"Effort thrombosis" of the subclavian vein associated with oral contraceptives.

We report a case of "effort thrombosis" of the subclavian vein in a 33-year-old woman with several thrombotic risk factors, including the use of oral contraceptives. The signs and symptoms associated with this syndrome, as well as concepts concerning diagnostic techniques and management, are discussed.

PIP: A case of "effort thrombosis" of the subclavian vein which occurred in a young woman with severe thrombotic risk factors is reported. The manifestations of this syndrome are summarized, and recent concepts regarding the management of subclavian vein obstruction are discussed. The 33 year old woman was admitted with a 3 day history of rapidly increasing pain and swelling of her right upper extremity and right breast. She recalled no previous trauma but did indicate that her vocation required frequent exertion of her right (dominant) arm. The involved extremity exhibited easy fatigability with intermittent "tingling numbness" of the hand. She had been taking oral contraceptives (OCs) for 4 years. On admission she was smoking 2-3 packs of cigarettes daily with a 15 year smoking history. She had essential hypertension of 14 years duration which was treated with a thiazide diuretic. On physical examination, the patient's right breast was found to be twice the size of the left and exhibited tenderness, peau d'orange appearance, and superficial venous prominence. The right upper extremity exhibited venous prominence and mottled cyanosis and was edematous with an upper arm circumference that was 2.5 cm greater than the left. The involved axilla was tender, with no palpable venous "cord" or enlarged lymph nodes. Adson's maneuver was negative. Noninvasive impedance plethysmography showed no evidence of obstruction to venous outflow in the upper or lower extremities, but venography taken with the arms abducted to 45 degrees showed complete thrombotic obstruction of the right subclavian vein (shown in a figure). At first the patient was treated conservatively with bedrest, arm elevation, discontinuation of OCs, and heparinization. She became asymptomatic during the ensuing week, but a repeat venogram after 7 days of heparin therapy displayed complete obstruction of the right subclavian vein. The patient was discharged on warfarin sodium therapy which was continued for 5 months, during which time antithrombin 3 levels rose to 100% activity. During the year following hospitalization, the patient has experienced monthly episodes of mild aching in her right arm, unaccompanied by swelling or discoloration, following exertion of the extremity. Due to the fact that the etiology of effort thrombosis is now considered to be related to thoracic outlet compression, more emphasis is being placed on the use of phlebography to demonstrate compression points along the subclavian vein. Conservative management with anticoagulants continues to be the mainstay of therapy, but surgical treatment with early thrombectomy promises to decrease the chronic morbidity so common to this condition.

Role of prolactin and the renin-angiotensin system in mediating dopaminergic control of aldosterone secretion in the rat.

Blockade of dopaminergic pathways increases aldosterone levels by mechanisms that are not well delineated. Since both prolactin (PRL) and plasma renin activity (PRA) also increase after administration of dopaminergic antagonists, the aldosterone increments may be secondary to these changes. To address these questions, the relationship between plasma aldosterone (PA) and PRL responses to 2 different dopamine receptor antagonists, haloperidol and metoclopramide (MCP) was examined in rats. The PA response to MCP was compared before and after blockade of the renin-angiotensin system with saralasin and after pre-administration of L-dopa. MCP administration produced significant and parallel increments in PA and PRL whereas haloperidol increased PRL without any change in PA or PRA. L-dopa pre-treatment suppressed the early PA response to MCP. Hypophysectomy prior to MCP administration eliminated the PRL response but did not significantly alter the PA response to MCP. Our findings suggest that dopamine has an inhibitory action on the adrenal gland production of aldosterone acting independently of changes in PRL and the renin-angiotensin system.

Plasma antithrombin III and thrombin generation time: correlation with hemoglobin A1 and fasting serum glucose in young diabetic women.

Three parameters of coagulability--thrombin generation time (TGT), antithrombin III (AT III), and activated partial thromboplastin time (ATPP)--and two parameters of diabetic control--serial measurements of fasting serum glucose (FG) and hemoglobin A1(HbA1)--were used to study the relationship between diabetic control and hypercoagulability. Four groups of females were studied consisting of 10 young normal, 10 young insulin-dependent diabetic, 10 pregnant nondiabetic, and 8 first-trimester, insulin-dependent, pregnant diabetic subjects. Fasting serum glucose values and HbA1 were higher (P < 0.005) in nonpregnant diabetic subjects (193.1 +/- 29.1 mg/dl, 12.9 +/- 1.1%) and pregnant diabetic subjects (111.0 +/- 13.6 mg/dl, 8.2 +/- 1.7%) than in controls (64.8 +/- 4.4 mg/dl, 5.9 +/- 0.1%) and the nondiabetic pregnant females (71.6 +/- 3.8 mg/dl, 6.1 +/- 0.2%). Young diabetic females, pregnant females, and pregnant diabetic subjects had a shorter (P < 0.01) TGT than did the controls. AT III was greater (P < 0.01) for controls (99.7 +/- 2.7%) than for pregnant nondiabetic (83.2 +/- 3.8%), diabetic (79.5 +/- 2.5%), and pregnant diabetic subjects (76.2 +/- 4.4%). There was a positive correlation (r = 0.88, P < 0.005) between HbA1 and FG in the 10 young diabetic and in the 8 pregnant diabetic subjects (r = 0.74, P < 0.05). In the 10 diabetic females there was a negative correlation between AT III and FG (r = -0.76, P < 0.01) and between AT III and HbA1 (r = -0.79, P < 0.01). Thus, AT III is depressed in both diabetes and pregnancy, with pregnant diabetic subjects displaying the lowest AT III levels. Our observation that depression of AT III levels in young diabetic females was closely correlated with elevations of fasting serum glucose and HbA1 suggests that strict diabetic control may help prevent hypercoagulability in diabetes.