Patients rights in India: an ethical perspective.

Patient autonomy is affected by a number of factors, including severity of illness, socio-economic status and dependence. Many patients find that they are not treated with due consideration and compassion, and also have no control over their own care.

Freedom from pain--a mirage or a possibility? Experience in attempts to change laws and practices in India.

The incidence of cancer increases exponentially with age and a large number of cancer patients are the older members of society. In many developing and some developed countries, the disease is usually detected at a stage when it is too late for aggressive anticancer therapy to have the desired effect. Most cancer patients suffer moderate to severe pain during the terminal phase of the disease. This pain is unpredictable and produces fear and anxiety in patients and family members. Morphine is the gold standard analgesic to control this pain, but its availability is restricted. The fear of diversion of morphine for non-medical uses has led to severe control on its availability. Studies have shown that diversion of medical morphine is not really an issue. This paper describes attempts to increase morphine availability through the courts in India. The courts have issued directives to improve the availability of the drug, yet 97% of Indian patients have very poor access to the drug. There is a need to improve access to pain-free end-of-life care. In the absence of morphine, physicians lack experience in its use. They need to be educated to provide for their patients a pain-free life. Patients and their families need to be educated that cancer need not end in a painful death. It is not adequate to be able to manage cancer alone; one needs to free the society from fear of cancer.

Inhibition of cell wall synthesis--is this the mechanism of action of penicillins?

Penicillins have been shown to inhibit bacterial cell wall synthesis, and interact with penicillin binding proteins, leading to bacterial lysis. These two mechanisms, the former more than the latter are believed to be responsible for their therapeutic potential. It has further been demonstrated that only actively multiplying cells are susceptible to bactericidal effects of the antibiotic, which is in accordance with the suggested mechanism of action. Bacterial growth takes place in terms of size and number, both requiring additional cell wall. An increase in bacterial size is due to an increase in the volume of cytosol and area of the cell wall. Presently there is no proof that the former is the cause of the latter or vice versa. Penicillin by inhibiting cell wall synthesis would inhibit both growth and multiplication. Since the antibiotic is bactericidal to rapidly multiplying cells, its effect on cell wall would interfere with its bactericidal action. As per the present understanding penicillin acts principally by inhibiting cell wall synthesis. There is however a discrepancy between its observed effects and what should logically be expected, which forces us to reexamine the mechanism of action of penicillin. We believe that the present understanding of the action of penicillin is incomplete if not outright faulty. It would be expedient to radically modify the same in view of its implication, for example on drug development.

The mechanism of action of aspirin--is there anything beyond cyclo-oxygenase?

Aspirin, today, is an established drug in the regime for the prevention of myocardial infarction, especially in high-risk groups. This use of aspirin has given it a new lease of life in its tenth decade of clinical use. Aspirin is probably the oldest synthetic drug in the Pharmacopoeias today; thus one would have imagined that understanding about the drug would have reached a zenith and if not, that at least there should be certainty about its mechanism of action. Most workers agree that aspirin inhibits the cyclo-oxygenase enzyme in the platelets leading to reduced formation of prostaglandin G2, the precursor of thromboxanes. This explanation does not appear to be complete, since the role of the platelet activating factor (PAF) seems to have been ignored. The precursor for PAF is the lysophospholipid that is almost always formed when membrane phospholipid breakdown takes place. Any effective antiplatelet drug would have to inhibit the formation and/or the action of PAF, if it were to prevent platelet aggregation. Alternatively, the pathophysiological role attributed to PAF is highly exaggerated and needs to be reassessed.

Salt restriction in hypertension.

Salt has had a long and controversial history. It is not known when man began to use salt in his diet, but it is logical to believe that salt has always been a part of human diet though we do not have scientific proof for this. Restriction of salt in hypertensive patients has been a popular measure adopted world wide. This paper examines the usefulness of salt restrictions and the effect it would cause. Most cases of hypertension are symptomless--using a therapy which drastically affects a patients food habits is a poor strategy to ensure compliance. We conclude that salt restriction is not very useful and probably harmful in some patients. Additionally it reduces the quality of life.

Studies on the mechanism of action of Semecarpus anacardium in rheumatoid arthritis.

Semecarpus anacardium nuts are used for variety of disorders in Ayurveda. A chloroform extract of the nut significantly reduced acute carrageenan-induced paw oedema in rats and was active against the secondary lesions of adjuvant-induced arthritis. Delayed hypersensitivity induced in mice by sheep red blood cells as an antigen was potentiated by the extract.

Phosphatidylethanolamide derivatives of prostaglandins E1 and E2.

Prostaglandins E1 (PGE1) and E2 (PGE2) have been coupled with the amine group of phosphatidylethanolamine (PE) by means of dicyclohexylcarbodiimide. These complexes basically mimic the relaxant and contractile effects of the corresponding free prostaglandins (PGs) on various smooth muscle preparations, but exhibit a delayed onset of action and a lower affinity for the PG receptors. The complexes are comparable with the free, parent PGs, in their intrinsic activities. The same holds true for the effects on blood pressure and on the motility of the uterus in situ. The PGE2-PE complex is hydrolysed to release obviously free PGE2 by cell-free homogenates prepared from various tissues, but not by blood plasma. The PGE2-PE complex is immunologically indistinguishable from the free PGE2.