pointed out that patients with T17P have been successfully treated with regimens that included drugs that suppress platelet function. His paper and at least one other recent review1 mentioned that in all the reports the patients received many other modes of therapy concomitant with the antiplatelet drug therapy, which leaves in doubt the efficacy of the latter. Nevertheless, in several instances the addition of platelet-suppressing drugs to the regimen coincided with the onset of remission. We recently reported the successful treatment of a 16-year-old girl with TTP by means of high doses of acetylsalicylic acid and dipyridamole without other concomitant treatment.' The disease has been in remission for over 8 months. We believe that our case is the first to be reported of a patient successfully treated with platelet-suppressing drugs alone and we think that it supports Dr. Neame's theory that disseminated intravascular platelet aggregation is involved in the pathogenesis of TTP. WILLIAM I. GUNDLACH, MD RALPH TARNAsKY, MD
Departments of hematology and pathology University of North Dakota school of medicine Bismarck, ND References 1. BuKowsKs RM, HEWLETr JS, HAxass JW, et al: Exchange transfusions in the treatment of thrombotic thrombocytopenic purpura.
Apresoline
the unique "ADD ON" antihypertensive
INDICATIONS: Various forms of hypertension: fixed essential hypertension, whether of benign or malignant character; hypertension associated with acute and chronic glomerulonephritis; nephrosclerosis; hypertensive toxemias of pregnancy, pre-eclampsia, and eclampsia. DOSAGE: Hypertension: Orally: In general after initiating therapy gradually increase dosage, adjusting according to individual response. As a single agent, initially 10mg, four times daily increasing slowly to a maximum practical dosage of 200mg daily. In combination with other hypotensive agents, lower dosages of APRESOLINE will be appropriate. Parenterally: When there is urgent need, therapy in the hospitalized patient may be initiated intravenously or intramuscularly. Usual dose is 20 to 40 mg, repeated as necessary. Certain patients, especially those with marked renal damage, may require a lower dose. Pressure may begin to fall within a few minutes after injection, with an average maximal decrease occurring in 10 to 80 minutes. Most patients can be transferred to oral APRESOLINE within 24 to 48 hours. Toxemia of Pregnancy: a) Early toxemia and hypertension of pregnancy: One 10-mg tablet orally 4 times daily, slowly increasing the dosage up to 400 mg per d8y, or until a therapeutic result is obtained. b) Late toxemia and pre-eclampsia: Give 20 to 40mg intramuscularly, or slowly by direct intravenous injection or infusion. Repeat as necessary. SIDE EFFECTS: Tachycardia, headache, palpitation, dizziness, weakness, nausea, vomiting, postural hypotension, numbness and tingling of the extremities, flushing, nasal congestion, lachrymation, conjunctival injection, dyspnea, anginal symptoms, rash, drug fever, reduction in hemoglobin and red cell count, giant urticaria, and a lupus-like syndrome (arthralgia) in some cases following administration for long periods. CAUTIONS: Use cautiously in the presence of advanced renal damage and recent coronary or cerebral ischemia. APRESOLINE may potentiate the narcotic effects of barbiturates and alcohol. Peripheral neuritis evidenced by paresthesias, numbness and tingling has been observed. Published evidence suggests an anti-pyridoxine effect and addition of pyridoxine to the regimen if symptoms develop. OVERDOSAGE: Symptoms: Hypotension and tachycardia. Treatment: Gastric lavage or, in the absence of coma, emetics. In the presence of hypotension, cautiously give norepinephrine (intravenously) or ephedrine to raise the blood pressure without increasing tachycardia. Avoid epinephrine. General supportive measures include intravenous fluids, external heat, and elevation of foot of bed. SUPPLIED: All forms contain hydralazine hydrochlorideTablets of 10mg (yellow, scored); bottles of 100. Tablets of 25mg (blue, coated); bottles of 100 and 500. Tablets of 50mg (pink, coated); bottles of 100 and 500. Ampoules of 1 ml aqueous solution containing 20 mg; boxes of 10.
Semin Hematol 13: 219, 1976
FIG. 3-Sulfur granule (Gram's stain; oil Immersion, x1024, reduced 50%).
2. GUNDLACH WJ, TARNASICY R: Thrombotic thrombocytopenic purpura: remission follow-
ing treatment with aspirin and dipyridamole. Minn Med (in press)
1194 CMA JOURNAL/DECEMBER 18, 1976/VOL. 115
CIBA
DORVAL, QUEBEC
C-5003
.
-.
64
1i4,
. FIG. 2-Sulfur granule (hematoxylin..eosin; x200, reduced 30%).
U,
'I
associated granules to establish the morphology of the organism pending more accurate identification by microbiologic methods. Plastic IUCDs should probably be changed at least every 2 years and copper-containing devices perhaps more often. At the time of changing, the removed device should undergo labo.ratory examination. P.K. O'BluEN, MB, FRcP[c]
L. Rom-Movo, MD, FRcP[c]
Department of pathology Etobicoke General Hospital 101 Humber College lllvd. Rexdale, Ont.
Thrombotic thrombocytopenic purpura To the editor: I read with interest the recent excellent review by Dr. P.B. Neame and his colleagues (Can Med Assoc J 114: 1108, 1976) of their experience and that of others with the treatment of thrombotic thrombocytopenic purpura (TTP). As Dr. Neame mentioned, therapy in TTP has been mainly empirical and has included exchange transfusion, heparin, steroids, splenectomy alone, steroids and splenectomy, fibrinolytic agents and hemodialysis. He also pointed out that patients with T17P have been successfully treated with regimens that included drugs that suppress platelet function. His paper and at least one other recent review1 mentioned that in all the reports the patients received many other modes of therapy concomitant with the antiplatelet drug therapy, which leaves in doubt the efficacy of the latter. Nevertheless, in several instances the addition of platelet-suppressing drugs to the regimen coincided with the onset of remission. We recently reported the successful treatment of a 16-year-old girl with TTP by means of high doses of acetylsalicylic acid and dipyridamole without other concomitant treatment.' The disease has been in remission for over 8 months. We believe that our case is the first to be reported of a patient successfully treated with platelet-suppressing drugs alone and we think that it supports Dr. Neame's theory that disseminated intravascular platelet aggregation is involved in the pathogenesis of TTP. WILLIAM I. GUNDLACH, MD RALPH TARNAsKY, MD
Departments of hematology and pathology University of North Dakota school of medicine Bismarck, ND References 1. BuKowsKs RM, HEWLETr JS, HAxass JW, et al: Exchange transfusions in the treatment of thrombotic thrombocytopenic purpura.
Apresoline
the unique "ADD ON" antihypertensive
INDICATIONS: Various forms of hypertension: fixed essential hypertension, whether of benign or malignant character; hypertension associated with acute and chronic glomerulonephritis; nephrosclerosis; hypertensive toxemias of pregnancy, pre-eclampsia, and eclampsia. DOSAGE: Hypertension: Orally: In general after initiating therapy gradually increase dosage, adjusting according to individual response. As a single agent, initially 10mg, four times daily increasing slowly to a maximum practical dosage of 200mg daily. In combination with other hypotensive agents, lower dosages of APRESOLINE will be appropriate. Parenterally: When there is urgent need, therapy in the hospitalized patient may be initiated intravenously or intramuscularly. Usual dose is 20 to 40 mg, repeated as necessary. Certain patients, especially those with marked renal damage, may require a lower dose. Pressure may begin to fall within a few minutes after injection, with an average maximal decrease occurring in 10 to 80 minutes. Most patients can be transferred to oral APRESOLINE within 24 to 48 hours. Toxemia of Pregnancy: a) Early toxemia and hypertension of pregnancy: One 10-mg tablet orally 4 times daily, slowly increasing the dosage up to 400 mg per d8y, or until a therapeutic result is obtained. b) Late toxemia and pre-eclampsia: Give 20 to 40mg intramuscularly, or slowly by direct intravenous injection or infusion. Repeat as necessary. SIDE EFFECTS: Tachycardia, headache, palpitation, dizziness, weakness, nausea, vomiting, postural hypotension, numbness and tingling of the extremities, flushing, nasal congestion, lachrymation, conjunctival injection, dyspnea, anginal symptoms, rash, drug fever, reduction in hemoglobin and red cell count, giant urticaria, and a lupus-like syndrome (arthralgia) in some cases following administration for long periods. CAUTIONS: Use cautiously in the presence of advanced renal damage and recent coronary or cerebral ischemia. APRESOLINE may potentiate the narcotic effects of barbiturates and alcohol. Peripheral neuritis evidenced by paresthesias, numbness and tingling has been observed. Published evidence suggests an anti-pyridoxine effect and addition of pyridoxine to the regimen if symptoms develop. OVERDOSAGE: Symptoms: Hypotension and tachycardia. Treatment: Gastric lavage or, in the absence of coma, emetics. In the presence of hypotension, cautiously give norepinephrine (intravenously) or ephedrine to raise the blood pressure without increasing tachycardia. Avoid epinephrine. General supportive measures include intravenous fluids, external heat, and elevation of foot of bed. SUPPLIED: All forms contain hydralazine hydrochlorideTablets of 10mg (yellow, scored); bottles of 100. Tablets of 25mg (blue, coated); bottles of 100 and 500. Tablets of 50mg (pink, coated); bottles of 100 and 500. Ampoules of 1 ml aqueous solution containing 20 mg; boxes of 10.
Semin Hematol 13: 219, 1976
FIG. 3-Sulfur granule (Gram's stain; oil Immersion, x1024, reduced 50%).
2. GUNDLACH WJ, TARNASICY R: Thrombotic thrombocytopenic purpura: remission follow-
ing treatment with aspirin and dipyridamole. Minn Med (in press)
1194 CMA JOURNAL/DECEMBER 18, 1976/VOL. 115
CIBA
DORVAL, QUEBEC
C-5003
