Fibrotic hepatic schistosomiasis caused by S. mansoni usually develops in around 5–15 years, while it can take less time for S. japonicum. Symptoms may include:
Esophageal varices (can cause life-threatening esophageal variceal bleed)
Ascites (end-stage)
Caput medusae
Enlarged spleen and liver
Complications may include:
Neuroschistosomiasis due to portosystemic anastomoses from portal hypertension
Pulmonary Schistosomiasis due to portosystemic anastomoses from portal hypertension

Pulmonary schistosomiasis
Portal hypertension secondary to hepatosplenic schistosomiasis can cause vessel connections between the portal (liver and gut) circulation and systemic circulation to develop, which creates a pathway for the eggs and worms to travel to the lungs. The eggs can be deposited around the alveolar capillary beds and causes granulomatous inflammation of the pulmonary arterioles followed by fibrosis. This leads to high blood pressure in the pulmonary circulation system (pulmonary hypertension), increased pressure in the right heart, enlargement of the pulmonary artery and right atria, and thickening of the right ventricular wall.Symptoms of pulmonary hypertension may include:

Shortness of breath
Chest pain
Feeling tired
Fainting during physical exertion

Urogenital schistosomiasis
The worms of S. haematobium migrate to the veins around the bladder and ureters where they reproduce. S. haematobium can produce up to 3000 eggs per day, these eggs migrate from the veins to the bladder and ureter lumens, but up to 50 percent of them can become trapped in the surrounding tissues causing granulomatous inflammation, polyps formation, and ulceration of bladder, ureter, and genital tract tissues. This can lead to blood in the urine 10 to 12 weeks after infection. Over time, fibrosis can lead to obstruction of the urinary tract, hydronephrosis, and kidney failure.
Methylenetetrahydrofolate reductase deficiency is the most common genetic cause of elevated serum levels of homocysteine (hyperhomocysteinemia). It is caused by genetic defects in MTHFR, which is an important enzyme in the methyl cycle.Common variants of MTHFR deficiency are asymptomatic and have only minor effects on disease risk. Severe variants (from nonsense mutations) are vanishingly rare. Symptoms
The common MTHFR deficiencies are usually asymptomatic, although the 677T variant can cause a mildly increased risk of some diseases. For individuals homozygous in the 677T variant, there is a mildly elevated risk of thromboembolism (odds ratio 1.2), and stroke (odds ratio 1.26). There is also an elevated risk of neural tube defects among children of individuals with the C677T polymorphism (odds ratio 1.38).For cardiovascular risk, common MTHFR deficiencies were once thought to be associated but meta-analyses indicate that correlation this was an artifact of publication bias. Causes
MTHFR is the rate-limiting enzyme in the methyl cycle, which includes the conversion of homocysteine into methionine. Defects in variants of MTHFR can therefore lead to hyperhomocysteinemia.There are two common variants of MTHFR deficiency. In the more significant of the two, the individual is homozygous for the 677T polymorphism. This variant in particular is the most common genetic cause of hyperhomocysteinemia. The resulting enzyme is thermolabile and in homozygotes, enzymatic activity is depressed to 35% of its usual level. The second variant is a milder one, caused by a homologous 1298C polymorphism. This leads to 68% of the control values of enzyme activity, and it normally does not lead to low serum folate.