Acebutolol is a cardioselective beta blocker with ISA (Intrinsic Sympathomimetic Activity, see article on Pindolol). It is therefore more suitable than non cardioselective beta blockers, if a patient with Asthma bronchiale or chronic obstructive lung disease (COLD) needs treatment with a beta blocker. In doses lower than 800mg daily its constricting effects on the bronchial system and smooth muscle vessels are only 10% to 30% of those observed under Propranolol treatment. But there is experimental evidence that the cardioselective properties diminish at doses of 800mg/day or more. The drug has lipophilic properties, this means that it crosses the Blood Brain Barrier. Acebutolol has no negative impact on serum lipids (cholesterol and triglycerides), in particular no HDL decrease has been observed. In this regard it is unlike to many other beta blockers which have this unfavourable property. The drug works in hypertensive patients with high or normal and low renin plasma concentrations, although acebutolol may be more efficient in patients with high or normal renin plasma concentrations. It seems that in clinical relevant concentrations a membrane stabilizing effect does not play an important role.

Pharmacokinetics

Acebutolol is well absorbed from the GI tract, but undergoes substantial first-pass-metabolization, leading to a bioavailability of only 35% to 50%. Peak plasma levels of acebutolol are reached within 2 to 2,5 hours after oral dosing, those of the active main metabolite diacetolol after 4 hours. Acebutolol has a halflife of 3 to 4 hours, diacetolol one of 8 to 13 hours. Acebutolol undergoes extensive hepatic metabolization resulting in the desbutyl amine acetolol which is readily converted into diacetolol. Diacetolol is as aktive as acebutolol (equipotency) and appears to have the same pharmakologic profile. Geriatric patients tend to have higher peak plasma levels of both acebutolol and diacetolol and a slightly prolonged excretion. Excretion is substantially prolonged in patients with renal impairment; a dose reduction may be needed. Liver cirrhosis does not seem to alter the pharmakokinetic profile of parent drug and metabolite.

Uses

hypertension
angina pectoris, including instable angina
ventricular and atrial cardiac arrhythmias
acute myocardial infarction in high risk patients

Contraindications and Precautions

See article on Propranolol. Acebutolol may be suitable in patients with Asthma bronchiale or COLD.

Side Effects

See article on Propranolol. The development of ANA (Anti-Nuclear-Antibodies) has been found in 10 to 30% of patients under treatment with acebutolol. A systemic disease with arthralgic pain and myalgias has been developed in 1%. A lupus erythematosus like syndrome with skin rash and multiforme organ involvement is even less frequent. The incidence of both ANA and symptomatic disease under acebutolol is higher than under Propranolol. Female patients develop these symptoms more likely than male patients. Also, a few cases of hepatotoxicity with increased liver enzymes (ALT, AST) have been seen. Altogether, 5 to 6% of all patients treated have to discontinue acebutolol due to intolerable side effects. The treatment should be, if possible, discontinued gradually in order to avoid a withdrawal syndrome with increased frequency of angina and even precipitation of myocardial infarction.

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Lupus erythematosus and lichen planus overlap syndrome
From Journal of Drugs in Dermatology, 5/1/04 by Hanna Kim

Abstract

A case of lupus erythematosus (LE) and lichen planus (LP) overlap syndrome in a 71-year-old woman is presented. This disease displays characteristics of both LE and LP. The clinical, histologic, and immunopathologic features of this disorder are reviewed.

**********

Case Report

A 71-year-old woman presented to the Bellevue Hospital Medical Center Dermatology Clinic in May, 1999 with a 1-year history of an erythematous eruption on the face, scalp (Figure 1), trunk (Figure 2), and upper extremities. An initial biopsy specimen from the right shoulder was interpreted as a lichenoid dermatitis, and she was treated with multiple topical corticosteroids with moderate improvement. A repeat biopsy specimen from the scalp was obtained in December, 2000. Past medical history included a history of deep venous thrombosis, hypercholesterolemia, and hypertension. Medications included warfarin, simvastatin, and atenolol.

[FIGURE 1 OMITTED]

[FIGURE 2 OMITTED]

Physical examination revealed scattered erythematous scaly papules, and plaques were present on the lower lip, upper back, chest, and forearms. On the vertex of the scalp was an erythematous, atrophic plaque with follicular plugging. No oral lesions were noted.

Evaluation of laboratory data including antinuclear antibody, anti-histone antibody, anti-SS-A antibody, anti-SS-B antibody, lupus anticoagulant, and anti-DNA antibody were negative. C3 and C4 levels were normal. A comprehensive metabolic panel including liver function tests was normal.

Histopathologic examination revealed a superficial and deep perivascular and perifollicular infiltrate of lymphocytes with vacuolar alteration at the dermoepidermal junction (Figure 3). There was also epidermal atrophy, follicular plugging, and dermal mucin. A PAS stain revealed a thickened basement membrane.

Direct immunofluorescence revealed no abnormal deposits of IgG, C3, IgM, IgA, or fibrin in the epidermis; granular, intermittent deposits of C3(+2), broad to granular deposits of IgM(+/-), and broad deposits of fibrin (+3) in the basement membrane zone; and no abnormal deposits of IgG, C3, IgM, IgA, or fibrin in the vascular space.

Discussion

Lupus erythematosus (LE) and lichen planus (LP) may occur as an overlap syndrome which displays clinical, histologic, and/or immunopathologic characteristics of both disorders. Although LE and LP are not uncommon dermatoses, their coexistence or overlap is rare. Approximately 50 cases of LE/LP overlap syndrome have been reported(1). Previous case reports have described two heterogeneous groups of lesions. One type occurs primarily on the extremities as bluish red, atrophic plaques while another type occurs as verrucous papules and nodules on the upper extremities(2,3). Cutaneous lesions have also been described in other sites, including the face, trunk, mucosa, and nails. The diagnosis, however, is based primarily on the combined presence of clinical, histologic, and/or immunologic features of both diseases occurring at the same time. Of note, different lesions occurring in the same patient may be consistent with either LP or LE.

It is important to differentiate between LE and LP in order to make an accurate diagnosis of this overlap syndrome. Both diseases may display similar histologic and immunologic findings of colloid bodies and basement membrane changes. Colloid bodies are generally more numerous and are situated deeper in LP. Basement membrane cleft formation (Max-Joseph spaces) is seen in LP, while areas of basement membrane thickening are more commonly seen in LE. On direct immunofluorescence microscopy, both LE and LP may reveal deposits of immunoglobulins or linear fibrinogen at the basement membrane zone. Immunoglobulin and complement deposition forms a granular pattern along the basement membrane zone in LE (lupus band), while a linear fibrinogen band is often seen at the basement membrane zone in LP(1).

Possible etiologies of LE/LP overlap syndrome include autoimmune, viral, and genetic predisposition. Isoniazid, procainamide, and acebutolol have also been reported as inducing drugs(1). Conversion of cutaneous LE into systemic LE has been shown to occur more frequently in LE-overlap syndromes and has been reported to have an estimated frequency of at least 5-10%(4). Like LE, LE/LP overlap syndrome is associated with a chronic course. Treatment options include systemic retinoids as well as cyclosporin, which has been reported to be effective(5).

[FIGURE 3 OMITTED]

References

1. Inaloz HS, et al. Lupus erythematosus/lichen planus overlap syndrome with scarring alopecia. J Eur Acad Dermatol Venereol 2000; 15(2):171-4.

2. Ahmed AR, et al. Coexistence of lichen planus and systemic lupus erythematosus. J Am Acad Dermatol 1982; 7(4):478-83.

3. Nieboer C. Lupus erythematosus/lichen planus (LE/LP) overlap syndrome. J Am Acad Dermatol 1985; 13(2):297.

4. Jablonska S, Blaszczyk M. Lupus erythematosus. What's new? J Eur Acad Dermatol Venereol 2000; 15(2):103-5.

5. Grabbe S, Kolde G. Coexisting lichen planus and subacute cutaneous lupus erythematosus. Clin Exp Dermatol 1995; 20(3):249-54.

HANNA KIM MD (1), MIRIAM K POMERANZ MD (2)

1 BOSTON UNIVERSITY DEPARTMENT OF DERMATOLOGY, BOSTON, MASSACHUSETTS

2 NYU MEDICAL CENTER, NEW YORK, NEW YORK

ADDRESS FOR CORRESPONDENCE:

Hanna Kim MD

Boston University Department of Dermatology

609 Albany Street, Boston MA 02118

Phone: 617-638-5500

Fax: 617-638-5515

E-mail: hannakim7@hotmail.com

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