female gp Singapore

Androgenetic alopecia, AGA, also known as common pattern baldness affects approximately 20 million American women. AGA in women is triggered by similar processes to those causing pattern baldness in men. In both genders, the onset of AGA may occur in early adulthood, though females tend to present signs and symptoms somewhat later than males.

Recent studies declare that women with some markers of insulin resistance are in significantly increased threat of female AGA. Moreover, a paternal history of baldness might be a strong predictor of female AGA.

Female pattern baldness has also been related to both hyperandrogenism and hirsutism. Most recently, female pattern hairloss has also been related to polycystic ovarian syndrome, PCOS, though epidemiological documentation with this female gp Singapore is, up to now, not statistically compelling. Nevertheless, the association between PCOS and insulin resistance is well documented.

What actually triggers pattern baldness in women?

From the susceptibility standpoint, the inheritance pattern in female pattern hairloss is polygenic, and the onset and incidence of the disorder closely parallels that observed in males. The disorder begins in susceptible hair follicles, where dihydrotestosterone, DHT, binds androgen receptor forming a molecular trigger that sets the procedure of baldness in motion.

The 5 alpha dihydrotestosterone hormone-receptor complex translocates to the cell nucleus of susceptible hair follicles, initiating a gene activation program that starts the gradual transformation of large terminal follicles to miniaturized follicles. This method occurs in just a genetically pre-determined anatomical region, or pattern of the scalp. The hair outside with this pattern remains unaffected. This is why the disorder is called pattern hair loss.

Strikingly, both females and males diagnosed with pattern baldness have higher degrees of 5-Alpha-Reductase, 5AR, in frontal hair follicles in comparison to occipital, back of the scalp behind the ears,. Other predisposing factors such as for instance differential cytochrome P450 levels in susceptible versus non-susceptible hair follicles are less well clearly worked out, but could have contributory relevance as well.

The diagnosis of AGA in women is supported by a design of increased thinning over the frontal/parietal scalp with greater density over the occipital scalp, a retention of the juvenile hairline, and the presence of miniaturized hairs in the effected zone of loss. The majority of women with AGA have normal menses and pregnancies. Extensive hormonal testing is normally not indicated unless signs & apparent symptoms of androgen excess are present such as for instance hirsutism, severe unresponsive cystic acne, virilization, or galactorrhea.

In most cases, the differential diagnosis of AGA is created based on the patient's history and clinical presentation. Typical differentials include alopecia areata, trichotillomania, and less commonly baldness associated with disorders such as for instance lupus erythematosis, scabies and other skin manifesting disease processes. Scalp biopsy and lab assay might be useful in elucidating a non-pattern baldness etiology but, in such cases, should generally only follow a preliminary clinical evaluation by way of a qualified treating physician.