Brief Answer:
Testosterone

Detailed Answer:
Sorry to hear about your condition.

1 Sustenon is a form of testosterone injection. It is the main male hormone in the body of a man

2 Masturbation has no known link with jaundice

3 If you still have jaundice you should be seeing your family doctor/ general MD physician or a gastroenterologist

4 Jaundice after sustenon is uncommon but can occur. You should definitely be monitored for recovery closely.

5 After thoroughly reading your compliants, this is what I would recommend if I saw someone like you in my practice, but once your jaundice/illness is gone and you are well overall for a few weeks:

Blood tests for
CBC
LFT
RFT
Electrolytes
Calcium
Glucose
TSH
Free T4
Total Testosterone
SHBG

If anything is abnormal in the results of these tests then further tests can be planned.

Ideally, you need to be examined in person by an endocrinologist

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Brief Answer:
Follow up

Detailed Answer:
I have reviewed the attached lab results

Your testosterone is low and your FSH / LH are high suggestive of 'Primary (or Hypergonadotrophic) Hypogonadism'. The meaning of this medical term is that your testicles are not making enough testosterone.

This requires systematic investigation such as:

History: did you have mumps as a child? or have you ever had significant trauma/ surgery/ radiation to the testicles? Have you had any chemotherapy for cancer in the past?

Examination: size and consistency of testicles. Other secondary sexual characteristics

Tests: Karyotype and semen analysis (in addition to tests mentioned above)

Once we get to the cause of this condition there will be a better understanding of the long term implications of this.

However, all this can be achieved only by seeing a qualified endocrinologist in person

To answer your other questions specifically:

1 No. Your low testosterone is not due to excessive masturbation

2 There are other forms of testosterone treatment such as gel, that can be considered.

3 There is no impact of dietary modification on this condition

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Brief Answer:
Second follow up

Detailed Answer:
I have reviewed all the attached laboratory test results.

The karyotype is strongly in favor of Klinefelter's syndrome. Essentially this is a genetic condition in which the testicles do not function properly in terms of making enough testosterone and sperms.
It is very important that you consult an endocrinologist in person to extensively go over the implications of this, particularly as you are a young gentleman

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Brief Answer:
Third follow up

Detailed Answer:
1 You were born with this genetic condition. It only got diagnosed now

2 Non veg diet or medication will not cure this. Nothing will reverse the genetic problem. There are treatments to improve some of the issues such as raising testosterone levels into normal range.

3 This genetic condition can occur for the first time in an individual. It is not always inherited.

4 Have you seen an Endocrinologist yet? If not, it is unlikely you will experience good outcomes.
I am providing extensive information underneath but trust me you are doing a great disservice to yourself by not establishing a long term relationship with a qualified endocrinologist who is the expert in managing this condition.

I have repeatedly tried to guide you in the right direction of seeing a specialist doctor because klinefelters syndrome is a complex condition to manage for the non-expert.
But since you insist on knowing details I will provide details here:
Klinefelter Syndrome
This syndrome was first described by XXXXXXX Klinefelter in 1942 as a clinical condition with small testes, azoospermia, gynecomastia and an elevated serum FSH (41). Only in 1959 was the chromosomal basis of the disorder described. Subsequently the diagnosis of Klinefelter syndrome has required the demonstration of the 47,XXY karyotype or one of its rarer variants.

The prevalence of Klinefelter syndrome appears to be approximately 1 in 660 males, and recent data suggest a rising incidence over the last decades (42, 43). It is the most frequent form of primary testicular dysfunction affecting spermatogenesis as well as hormone production and is found in about 12% of men presenting with azoospermia. It appears that at least half of the cases remain undiagnosed and untreated throughout life (42).

A non-mosaic 47,XXY karyotype is found in 80 – 90 percent of Klinefelter patients. A mosaic is seen in another 5 – 10 percent of patients. The 47,XXY/46,XY mosaicism is most common. The 48,XXXY, 48,XXYY and 49,XXXXY karyotypes constitute 4 – 5 percent of all Klinefelter syndrome karyotypes, structurally abnormal extra X chromosomes are found in less than one percent of patients. Apart for karyotype analysis, molecular genetics methods can be used to quantify the number of X chromosomes, for example by quantitative PCR analysis of the androgen receptor gene located on the X chromosome (44).

The numerical aberration in non-mosaic 47,XXY is derived with equal likelihood from maternal or paternal meiotic error (45). Most cases are caused by meiosis without X/Y or X/X recombination. Advanced maternal age seems to be a risk factor (42). It is not known whether the 47,XXY karyotype is slightly over-represented among spontaneous abortions and stillbirths. However, in contrast to many other aneuploidies, Klinefelter syndrome seems to be only a minor risk factor and most pregnancies result in a live-birth.

Patients with Klinefelter syndrome are usually inconspicuous until puberty. Interestingly the velocity of height gain can be increased in the pre-pubertal years. Men with Klinefelter syndrome tend to be tall (mean adult height is about the 80th percentile for the population) and to have relatively long legs compared to their overall height.

In most patients, early stages of puberty proceed normally. Post-pubertally the syndrome is characterized by the small testes with firm consistency remaining in the range of 1 – 4 ml. Most patients with Klinefelter syndrome are infertile because of azoospermia. Testicular histopathology in adult men with Klinefelter syndrome displays various patterns. Classically, germ cell aplasia, total tubular atrophy or hyalinizing fibrosis and relative hyperplasia of Leydig cells are found. However, in some adult Klinefelter patients, foci of spermatogenesis up to the stage of mature testicular sperm can be detected (46, see below).

The degree of virilization varies widely. In early puberty, LH and FSH increase while serum levels of testosterone plateaus at or just below the lower limit of the normal range. After the age of 25, about 80% of patients have reduced serum testosterone levels and complain of decreasing libido and potency. On average serum estradiol levels are high normal or may exceed the normal range. LH and especially FSH levels are exceedingly high, serum levels of inhibin B are very low or undetectable (47, 48).

During puberty bilateral painless gynecomastia of varying degrees develops in about half of the patients. In a large XXXXXXX study covering 696 men with Klinefelter syndrome no evidence for a substantial increase in the overall cancer rate was found (49). The risk of developing mammary carcinoma may be increased relative to normal men but remains a rare occurrence and routine surveillances is not recommended (49, 50). A significantly increased risk was found for the rare mediastinal malignant germ cell tumors, which occur preferentially at the age of 14 to 29 years (49).

The intelligence of Klinefelter patients is very variable. The group difference between boys with Klinefelter syndrome and controls amounts to 11 points in full scale IQ (92 versus 103), and deficits are observed primarily in verbal and cognitive abilities (51). Some of the young patients attract attention because of learning difficulties and school problems. In general, they fail to reach the level of achievement or professional expectations of their families (52, 53). Compared with their classmates certain abnormal physical and psychological characteristics of the patients become obvious and they may become socially alienated. Higher-grade aneuploidy of the sex-chromosomes (48,XXXY, 48,XXYY and 49,XXXXY) is associated with mild mental retardation. Klinefelter patients with chromosome mosaics (47,XXY/46,XY) may show very few clinical symptoms.

In general, the variability of the clinical features in patients with Klinefelter syndrome is related to degree of androgenisation, which, in turn, depends on the pattern of inactivation of one copy of the androgen receptor gene. In particular, a significant genotype-phenotype association exists in Klinefelter patients and androgen effects on appearance and social characteristics are modulated by the androgen receptor CAGn polymorphism (54).

Regarding infertility treatment, it should be noted that in rare cases sperm could be found in the ejaculate and, exceptionally, spontaneous paternity has been described (55). The rate of diploidy of sperm as well as disomy for gonosomes and autosomes seems to be increased in patients with Klinefelter syndrome, however, the majority of sperm appear to be normal (56 – 59). Preliminary data suggest that in about 20 – 50 percent of patients with Klinefelter syndrome it may be possible to retrieve sperm by TESE (46, 60, 61). Several pregnancies have been achieved with testicular sperm used for ISCI (62). The embryos show normal or aneuploid karyotypes which can be identified by preimplantation or prenatal diagnosis (62). Interestingly, the birth of normal children conceived by assisted reproductive techniques seems to be rule (62), suggesting that the few sperm which can be found in about 50% of patients with Klinefelter syndrome possibly derive from the clonal expansion of spermatogonia with normal karyotype.

When testosterone serum levels are reduced, substitution with testosterone is necessary. To avoid symptoms of androgen deficiency hormone replacement therapy should be initiated as early as needed. In particular, Nielsen et al. (63) showed that early testosterone replacement not only relieves biological symptoms such as anemia, osteoporosis, muscular weakness and impotence, but also leads to better social adjustment and integration. Testosterone replacement must be considered a lifelong therapy in Klinefelter patients to assure quality of life. Usually gynecomastia is not influenced by hormone therapy. If it disturbs the patient, a plastic surgeon experienced in cosmetic breast surgery could perform a mastectomy.

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